Introduction to Neuroscience, Part 3

History of Studying the Amygdala

1819 - Brudach named a region in the medial temporal lobe the amygdala based on its resemble to an almond 1888 - Brown and Schaffer found that monkeys became very tame and fearless after removal of bilateral temporal lobes ∙collections of symptoms associated with removal of the temporal lobes is called Kluver-Bucy syndrome ∙characteristic changes are absence of fear and anger, hypermetamorphosis (Excessive examination of objects), hyperorality (fixation with putting objects in mouth), hypersexuality, and changes in dietary habits ∙bilateral removal of only the amygdala causes disruption of social hierarchy, flat affect, and lack of aggression ∙if dominant monkey has bilateral amygdala removal, it becomes the lowest ranked monkey and an outcast

Roles of the ACC and PFC in Cognitive Control

3 different types of conflict that initiate activity in the anterior cingulated cortex (ACC) ∙response overriding is like the Stroop Task, where conflict is different response possibilities and you override the incorrect ones to prioritize one task module over another ∙Underdetermined responding happens when there is a conflict that has different ways of responding, like a stem completion →in a stem completion test, a subject is asked to completel a word after being given the first few letters, leaving them many options and conflict Error in speeded responses activates the ACC cognitive control tests using fMRI to measure the activity in the ACC show that these similar areas are activated during different types of conflict, providing support for the "conflict monitoring" hypothesis ∙graph shows varied responses from 4 variations of Stroop Task ∙"C" represents subject expecting congruent words, "I" indicates expecting incongruent words ∙"c" and "i" denote if the word was actually congruent or incongruent ∙C/i trials showed high ACC activity in response to shift from no conflict to conflict ∙in contrast, C/c trials are easy throughout and ACC activity is low ∙ACC activity is low for both I/i and I/c trials b/c they have been difficult the entire time High adjustment correlates with high ACC activation ∙for iI trials (all incongruent tets), there is no conflict and high adjustment corresponds to short rxn times ∙for post-error trials, high adjustment corresponds with long rxn times b/c errors induce ACC activation and we want to avoid making more mistakes

Memory

3 major types: Very short-term (immediate), short-term (aka working), and long-term memory

PFC and Executive Function

PFC is involved in the coordination of all of the other regions of the brain → executive function executive function is the ability to direct our cognitive resources to reach a goal it requires both working memory and cognitive control (suppression of irrelevant information and enhancement of relevant data) ∙we require this control to be able to pay attention to important information, but we also must be able to adapt to changing circumstances so that we can switch our attention, if, say, someone shouts fire in the library and we have to evacuate Sequencing and prioritizing information, shifting our actions when necessary, and the ability to monitor our actions and our progress are all important requirements for executive function

Brain MRIs of SCA cases

SCA6 can see major atrophy of cerebellum SCA3 can show major atrophy of pons AND cerebellum

Temporal vs. Spatial Resolution

temporal resolution is important for tasks where things can happen very rapidly spatial resolution is important to see what parts of the brain are creating a specific action

The "Error Likelihood" Theory of Cognitive Control

a horizontal line is shown to a subject, which turns into an arrow this image disappears and is followed by either an identical "go" arrow, or a conflicting "change" arrow the delay time b/w the first and second arrows is varied ∙short delay corresponds to few errors b/c the subject has no compared responses ∙when the delay time increases, there are more errors b/c the subject had more time to focus on the first arrow, creating more conflict color was added to this experiment to allow the subject to predict the difficulty of the test ∙white arrows were short delay and easier, while blue arrows were used for longer delay and thus the harder test ∙blue arrows represent a need for cognitive control ∙responses in the ACC changed depending on the 4 different conditions: Change vs. Go arrows, High vs. Low difficulty →ACC activity was highest w/ high/change arrows (long delay blue arrows that switched direction) →as anticipation of error increased, so did ACC activity and cognitive control in the error-likelihood model, ACC activation is more compatiable with "error likelihood" than conflict ∙it is conflict monitoring, taking the situation, or context, into account

Attention in the absence of top-down cues: Concept of saliency and how it can be computed: the Itti, Nieber, Koch model

a stimulus/cue that stands out over other stimuli/cues is said to be more salient than the surrounding stimuli/cues Itti, Niebur, Koch model = visual scene/stimuli → brain → different features → visual maps → salience map → eyes focus on the biggest salient part of scene

Cognitive Neurogenetics: A Clinical Application

a study investigating the effects of two Alzheimer's genetic risk factors on brain activity in young people ∙APOE-e4 - strongest risk factor - evidence of effects on brain activity in young people ∙CLU-C (also called APOJ) - a secondary risk factor identified by GWAS Shared properties ∙both are among a small group of proteins associated with brain lipoproteins ∙interact w/ a shared set of cell surface receptors ∙both promote neurite growth ∙elimination has a similar effect on Aβ accumulation in mice Our question: Do the risk alleles for APOE and CLE 9e4 and C have an additive effect on brain activity (common pathway)? ∙basically, more e4 or C alleles = higher risk score Approach: tested whether a combined APOE and CLU genotype variable (Risk score) predicted brain activity in young participants (college students) ∙fMRI task = MSIT decreased activity associated with increased genetic risk ∙higher risk score = less activity ∙medial temporal lobe, posterior cingulated, medial PFC

Flanker Test

a subject is asked to look at a series of arrows and indicate the direction that the center arrow is pointing (left or right) by pushing a matching button other arrows flank the middle arrow the test can be made easy, by having congruent arrows, flanking arrows that point in the same direction as the middle arrow the test can also be made difficult, by using incongruent arrows, flanking arrows that point in opposite direction Response time increases when incongruent arrows are used

The Error-Related Negativity

a subject is given a flanker test in which they respond with S or H, matching the central letter ∙the central letter is incongruent (flanked by different stimulus) the subject is supposed to respond S, but answers H, and realizes right away that they made a mistake Brain response is studied with EEG and compared to time of response Brain activity changes soon after the subject realizes that they made a mistake ∙there is more brain activity shortly after a mistake is made and an incorrect answer is given → this is error-related negativity (ERN) the ERN is localized to the medial frontal cortex, the part of the brain that is activated when an error is made errors mean that there needs to be a change to how the task modulators are activated b/c cognitive control failed ∙however, we do not want to rely on error to activate cognitive control, cognitive control should act earlier, i.e. when a conflict between task modules is detected

Why Multiple Mediation Modeling?

able to test mediation can incorporate multiple brain regions w/ different relationships to genotype and phenotype more rigorous (requires at least 3 relationships b/w at least 3 variables, instead of one relationship b/w 2 variables) Drawbacks: ∙requires some assumptions, including directionality of effect (gene→brain→cognition, and no other way) ∙requires large samples for sufficient power (difficult b/c brain imaging is expensive and takes a long time)

Working Memory

active maintenance of information that is relevant to the task you are performing is our working memory What is the neuronal mechanism in the brain that enables this memory to exist? ∙demonstrated by Goldman-Rakic ∙had monkeys look at a target area for a trigger through a period of delay where there was no stimulus reminding the monkey to continue looking at that area ∙this delay period is the key time we need to understand, when the monkeys were holding that information in their working memory ∙prefrontal neurons fired much more during this delay period than when the target area was given to the monkeys or after the trigger was shown, demonstrating that the PFC is responsible for the working memory during that delay period when the cue was kept "out of sight but in mind" ∙extending delay period from a few seconds to a few minutes forces the information to move into longer-term storage and is no longer held in the working memory ∙this temporally limited delay period is the key to understanding working memory Researchers wanted to know if there was a separation of spatial and object identification oriented working memory ∙found that monkeys have a dorsal/ventral pathway separation similar to what we saw w/ the posterior audiovisual pathways ∙information is not stored in these pathways, but this is where we get activation when information is pulled from different portions of the brain to be held in the working memory of the PFC ∙HOWEVER, does not hold true in humans brains ∙instead, we have similar bilateral activation for both spatial and identification tasks ∙the information that allows the subject to identify an image is held in the posterior extrastriate cortex, but that information is called up to the working memory in the PFC while performing this task, so we see activation in both areas ∙lack of dorsoventral separation may be b/c we have language w/ which we can describe and categorize what we see

Associative Learning

aka Pavlovian Conditioning we eventually learn to associate a neutral stimulus (i.e. a beep or tone) with another stimulus (i.e. food) to get a physiological response to the neutral stimulus itself associative learning can be applied to two specific models: ∙musculoskeletal responses, which happen in the cerebellum ∙emotional responses, which happen in the amygdala

Multifactorial inheritance

aka polygenic inheritance mutations in different genes Examples: Alzheimers, diabetes, obesity, cancer, arthritis, heart diseases

Deficits in Working Memory

damaged to the involved areas (via stroke/trauma) like frontal or parietal regions ∙frontal b/c the pre-frontal cortex is here ∙Parietal b/c Broca's area receives some projections from the parietal lobe Phenylketonuria will also lead to deficits ∙PKU is a disease that reflects an inability to metabolize phenylalanine to tyrosine ∙phenylalanine in high quantities is toxic to the brain, so accumulation will lead to mental retardation ∙equally important, if phenylalanine is not converted to tyrosine, dopamine will not be formed →Synthesis pathway = Tyrosine → L-DOPA → Dopamine →as dopamine is implicated in some forms of memory, especially in the frontal lobe, PKU will present with working memory deficits ∙Solution = remove phenylalanine from diet

Aphasias

defined as an acquired primary impairment in all different aspects of language (expression, comprehension, and manipulation of sounds, meaning, syntax and lexicon) in the L hemisphere are usually observed following L hemisphere stroke or injury anomia = difficulty retrieving words ∙characteristic of all patients w/ phasia aphasias are further categorized into anterior and posterior aphasia (of the L temporal hemisphere) based on degree of fluency, grammatical deficit, articulation and paraphasias ∙distinctions are not very clear cut Anterior aphasias are characterized by non-fluent speech ∙limited output and short phrases usually, with nouns and verbs only ∙Agrammatism, or the deletion of syntactical words, is typically observed in anterior aphasias ∙Articulatory problems, distorted production of phoneme of a word are also common in anterior aphasias b/c the lesion may be near the motor strip Posterior aphasia are characterized by fluent speech: normal output, grammar and phrase length, w/ some trouble w/ nouns and verbs ∙paragrammatism (not-as-obvious disordered use of syntactic words, is typical in posterior aphasias) ∙note the fluent speech to produce a whole sentence, w/ words reversed ∙Paraphagias are typically observed in posterior aphasias

Any addictive behavior depends on changes in electrical activity of specific brain regions

drugs of abuse alter the number of synapses and ion channels goal is to erase physiological memories that drugs of abuse produce to return to a physiological baseline

EEGs

electroencephalography = the recording of electric currents generated in the brain, by means of electrodes applied to the scalp, to the surface of the brain (intracranial), or placed within the substance of the brain (depth) Electroencephalogram (EEG) = a recording of the potentials on the scalp generated by currents emanating from the nerve cells in the brain EEGs are simple, fast and have good temporal resolution (milliseconds) ∙they have poor spatial resolution and cannot map beyond the level of neural maps (centimeters) pyramidal neurons orient radially and line up ∙if they are activated you get a current going to an electric field that you can pick up with the electrodes on the surface

Emotion

emotion is defined as a positive or negative mental state that is associated with a particular pattern of physiological activity it turns out that we cannot make decisions w/o emotions, as evidenced by people w/ frontal lobe damage ∙these patients cannot integrate emotions into their reasoning processes, and thus cannot make decisions emotion is different from mood, temperament and affect ∙mood is more long term, self-sustaining response that does not involve response to external stimuli ∙temperament is the tendency for a person to experience certain moods or emotions ∙affect is the outward expression of emotions

Juvenile HD

juvenile onset HD has rigidity rather than chorea seizures are common more widespread brain changes (Astrocytosis and neuronal loss can be seen in the cerebellum, hippocampus)

Why is attention necessary?

oftentimes we need to focus on a particular object, but when there are tons of stimuli coming at us, we need to somehow enhance the relevant stimulus information while suppressing the irrelevant information attention helps us do that by helping us allocate "resources" (perceptual and/or cognitive) to what we want to focus on

Testing Neural Mediation

pair-wise relationships are informative ∙however, they cannot test mediation the development of cognitive neurogenetics requires a different approach in order to combine all 3 data types and test mediation also, pair-wise relationships have reported seemingly conflicting results so far ∙some studies report increased brain activity associated with a particular genotype in one brain region, other studies report decreased brain activity with the same genotype

Visual Search: Serial and Pop-Out

pop-out visual search has an overall shorter reaction time and uses more "bottom-up" processing via the parietal lobe visual search has on overall longer reaction time and uses more "top-down" processing

Cognitive Neurogenetics: Clinical Potential

potential to prevent disease by treating neural markers of genetic risk before disease onset Alzheimer's is a prime example ∙known genetic risk factors (i.e. APOE-e4 and CLU-C) ∙genetic risk factors affect brain function in healthy people before disease onset ∙waiting until disease onset appears to be too late for treatment ∙some candidates for prevention (e.g. NSAIDs, exercise) →seem to have strongest effects in carriers of risk alleles) The big question: can treatment make high-risk young brains look more like low-risk young brains?

Theories on How Short-Term Memory Works

Alan Baddeley's Theory suggests that there is a chief controller (like a CEO) part of the brain that coordinates two sub-systems: storage and rehearsal ∙think of the storage sub-system as the part of your brain that literally allows you to hold information for a very temporary amount of time, while the rehearsal sub-system is another part of the brain that allows you to take the inform from that storage component and practice rehearsing it to eventually remember it Nelson Cowan's theory (apparently more correct) says that the brain consults areas responsible for long-term memory to help store the information ∙i.e. remembering a phone number by associating an area code with an area

Cognitive Neurogenetics

Central hypothesis: specific properties of the brain mediate relationships b/w genes and cognition genes change our behaviors, but they must do this through specific pathways ∙basically, neural mediation via genes

Factors that Obstruct the Development of Declarative Memory

E4 allele in the APOE gene, a major risk for Alzheimer's Methionine point-mutation in BDNF gene - correlated w/ decreased hippocampal size

Genetics of Alzheimer's Disease

Familial Alzheimer's disease ∙amyloid precursor gene (chromosome 21) ∙presenilin gene (chromosome 14) ∙presenilin gene 2 (chromosome 1) autosomal dominant disease that affects the processing of amyloid protein leading to amyloid plaques early onset (age 30-60)

Non Polyglutamine Diseases

Fragile X mental retardation 1 (FMR1) Fragile XE mental retardation (FMR2) Friedreich's ataxia (FRDA) Spinocerebellar ataxia (types 8 and 12)

Toxic Theories

Gain of function effect ∙new function of the mutated protein ∙accumulation of mutant protein →proteins tend to form secondary structures (i.e. beta sheets) so that they cannot be removed by neurons and they accumulate Dominant negative ∙the mutant allele interferes with the remaining allele

PolyQ Diseases

Huntington's disease Spinocerebellar ataxia (types 1, 2, 3, 6, 7, 17) spinobulbar muscular atrophy (Kennedy disease) Dentatorubropallidoluysian atrophy (DRPLA)

Internal vs. External Feedback

Internal feedback = notable change in brain activity (i.e. ERN) when the subject realizes that they have made an error ∙if the subject did not realize that they made an error, there would be no change in brain activity External feedback - when you make a mistake and someone tells you that you made a mistake ∙a negative signal, or ERN, is also generated with external feedback

LTP and Dopamine Neurons

LTP is one of the foundations of learning and memory processes LTP of AMPAR is present in dopaminergic sites

Factors that Facilitate the Development of Declarative Memory

Long-Term Potentiation ∙neurons that fire together, wire together ∙newly formed connections will enhance learning ability E2/E3 alleles in the APOE gene Valine point-mutation in the BDNF gene Estrogens

Spatial Attention

Spatial attention is when you're told to focus your attention around a particular area or region ∙"look over there!" ∙there is something that occurs that increases the contrast in that particular region ∙results in an increase in the target object's perceived contrast and/or decrease in the contrast of the unattended region

Amygdala is connected to many subcortical structures w/ different functions

Striatum - motor response, reward, goal-direct behavior Bed nucleus of the Stria Terminalis - anxiety Olfactory system - olfaction basal forebrain - aggression and motivation thalamus - sensory and memory hypothalamus - neuroendocrine, autonomic and visceral functions, defensive reactions Brain stem - physiological changes include autonomic, respiratory, and cardiovascular functions

Interpreting Our Emotions

The James-Lange Theory posits that emotional context directly affects our physiology and behavior, and our mind interprets these specific patterns of behavior associated with each emotion as evidence that something in the environment is causing these responses, and from that generates an emotion ∙basically, physical events cause physical states, and interpretation of these physical states causes a mental event, aka emotion the Facial-Feedback Hypothesis proposes that what your body does causes your mind to experience different physiological states ∙theory is Cartesian, suggesting that mind and body are distinct phenomenon, and generally bogus facial-beedback does occur in a gross, general way, but overall James and Lange are way off ∙some problems are theory are that emotions are instantaneous but physiological changes lag, people who are not as sensitive to changes in the body still experience emotion, and finally that James and Lange require specific ANS changes w/ an emotion, which is not always the case the Cannon-Bard Theory stipulates that emotional events cause both physiological and behavioral changes, as well as subjective feelings directly ∙first group to talk about brain's role in emotion, stating that the hypothalamus generates basic emotional responses and sends output to the cortex that generates emotional feelings ∙findings were substantiated by studies on decorticated animals that showed integrated emotional responses ∙problem: they didn't grasp how important intepretation was Schachter-Singer Theory states that we experience undifferentiated ANS arousal, and we interpret this change in arousal as separate emotions on the basis of our current context ∙injected patients with adrenaline, told half of them, and then put them in room with either grumpy or fun human ∙discovered that subjects who were w/ grumpy and did not know they had adrenaline were angry, while others understood body state due to adrenaline ∙this lead to the idea that most emotional feeling states can be quantified, and that context is what dictates whether changes in ANS arousal are interpreted as positive or negative

The Neural Correlate of Conflict: The N2

The N2 is the component of EEG that correlates to conflict the same mechanism demanding cognitive control is used if an error is made or if there is conflict N2 and ERN have the same neural locus (where they come from) in the medial frontal cortex, indicating that conflict monitoring and response to error come from the same circuitry makes sense, b/c both conflict monitoring and error response require increased cognitive control

The "Predicted Response Outcome" Model

The Predicted Response Outcome model (PRO) of ACC function reinterprets error effects in the medial prefrontal cortex as unexpected outcomes neurons can adjust their signaling based on a learned prediction of both the probability and timing of various possible outcomes of an action if that action actually occurs, the prediction signals are inhibited activity is highest when an expected outcome does not occur the medial prefrontal cortex signals when there is a surprise non-occurrence of a predicted outcome PRO model can account for the "unexpected outcome" data

Non-Declarative Memory

all forms of non-declarative memory are implicit Procedural memory refers to the memory of how to do things, like motor/cognitive skills and habits ∙occurs in the basal ganglia, pre-motor cortex, and cerebellum ∙if any of these areas is damaged, big problems occur with procedural memory ∙damage to the basal ganglia (i.e. Parkinson's or Huntington's) will lead to deficits in learning new skills/habits Priming is a form of learning that involves improvement in a reponse to an object after being primed/acquainted with a related item beforehand ∙basically, if you are shown a picture of a kitten, you will have an increased response (perhaps in the form of quicker identification) to another picture of a kitten (identity priming), a picture of a mitten (phonological priming) and a picture of a puppy (semantic priming) ∙the neocortex is responsible for these long-term memories - i.e. visual cortical areas are responsible for visually-related priming →damage to these cortical areas will lead to deficits in priming

Fear circuitry and conditioning

amygdala is highly involved in fear responses and fear conditioning fear has two distinct neural pathways: thalamic pathway and cortical pathway ∙in both pathways, the amygdala acts on the periventricular nucleus to affect endocrine function, the central gray area to elicit freezing behavior and the lateral hypothalamus for sympathetic activation thalamic pathway is fast, responsible for immediate detection and responses to danger ∙sensory information passes through the thalamus then directly to the amygdala and to the brain stem to elicit an immediate response the cortical pathway is longer, involves processing and assessing danger to mediate the correct response ∙sensory information passes through the thalamus to various sensory and association cortices, as well as the hippocampus ∙the signals from the cortex then act on the amygdala to mediate the initial response to become an appropriate response based on the amount and context of the danger fear conditioning occurs via classical Pavlovian conditioning (i.e. dogs salivating in response to bells) ∙essentially a beep (conditioned stimulus) is played at the same time as the floor of the cage is shocked (unconditioned stimulus) ∙both sensory systems feed into the amygdala at the same time and eventually stimulate plasticity by the principal that neurons that fire together wire together ∙this causes the conditioned stimulus to elicit the same response as being shocked without the actual shock Fear processing studies have been performed in nonhuman primates by using excitotoxic lesion studies ∙amygdala neurons were pharmacologically overstimulated, causing them to become temporarily dysfunctional ∙these lesions caused several effects, including reduced fear and aggression, increased submission, excess manual and oral examination, blunted emotional response to a snake, and decreased defensive freezing in response to an intruder facial expressions have been shown to elicit specific responses and emotions depending on the particular expression ∙emotionally significant expressions elicit specific responses and emoions depending on the particular expression ∙emotionally significant facial expressions activate the amygdala much more than emotionally neutral faces ∙of the emotional expressions, those showing fear activated the amygdala more than all of the others

Amygdala and Lateral Nucleus

amygdala receives inputs via the lateral nucleus from a large range of sensory areas, however, the only direct input is from the rhinal cortex all sensory information from the cortex must feed into the rhinal areas before it can reach the amygdala overall, amygdala has significantly more inputs that outputs information enters the lateral nucleus, and then is passed around the various nuclei, eventually exiting mostly via the central nucleus and also the basal nucleus to the orbitofrontal cortex

Autosomal Dominant Cerebellar Ataxias (ADCA)

ataxia = abnormal movement seen in the limbs and sometimes in the trunk ∙i.e. ataxic speech or ataxic gate Nystagmus - rapid, involuntary, side-to-side eye movement affects mainly the cerebellum, brain stem and spinal cord ∙creates lack of coordination repeated CAG mutation is Ataxin-1

Effects of attention at the neuronal level: Amplitude Modulation and Decorrelations

attention does not just modulate response amplitudes, it also decorrelates responses among neurons neurons that like the attended stimulus respond more independently so that total information transmitted is increased, while redundancy is decreased

Similarities and differences b/w cognitive control and attention: Where and how to modulate along the cortical processing hierarchy

attention reduces interference b/w two different stimuli by modulating response in the sensory processing hierarchy from retina to cortex, proceeding from simple to complex features ∙attention modulations are done at the sensory level Cognitive control deals w/ interference at the level of task modules, which is the top level of hierarchy ∙happens in the prefrontal cortex ∙the prefrontal cortex is much larger in humans as compared to other animals, which allows for increased cognitive control There are different ways to respond to the same stimulus, like reading a word vs. seeing a color, and different task modules can be activated ∙however, there is only one correct response, and this is determined by cognitive control in the prefrontal area When there are conflicting answers, or several task modules responding to the same stimuli, we need cognitive control Interference occurs when these task modules produces conflicting responses for a given sensory input ∙allows us to have flexibility in response to stimuli, as our response can be modulated depending on what is necessary through inhibition and choice by the prefrontal cortex Cognitive control takes effort to switch b/w tasks (Activating the relevant task and suppressing the conflicting task in the prefrontal cortex) so we do not want to use it unless it is necessary ∙the problem is when should we modulate activity with cognitive control? ∙example used was Stroop test → both the display color and the word provide input to task module and the task can be either color naming or word naming ∙for color naming, you connect it to the display color units ∙for word naming, you need it to the word units cognitive control is often activated after the subject makes an initial error in their response, showing control is needed when we make errors ∙if we are making errors, we know that we need more control

Huntington's Disease

autosomal dominantly inherited disease slowly progressing neurodegenerative disease ∙15-20 year duration adult onset, generally >39 CAG repeats confers disease ∙age of onset and rate of progression are CAG length-dependent common to see suicide w/ these patients, because they are very depressed, even when taking antidepressants

Neural Basis of Emotion

brain structures associated with emotion are not totally clear, but we talk about the limbic system early on, it was shown that monkeys w/ excised temporal lobes had out of control emotions Papez then coined the term limbic system and theorized that the circuits for emotional responses resided in the medial wall of the forebrain and included the thalamus, hypothalamus and cingulated gyrus (b/c they all had monosynaptic connects to the HT ∙also theorized that the limbic system was divided into a thought stream (thalamus, sensory neocortex, cingulated gyrus) and a feeling streem (Thalamus, HT, cingulated gyrus) this lead to MacLean's "visceral brain" that included evolutionarily old structures essential to survival: thalamus, HT, cingulated gyrus, temporal cortices, BG, amygdala, orbitofrontal cortex, and hippocampus ∙believed hippocampus was center of emotion Ledoux decided to look at structures involved in particular emotions (specifically fear and thalamus, amygdala and sensory cortex) ∙states there is a low road that rapidly sends rough and grainy information from thalamus straight to the amygdala to immediately alert ANS →in fear, this results in increased HR, BP and RR, etc. ∙there is also a slower, more precise high road that simultaneously sends information to the visual and auditory cortex for interpretation, then re-routes to the amygdala to refine the response ∙From this we can say that the amygdala: →rapidly codes for valence (how good or bad something is) →plays a role in a variety of emotions, mostly fear

Characteristics of Glutamine (polyQ) diseases

characterized by expansion of CAG (glutamine) repeats in various genes triplet repeat expansion occurs w/in the coding DNA region (polyQ) or more rarely in introns (non-polyQ) selective vulnerability of specific neuronal populations ∙disease effects depend on location of affected neurons

Pathology of Huntington's Disease

characterized by loss of cortex and striatum ∙the cortex undergoes atrophy ∙the caudate shrinks the ventricles are really enlarged notice the pale color of the cortex: means there is more astrogliosis going on than in normal brain Targeted: spiny projection neurons that contain GABA Spared: aspiny interneurons (contain ACh) also see deposition of aggregates

Cognitive Control

cognitive control is how the brain processes specific stimuli in relation to their current context, and guides perceptual and motor action the task center determines how you respond to a certain stimulus what action you take is dependent on the context of the stimuli ∙i.e. answering the phone at your house vs. at a friend's house

Conflict Monitoring Theory of Cognitive Control

cognitive control is needed when there is conflict b/w task modules, like in the Stroop test, to prevent errors the conflict monitoring hypothesis of cognitive control states that "errors occur when the wrong task module wins out, so to prevent error, we need to monitor for conflicting activation" there is a cyclical interaction b/w control and conflict ∙control serves to reduce conflict, but if conflict occurs we need more control Response conflict is the need for cognitive control and is measured as energy, or activation, in the response layer of the brain ∙if there is one possible response, or no conflict, minimal energy is used and control is not needed ∙if conflict exists, there is a lot of brain activity and control is necessary ∙with more conflict there is more activation in the response layer and more control is required to make sure that the correct response is selected and the incorrect response is suppressed Cognitive control tests administered w/ fMRI show in more detail what area of the brain is activated when there is interference, or what area is modulated by conflict ∙the same mechanism is used for conflict monitoring and error response

Interactions of sensory and prefrontal modulations in cognitive control

cognitive control suppresses task-irrelevant circuits and emphasizes other task modules in addition to restraining our cognitive control of task modules, we can also suppress lower brain level sensory circuits, showing that there is some control at this basic level to modulation our reactions comparison of modulation by subjects in the Stoop test indicates sensory modulation in cognitive control ∙on average, the color areas has stronger responses and the word area has lower responses ∙at the sensory level there is modulation that fits w/in cognitive control, as there is decreased response to words, and increased response to color, in order to do the task better the brain changes the way it sees the world to help you do the task better ∙implements specific tasks at both higher cognitive levels, and lower basic sensory levels there is variability across subjects as to how well they can deploy cognitive control, as indicated by task switching ∙subjects were shown a face, w/ word written on top of face ∙red boxes indicated the subject should remember the gender of the face, and blue boxes meant that the subject should remember the word ∙when the color of boxes switched from red to blue, the subject had to suppress the face input and activate the word input ∙subjects had more difficulty if the preceding image was the opposite task, indicating that it is harder to switch b/w tasks

Are drugs of abuse capable of producing LTP?

even a single injection of cocaine can induce memory for around a week repeated cocaine has a similar effect cocaine self-administration has an entirely different effect ∙lasts 3 months for a rat (~5 years for human) from beginning of abstinence in comparison, with reward-related learning, LTP lasts only until day 3 ∙once the rats learn it on day 4, there is no longer LTP

Similarities and Differences b/w Spatial and Featural Attention

featural attention is a global effect, meaning that if the feature you are focusing on is a red hat, it could be anywhere it your visual field (not just in one area, as is the case w/ spatial attention), so all the neurons that code for that one feature experience an increase in response Spatial attention is very localized and if you are told to look to one side, you get suppression in other regions in your hemispheres/hemifields in featural attention, your whole brain is affected and the neurons are modulated according to the feature to which you are attending

Featural Attention

featural attention is looking for a red soda can or a blue shirt, etc. results in attention on a particular trait, i.e. a color, shape, or orientation

Posner's Cost-Benefit Paradigm

for this, the subject is performing a task where there is a cross in the center, a delay period, and then after a while, a spot is projected on either the right or left side and the subject has to respond to which side the spot was on ∙more of a reaction time task than anything else however, attention was tested when, instead of a cross at the center, there was an arrow that pointed in a direction (i.e. right) ∙then, for "valid" trials, after a delay, a spot was projected on the right (side which the arrow pointed), while for "invalid" trials, after a delay, a spot was projected on the left ∙in valid test conditions, the reaction time was faster, while invalid conditions had a slower reaction time this is where the cost-benefit paradigm arose: if you give a cue to focus in a particular area, you're faster at detecting change in that region, but slower at detecting change that occurs outside region take is that that selective attention comes with a cost: whatever you focus on takes away your ability to notice objects outside of the area on which you were focusing, but increases your ability to notice objects inside the area on which you are focusing

Neuronal basis of attentional modulations: Involvement of frontal and parietal areas, different roles "bottom-up, stimulus-driven" vs. "top-down, task-driven" attention

frontal and parietal area involvement: both areas showed cue-triggered delay activity in a task where subjects had to attend to a particular location ∙parietal area detects "bottom-up" pop-out targets first, while the frontal area detects "top-down" targets first ∙damage to the frontoparietal areas can lead to spatial neglect "Bottom-up, stimulus-driven" attention: explains about 50% of inter-subject variability "Top-down, task-driven" attention: shows how a task influences where the eyes look and focus on, therefore, saliency also depends on the task we must complete

fMRI

functional magnetic resonance imaging another method that can be used to visualize brain activity during cognitive control and conflict fMRI has high spatial resolution (millimeters) which provides us with information about where in 3D space things are occurring, but poor temporal resolution (seconds)

Approaches to Combining Data Types

genetic data, cognitive phenotype data and neural data behavioral genetics = looking at genetic variations and how they affect behavior Neurogenetics = association of variant in genotype to variation in brain structure/function Cognitive neuroscience = comparison of brain activity/structure and behavior

Hemineglect

hemineglect is a deficit in attention to and awareness of one side of space

Amygdala interacts w/ several different cortical areas

hippocampus - context and memory orbitofrontal cortex - goal directed behavior medial prefrontal dorstolateral prefrontal insular cortex - HR, taste, and gustatory responses cingulated cortex temporal cortex - visual processing

Non-Associative Learning

involves habituation and dishabituation in habituation, you basically get used to receiving the same stimulus over and over dishabituation is the process of getting re-sensitized to the stimulus after being presented with a strong stimulus non-associative learning is not confined to a specific region of the brain, but rather occurs via synaptic modification

Amygdala

humans care more about losses: a negative event w/ same absolute value as a positive event is more significant Prospect Theory is the idea that subjective experiences of emotion are different than objective things that happen in the world 2 components of emotional judgment: ∙avoiding losses matters more than acquiring gains ∙as losses or gains increase in magnitude, any loss/gain increment means less this theory highlights the framing effect in explaining scenarios, and how reactions vary individuals w/ damaged amygdalae do not have fear and cannot recognize fear in others ∙empathy is the basic process of mapping one's own experiences onto the experiences others are having, and it relies on the amygdala

Symptoms of Huntington's Disease

hyperkinesia (Excessive motor activity) ∙symptoms include involuntary movements (dyskinesia), chorea (jerky movements of limbs and orofacial structures) decreased muscle tone dementia mood disturbances

Strength and Efficiency in Parallel

increased AND decreased activity in separate regions (positive and negative path coefficients) associated with MSIT and IQ performance

Long-Term Memory

lifetime Function: long-term storage/usage of memory Capacity: huge Types/Location: ∙Declarative Memory System: MTL (Medial Temporal Lobe structures like the hippocampus, entorhinal cortex, perirhinal cortex, and structures connected to the MTL like the fornix and mammillary bodies →this system includes recollection of both facts and events, and encompasses both explicit and implicit forms of memory ∙Non-Declarative Memory System: ONLY IMPLICIT (subconscious) memory →procedural memory system (basal ganglia, pre-motor cortex, motor cortex, cerebellum) → skills, habits, and grammar →Priming (neocortex) →Associative Learning →→→musculoskeletal responses (cerebellum) →→→emotional responses (amygdala) →Non-Associative Learning (takes place at level of synapses) Note: Priming, associative learning and non-associative learning are not really system, but instead FORMS of learning

Paraphasias

literal paraphasia is when one phoneme is substituted for another → the correct production of an incorrect phoneme ∙i.e. "I lotused (noticed) a funny thing" ∙literal paraphasias are observed in both fluent and non-fluent aphasias Verbal paraphasia is the substitution of a real word for another real word ∙can be further characterized into 3 phenomena ∙Semantic paraphasia (observed in both fluent and non-fluent aphasia) is when the substituted word is related in meaning to the intended word, i.e. synonyms or similar words ∙Neologism is the production of a nonsense word so far removed from the intended word that one cannot determine the target word ∙Jargon is the substitution of a completely unrelated word or phrase both neologism and jargon are more commonly observed in fluent aphasias

Feature Similarity Gain Model of Attention

main model through which brain pays attention to an object ∙the effect of attention at a neuronal level this model states that attention changes the strength of neurons depending on the similarity between the attended stimulus feature and the neuron's preferred feature ∙basically, there is an up-modulation in the activity of neurons that prefer the attended features and down-modulations in the activity of neurons that do not prefer the attended feature

Dopamine and PFC

mechanistically, dopamine release facilitates the increased firing of PFC neurons during the delay period the level of dopamine has to be closely controlled for optimal PFC function working memory is strongly affected in kids with ADHD and adults with schizophrenia, and both conditions are treated with dopamingeric medications

Very Short-Term Memory

milliseconds-seconds Function: sensory register, which refers to the instatneous memory that comes through your eyes and ears before your brain is even able to process it Storage capacity: LARGE Types/Location: ∙iconic memory (located in Low-level VISUAL circuits) → i.e. briefly seeing a sheet of numbers and being asked to recall it a few seconds later ∙echoic memory (located in low-level AUDITORY circuits) → replaying or echoing in your head what someone just said to you

Fragile X Mental Retardation 1

mutation in X chromosome CGG repeat (non polyQ) gene undergoes hypermethylation resulting in lack of protein ∙there is very little RNA produced, and in the end, this patient exhibits abnormal dendritic development causes impaired cognitive and reproductive development

DRN is a major input to VTA

neurons in the dorsal raphe nucleus are the strongest input to the VTA electrical stimulation of the DRN is rewarding but there are many cell types ∙dopamine activation, but not dopamine cell body is rewarding ∙Rewarding aspect seems mediated by glutamate inputs which excite DA neurons ∙DRN serotonin cell bodies are NOT rewarding ∙Non-serotonin DRN output is rewarding, and they also project primarily to the VTA

Friedreich's Ataxia

recessive located on chromosome on 9Q onset can be very early in life repeat is GAA Frataxin gene codes for mitochondrial protein that regulates iron flow ∙impairment causes build-up of iron of mitochondria Symptoms include ∙muscle weakness (arms and legs) ∙loss of coordination ∙vision and hearing impairment ∙slurred speech ∙diabetes ∙heart disorders Can see some problems with dorsal root ganglia, atrophy in the superior vermis and posterior lobes of cerebellum

Late-Onset Alzheimer's Disease

related to apolipoprotein E gene (chromosome 19) ∙involves cholesterol transport and metabolism three alleles ApoE ε2, ApoE ε3, and ApoE ε4 ∙risk factor (not definite cause) ∙if you have problem w/ ε4 you most likely have the disease

Short-Term Memory

seconds - hours Function: Keeping info in your mind ∙key here is you must be rehearsing or actively paying attention to it Capacity: limited Types/location: ∙Executive/attentional (prefrontal cortex, especially dorsolateral PFC aka BA 46) ∙Storage (tonotopic organization, i.e. memory for phonology/word sounds will be located in left inferior parietal lobe, memory for visual word forms located in inferior temporal lobe which is where ventral visual stream starts) ∙Rehearsal (pre-motor cortex & Broca's area)

Social Behavior

social behavior is a complex system that involves the fronto-temporal network the cortex receives a sensory stimulus such as a slap or bark that then projects to the lateral nucleus of the amygdala ∙this activates the normal amygdala responses to effect endocrine and autonomic function ∙the basal nucleus of the amygdala also projects to the orbitofrontal cortex in order to analyze the context and determine the proper response ∙the orbitofrontal cortex then organizes the response to stimulate the fight or flight response or other appropriate responses Amygdala lesions can cause a major disruption of social hierarchy and behavior ∙bilateral ablation has been shown to decrease social interactions in lab and natural settings ∙neurotoxic lesions cause increased interactions due to reduced fear and aggression →neurotoxic lesions also cause decreased social affliation and increased exploration and the effects tend to be less severe than ablation amygdala lesions that occur during infancy have a significant impact on social behaviors ∙at 6 months, the time spent in social contact is significantly reduced compared to normal, w/ lesions to the amygdala or temporal cortex ∙however, at 4-5 years, the social contact w/ lesions to the temporal lobe increases to almost normal, but with a lesion to the amygdala, the level of social contact remains low ∙there is also a significant decrease in social contact when the amygdala lesion occurs in a neonate as compared to occurring in an adult

Patient awareness of deficits

some patients can be aware of the changes in their behavior and the errors that they are making these disorders are on a spectrum, so some may be unaware as well the size of the lesion is very important in determining where on this spectrum an individual patient falls

Building a Gene-Brain-Cognition Model

start with a gene, in this case COMT ∙COMT gene codes for an enzyme that deactivates catecholamines in the synaptic cleft ∙there is one particular sequence where if there is MET instead of VAL, the enzyme works much slower → means that more dopamine is available ∙this is important, b/c dopamine is needed for higher degrees of mental function, and there is no re-uptake in the PFC so this is one of the major determinants of dopamine availability there have been conflicting results ∙in general COMT MET allele is associated with better cognitive function, BUT some people report that this improved function is associated with increased activity (recruitment strength) and some report that it is associated with decreased activity (neural efficiency) the cognitive part of the model is cognitive control ∙ability to tell attention what to pay attention to ∙used the MSIT task b/c it is a well-validated measure of cognitive control →designed for use w/ fMRI, which is important, b/c a lot of brain studies are not →reliably recruits a consistent set of prefrontal brain regions →good predictor of general intelligence and IG b/c cognitive control supports IQ performance the regional activation associated with the MSIT ∙SFG, ACC, MGF, and IFG

The Spotlight Theory of Attention and Experimental Support

states that when we look at a scene, there are certain objects that pop out to use that our eyes move to first McMains & Somers (2004) - showed we can have multiple spotlights of attention Muller & Hubner (2002) - showed that we can have spotlight of attention with complex shapes, i.e. a donut shape

The Simon Task

subject is shown a series of slides w/ 2 boxes in each slide, one of the boxes will be colored either red or green for red boxes, the subject responds with their left finger, and for green boxes, the subject responds with their right finger cognitive control is tested b/c we have different ways of responding, by what color is used and by which box (left or right) is filled ∙the subject responds faster when the color matches the sidedness of the finger used to respond to that color ∙the conflict is b/w where the stimulus appears and how you are supposed to respond to that stimulus, or interference at the level of response selection

Stroop Test

subject is shown a series of words and asked to name the color of the ink of each word in the control trial, congruent words are used (words that are not associated with a specific color) in the Stroop Trial, incongruent words are used (words that are names of colors written in different colored ink) In the Stroop trial, there is interference at the stimulus level ∙when incongruent words are used, the reader has to suppress the automatic reading response of the brain and only pay attention to the color of the ink, not the meaning of the word Cognitive control is how we suppress the reading part of our brain and respond appropriately to the ink color Subjects have a longer response time in Stroop conditions than control conditions b/c of interference of reading and color naming ∙have to suppress reading, or respond to reading, which slows down response time

Maturation of the Prefrontal Cortex

the PFC is the last region of the brain to mature, which is why a 30 y/o has better problem solving skills than a 13 y/o the rate of development and the overall level of development of the PFC vary from one individual to the next, which helps explain why there can be significant differences in the learning abilities of children the same age damage to the PFC does not cause memory less ∙an individual with a PFC lesion might perform well on a basic memory test, but if we were to tell them a story, they would have difficulty retelling it in the correct sequence ∙this is the difference b/w recall and recognition ∙if the PFC does not function normally, the brain's capacity to perform within a social situation is diminished → it cannot maintain multiple streams of conversation or adapt to the changing flow of a conversation and the reactions of people w/ whom they are speaking

Diagnostics of the PFC

the Wisconsin Sorting Card Test (WSCT) is used as a measurement of PFC function ∙as the subject orders the cards and is corrected by the experimenter, the subject is forced to act in uncertain conditions, to absorb and respond to feedback from the experimenter, adapting to changing experimental conditions ∙an individual with PFC damage would know that the feedback they were receiving was negative and that they were sorting the cards incorrectly, but they would be unable to adapt to the change and continue to sort the cards according to the first strategy they used ∙this would not be the case w/ almost any other kind of brain damage, so the WSCT is fairly diagnostic of PFC damage another diagnostic test that is used to test verbal fluency gives you specific category of words (i.e. words beginning with J, sports, etc.) and asks you to come up with as many words as you can within a few minutes ∙normal individuals come up with 10-15 words, while a patient with PFC damage might only come up with 4 or 5 ∙in order to perform well in this test, we must be able to suppress recurring words that we have already listed and come up with various strategies that allow us to think of many words within that given category

Circuitry and Functional Anatomy of the Amygdala

the amygdala is a complex of nuclei separated into two evolutionarily distinct sections ∙the primitive amygdala includes the central, medial and cortical nuclei w/ projections to the olfactory bulb ∙the newer amygdala includes lateral, basal and accessory basal nuclei with projections to the cortex amygdala nuclei can also be divided based on their anatomical distribution ∙deep nuclei include the lateral, basal and accessory basal (also collectively called the basolateral nuclei) →lateral nucleus receives cortical and subcortical inputs and distributes to the various other nuclei →the basal nucleus receives inputs from the lateral nucleus and sends projection to other amygdala nuclei and orbital frontal cortex for goal-direct behavior ∙the superficial nuclei include the medial nucleus and an assortment of other nuclei and process involved involved in amygdala function ∙the central nucleus is the major output nucleus and sends projections mostly to the hypothalamus and striatum

Split Brain Studies

the corpus callosum is cut in patients with intractable epilepsy, and studies have been done using these patients to try and localize language centers in the brain ∙since the optic chiasm is still intact but the corpus callosum is cut, visual field information will remained isolated in the receiving hemisphere Bird is shown in L visual field ∙information travels via the optic chiasm to the R occipital lobe ∙since the dominant (L) hemisphere controls the motor aspect of speech, the patient cannot use words to describe the image ∙however, he can use his L hand to point to the correct picture, b/c the R hemisphere controls the L hand Deer shown In R visual field ∙information travels via optic chiasm to the L occipital lobe ∙patient is able to verbally identify the image here, and can correctly point to image w/ R hand

Anatomy of the PFC

the frontal cortex is everything anterior to the central sulcus the PFC is everything anterior to the premotor cortex the lateral PFC is the region where our working memory and cognitive control seem to be located the ventromedial PFC integrates these lateral functions with our emotions/the limbic system the anterior cingulated gyrus is important in cognitive control

Multiple Mediation Modeling (to test neural mediation)

the idea is that if you have a behavioral association with a gene, can we identify a way in which specific structure/function underlies that behavior? Goal: Gene→Brain→Cognition pathways ∙in math terms, does this effect transmit from here to there to there?

Effect of attentional modulations on neural codes: Experiment (2008)

the neuronal response for each task doesn't change regardless of the difficulty if the monkey is paying attention if the monkey was not paying attention, there was a progressive decrease in neuronal response as the task got harder turns out that there are inhibitory neurons that increase in response when attending to an object ∙these inhibitory neurons then tell the surrounding neurons to respond less Note: neurons selected for orientation/direction tend to get suppressed, while the neurons that have low selectivity tend to get enhanced

Positive Emotions and Reward

the reward system involves four brain areas: the ventral tegmental area, basolateral amygdala, orbitofrontal cortex, and nucleus accumbens ∙the VTA receives the reward inducing stimulus and sends dopaminergic projections to the BLA, OFC and NAcc ∙the BLA creates/associates the feeling of reward w/ the stimulus and sends glutamate projections to the OFC and NAcc ∙the OFC is involved in consequence evaluation and modifies behavior to maximize the positive emotions associated with rewards and sends glutamate projections to the BLA and NAcc ∙the NAcc is involved in detecting and registering the positive emotions of reward and acts as the final portion and integrates all the signal from other regions

Components of Emotion

there is the subjective feeling and the context ∙an example is that the subjective feeling is fear, and the context is a perceived threat these are accompanied by physiological changes that are modulated by the ANS (via SNS and PSNS) ∙in the case of fear, people experience increases in HR, BP and RR w/ sweating and muscle tension ∙this is regulated at the level of the brain by the hypothalamus (w/ other subcortical inputs) there are associated behavioral/somatic changes as well, such as avoidance, shrieking and running (in case of fear)

Syndromes of Aphasia

these are commonly co-occuring deficits results from lesions to language areas of the brain ∙they are determined by categorization as good vs. poor fluency (output), repetition, and comprehension ∙patients are NOT categorized as having present vs. absent comprehension, since everything is relative ∙rather, it is the relative degree of comprehension and/or repetition deficit that distinguishes b/w the 8 different aphasias Comprehension tends to be impaired in all aphasics, and impairments can be elucidated by difficulty comprehending reversible passives and following complex commands (due to trouble holding onto long strings of words) Repetition may be significantly impaired even if the patient speaks and comprehends well ∙poor repetition is characterized by phonologic processing deficit near the posterior temporal or parietal lobe that results in difficulty saying tongue twisters and inability to repeat words w/o semantic value, such as if, and, but what, etc ∙patient w/ repitition deficit likely processes meaning rather than sound, so an intended phrase may be repeated with different words but with same overall meaning (book on couch → novel on sofa) Broca's (anterior) aphasia is characterized by non-fluent agrammatic speech (short/single-word phrases), articulatory problems, good but imperfect comprehension, and R hemiparesis/hemisensory loss resulting from a lesion near the L motor strip ∙Broca's area is defined as the posterior inferior frontal gyrus of the L hemisphere ∙a lesion here itself will not cause Broca's aphasia → lesion must extend from Broca's area to other areas involved w/ language to cause it Wernicke's (posterior) aphasia is characterized by fluent paragrammatic speech (verbose, full sentences) w/ poor comprehension, poor repitition, and semantic & lateral paraphasias ∙Unlike Broca's aphasics, Wernickes' aphasic do not exhibit motor impairments ∙Wernicke's area is defined as the posterior superior temporal gyrus ∙Wernicke's aphasics have lesions including, but not limited to, Wernicke's area Neologistic jargon aphasia is a severe form of Wernicke's aphasia

Declarative Memory

think of this as events, facts and words encompasses both explicit (consciously accessible) and implicit (sub-conscious, aka things that we know how to do that we really aren't aware of) forms of memory can be divided into episodic and semantic memory ∙episodic refers to memory of personal events, and can best be summed up with the word "remembering" - like remembering what you ate last night ∙semantic refers to general knowledge of facts or words that are NOT linked to a personal event, or "knowing" - i.e. Paris is the capital of France declarative memories form in the MEDIAL TEMPORAL LOBE (hippocampus, perirhinal cortex, entorhinal cortex) and its associated structures (fornix, mammillary bodies) ∙Episodic memories occur in the hippocampus ∙Semantic memories occur in the perirhinal/entorhinal cortex it now known that the medial temporal lobe is not the only region involved in the learning and consolidation of these new memories → areas of the neocortex play an important role in forming long-term declarative memories ∙example: memories about how to use a hammer, or even that hammer is associated with hitting nails, are localized to motor cortex ∙sleep helps in memory consolidation if the medial temporal lobe gets damaged, you will see Anterograde Amnesia and Temporally Graded Retrograde Amnesia (both are impairments in declarative memory) damage to the neocortex will lead to long-term memory deficits, particularly in semantic memory Pick's Disease, which leads to semantic dementia, is the degeneration of the temporal lobe, which is an area of brain responsible for storing a lot of semantic memory

Unilateral Tactile Anomia

this is a phenomenon in which a subject is blindfolded, given an object to touch, but cannot name it if placed in left hand subject is immediately able to name the object if placed in R hand, b/c the tactile information from her R hand travels to the dominant hemisphere, which is responsible for control of motor aspects of speech production

LTD is blunted in the Thorase Knockout Mouse

this is important because AMPA function is upregulated, and the AMPA/NMDA ratio is increased causes an imbalance b/w GABA and glutamate, as well as AMPA receptors and GABA receptors ∙imbalance favoring glutamate and AMPA receptors this imbalance means that you effectively remove the ability of the AMPA receptors to learn ∙they can no longer go up and down, and effectively cannot learn, because they cannot be depressed ∙this does not make you smarter, or learn things more easily, it actually has the opposite effect → they stop helping you ∙in mice, there is a decrease in Pavlovian appetite learning that demonstrates this ∙FLEXIBILITY IS MORE IMPORTANT

The Biased Competition Model of Attention

this model essentially states that the object we end up giving our attention to is "chosen/given priority" based on other mental processes - i.e. bottom-up, top-down and/or working memory - that prioritize (and bias) certain features of an object for attention and processing

Cognitive Behavioral Therapy

thought to be one of the most effective forms of therapy, especially for anxiety disorders and depression this form of therapy involves teaching people how to reinterpret their context in more adaptive ways to reduce the sadness or anxiety they feel individuals prone to depression tend to interpret bad things as global, stable and internal this is equally as effective as pharmacological therapies, w/o side effects and is long lasting

Trinucleotide repeat disorders

two kinds: glutamine repeat (polyQ) or nonpolyQ diseases

Thorase

uses ATP to traffic AMPA receptors into the cell, and the AMPA receptors become internalized cells without thorase cannot do this, and AMPA receptors stay on the cell surface ∙these receptors are not just stuck in the membrane, they are MORE FUNCTIONAL

Optogenetics

uses light to control neurons which have been genetically sensitized to light neuromodulation technique used to control and monitor the activities of individual neurons within living animals to precisely measure the effects of those manipulations in real-time

Language Processing

with regards to language, the left hemisphere is said to be dominant ∙95-98% of right handed people have their primary language cortex situated in the left hemisphere ∙70% of left handed people also have primary language cortex in left hemisphere the dominant hemisphere controls motor aspects of speech → it is responsible for producing speech ∙in addition, phonologic processing occurs here - which has to do with the sounds of words and how they are heard and processed ∙syntax (grammar) and orthography-to-phonology (involved in reading and spelling) are also controlled by the dominant hemisphere the non-dominant hemisphere is involved in single word comprehension and humor ∙also controls prosody, which has to do w/ sentence intonation to reflect different meanings (i.e. inflection of phrase Oh Boy to mean either good or bad things) ∙pragmatics (language in context) is based in the non-dominant hemisphere (i.e. saying "can you pass the salt?" which means "pass the salt") ∙non-dominant hemisphere is responsible for the abstract use of language → metaphors & idioms, patients w/ lesions here may only understand literal sense of the phrase Semantic information is much less localized ∙since it encodes a variety of sensory information, it activates different areas of the cortex and is present in both the dominant and non-dominant hemispheres keep in mind that hemispheric dominance is not clear cut, and that mixed dominance exists

Symptoms of PFC Damage

you will see psychological inertia in individuals with PFC damage = a mind devoid of ideas, leading to a lack of motivation to get out of bed or do much of anything ∙patients with this symptom will be very matter of fact about what has happened to them and will seem to be emotionally affected by the changes perseveration is when you keep doing an action over and over again, like continuing to brush you teeth even after your gums have started to bleed environmental dependency syndrome can manifest in several different ways, such as picking up the objects around them and performing actions associated with those objects ∙examples: putting on a pair of glasses that are not yours, drinking a cup of coffee when you aren't thirsty ∙may also mimic the behavior or actions of those around them ∙KEY: they know what they are doing in inappropriate, but they are unable to stop themselves some of these symptoms are seen in psychiatric disorders, such as a lack of a motivation in depressed individuals ∙the different b/w psychiatric and neurological disorders is that we can pinpoint a physical cause for neurological disorders, while the biological cause of psychiatric disorders cannot yet be found on an MRI or similar empirical diagnostic tool ∙however, the function of an individual can be similarly affected by either disorder patients w/ PFC damage will have difficulty with cognitive estimation deficits (being asked to estimate a distance or the size of an object off the top of their heads) ∙this demonstrates difficulty with deductive reasoning ∙it can also manifest as a mis-estimation of their own abilities, like a 120-pound woman thinking she can lift a car Deficits in temporal organizations of thought ∙basically, if you can't tell someone how to perform a simple, sequential, organized task, you might have PFC damage →example: how to cook an omelette can also see deficits in emotional/affective responses after damage to the ventromedial PFC, resulting in a flat affect or failure to show emotion through facial expression, body language, or tone of voice ∙might even see loss of socially acceptable behavior or personality changes

Cognitive Control Tests

∙Flanker Test ∙Stroop Test ∙The Simon Task

Major functions of the amygdala

∙fear and aggression ∙emotion ∙reward ∙social interactions