Exam Three Study Guide - Psy 319

Ryback and Lewis (1971)

function of sleep; 6 weeks of bed rest and no decreases in SWS or REM - suggests that sleep is not needed to provide rest after physical activity

Roffwarg et al (1962)

eye movements during REM sleep; recorded eye movements during dreaming; similar to waking eye movements (same type of scene)

Desynchronous

having different periods and phases; in EEG, represents high levels of brain activity

Sleep Spindles

short bursts of waves of 12-14 Hz that occur two to five times a minute during stages 1-3 (mainly 2) of sleep; they play a role in consolidation of memories, and increased number of sleep spindles are correlated to increased scores of intelligence.

environmental factors (stop a meal)

short term signal; can shorten or lengthen a meal

Insulin (when glucose levels are high)

short term signal; insulin receptors in hypothalamus; evidence: intraventricular injections- decreases eating

Liver

short term signals; has glucose detectors; evidence: glucose/fructose into hepatic portal vein-decreased food intake

Strumbreys et al. (2013)

used transcranial direct current stimulation (tDCS) and discovered prefrontal cortex is more active in lucid dreamers

arousal systems

Five arousal systems: 1. ACh: cortical arousal, alertness 2. NE: Vigilance 3. 5-HT: ongoing movements 4. Histamine: novel stimuli 5. Orexin: exploratory behavior

Histamine

In the tuberomammillary nucleus (TMN); Implicated in the control of wakefulness and arousal; the activity of the histaminergic neurons is high during waking and low during SWS and REM sleep.

PYY

Peptide YY3-36; a peptide released by the gastrointestinal system after a meal in amounts proportional to the size of the meal

Control of REM sleep components by REM on

REM ON cells activate inhibitory interneurons in spinal cord causing paralysis Purpose: (theory) motor systems of the brain are rehearsing movements learned during the day-nondeclarative memory consolidation

Stage 2 sleep (NREM)

A sleep deeper than that of stage 1, characterized by a slower, more regular wave pattern (at about 12-14 Hz), along with momentary interruptions of "sleep spindles."; generally shows an irregular EEG, but contains periods of theta activity, sleep spindles, and K complexes (precursor for Stage 3).

intestinal factors

a.) Duodenum detects fats: released cholecystokinin or CCK: I. Bile is released from gall bladdar II. Slows movement of food into duodenum III. CCK receptors (stomach/duodenum) activates Vegus Nerve) IV. May also signal the brain (satiety signal) b.) peptide YY (PYY): I. Released by small intestines after a meal II. Its release is directly proportional to the number of calories consumed.

caffeine

block adenosine receptors on neurons so it decreases adenosine's "sleep signal"

REM sleep behavior disorder

a neurological disorder in which the person does not become paralyzed during REM sleep and thus acts out dreams; caused by damage to REM regions, its hereditary: genetic neurodegeneration, and also occurs with other neurodegenerative diseases Treatment: Clonazepam (Benzodiazepine)

adenosine

a neuromodulator that is released by neurons engaging in high levels of metabolic activity; may play a primary role in the initiation of sleep; the accumulation of adenosine serves as a sleep-promoting substance; inhibits neural activity

a-Melanocyte-Stimulating Hormone (a-MSH)

a neuropeptide that acts as an agonist at MC-4 receptors and inhibits eating

Agouti-related protein (AGRP)

a neuropeptide that acts as an antagonist at MC-4 receptors and increases eating

arcuate nucleus of the hypothalamus

a nucleus in the base of the hypothalamus that controls secretions of the anterior pituitary gland; contains NPY-secreting neurons involved in feeding and control of metabolism; ghrelin (from blood stream) and medulla (NPY neurons) activate the arcuate nucleus

insulin

a pancreatic hormone that facilitates the entry of glucose and amino acids into the cell, conversion of glucose into glycogen (stored glucose), and transport of fats into adipose tissue

glucagon

a pancreatic hormone that promotes the conversion of liver glycogen into glucose

ghrelin

a peptide hormone released by the stomach that increases eating; also produced by neurons in the brain

melanin-concentrating hormone (MCH)

a peptide neurotransmitter found in a system of lateral hypothalamic neurons that stimulate appetite and reduce metabolic rate

cocain- and amphetamine- regulated transcript (CART)

a peptide neurotransmitter found in a system of neurons of the arcuate nucleus that inhibit feeding

neuropeptide Y (NPY)

a peptide neurotransmitter found in a system of neurons of the arcuate nucleus that stimulate feeding, insulin and glucocorticoid secretion; decrease the breakdown of triglycerides; and decrease body temperature

Orexin

a peptide neurotransmitter involved in the neutral control of arousal; in lateral hypothalamus (LH); helps stabilize the sleep/waking flip-flop through their excitatory connections to the wakefulness neurons; allosteric factors (like hunger and thirst) and circadian factors (biological clock) activate orexin; homeostatic factors (increased adenosine and vlPOA activity) inhibit orexin

REM sleep

a period of desynchronized EEG activity during sleep, at which time dreaming, rapid eye movements, and muscular paralysis occur; also called paradoxical sleep; when a person is awakened from REM sleep, they will appear alert and attentive; 90 minute sleep cycle/ 20-30 minute REM episode so 4-5 REM periods per 8 hours of sleep; low activity in striate cortex (no visual input), high activity in extrastriate cortex (visual hallucinations: dreams), low activity in prefrontal cortex (why dreams are not well organized)

melanopsin

a photopigment present in ganglion cells in the retina whose axons transmit information to the SCN, the thalamus, and the olivary pretectal nuclei

MC4 receptor

a receptor found in the brain that binds with a-MSH (suppresses eating) and agouti-related protein (induces eating); plays a role in control of appetite

Ventrolateral periaqueductal gray matter (vlPAG)

a region of the dorsal midbrain that forms the REM-OFF portion of the REM sleep flip-flop

sublaterodorsal nucleus (SLD)

a region of the dorsal pons, just ventral to the locus coeruleus, that forms the REM-ON portion of the REM sleep flip-flop

Mednick et al (2003)

consolidation of non-declarative memories (consolidation of a memory means converting a short term memory into a long term memory) used visual discrimination task

VTA Dopamine

contain ghrelin receptors; intra VTA: increases eating

triglycerides

the form of fat storage in adipose cells; consists of a molecule of glycerol joined with three fatty acids

carbohydrates

glucose levels in blood increase; pancreas releases insulin: glucose available to all cells in body; excess glucose: short-term storage (as glycogen)/long-term storage (as triglycerides)

glycogen

glycogen is used up during the day and is restored in astrocytes during SWS

Stage 1 sleep (NREM)

marked by the presence of theta wave activity (EEG activity of 3.5-7.5 Hz); increased synchrony of cortical neurons; hypnic jerks (feeling like you're falling); lasts about 10 minutes

brain mechanisms: hunger

neurochemicals that stimulate eating: 1. melanin-concentrating hormone (MCH) 2. orexin 3. neuropeptide Y (NPY) 4. agouti-related protein (AGRP)

lateral hypothalamus

neurons that contain: - melanin-concentrating hormone (MCH): intraventricular injections induces eating - orexin: intraventricular injections induce eating *sleep-eating relationship arcuate nucleus neurons (NPY and AGRP) activate LH

absorptive phase of metabolism

the phase of metabolism during which nutrients are absorbed from the digestive system; glucose and amino acids constitute the principal source of energy for cells during this phase, and excess nutrients are stored in adipose tissue in the form of triglycerides

sleep/waking flip-flop

uses orexinergic neurons to help stabilize it; when adenosine accumulation is high, the flip-flop is off and it inhibits the wake promoting areas and the arousal systems; when flip-flop is on, the sleep-promoting region in vlPOA is inhibited

vlPOA

ventrolateral preoptic area; Nucleus of Hypothalamus critical in initiating sleep (also assesses & regulates body temp)

Circadian factors

wakes up and sleeps at a certain time of the day

Horne and Minard (1985)

waking: large amount of cognitive activity, minimal physical activity (participants go to museum, zoo, etc) Sleep: duration was normal; SWS increased conclusion: SWS provides rest after high cognitive activity during waking hours; increase cognitive activity-increased SWS

Subparaventricular zone (SPZ)

primary (efferent-away) output of SCN, SCN to SPZ to VLPO

declarative memory

refers to recalling episodes of our lives (ex: remembering a specific vacation you've had)

adenosine receptors

regulate channels that are inhibitory/make neurons less active/make you sleepy; caffeine inhibits these by binding to them and preventing the process

gastric factors (empty stomach-start a meal)

release of ghrelin by stomach (travels to the brain via bloodstream); ghrelin detectors: in hypothalamus and initiates eating

sensory factors

shortens a meal; taste can provide caloric information

REM flip-flop

similar to the sleep/waking flip flop; controls the time in SWS vs. REM sleep; REM-ON: sublaterodorsal nucleus (dorsal pons); REM-OFF: ventrolateral periaqueductal grey matter (dorsal midbrain)

Ramanathan et al (2002)

sleep deprivation on rats; high metabolic activity in the brain: produces free radicals (creates oxidative stress which is damaging to the neurons) - suggests low metabolic rate of SWS allows for removal of free radicals; increased metabolism-increased free radicals (potential damage)

sleep regulation

sleep is regulated by adenosine; the amount of slow-wave sleep that a person obtains during a daytime nap is deducted from the amount of SWS they obtain the next night; astrocytes use stored glycogen to deliver energy to neurons-releases adenosine

REM ON

stimulation of the REM-ON region with infusions of glutamate agonists produces most of the elements of REM sleep (like muscle paralysis), whereas inhibition of this region with GABA agonists disrupts REM sleep; (REM-ON = promotes REM sleep)

Youngstedt (2003)

does exercise improve sleep? - maybe, but only by a small amount

gastric factors

nutrient detectors; shortens a meal

starvation and eating disorders demonstrate:

-preoccupation with food and eating -ritualistic eating -hoarding food or other objects

treatment of eating disorders

1. cognitive behavioral: success rate less than 50% 2. Pharmacological: fluoxetine may help bulimia, but does not aid anorexia/LDX (lisdexamfetamine) may help binge eating disorder 3. Alternative therapies under development: -behavioral treatment targeting time needed to consume a meal -deep brain stimulation: cingulate cortex -oxytocin treatment

flip-flop circuit integration

1. wake state: 5 arousal regions active 2. adenosine accumulation: vlPOA is active (SWS) 3.NE, 5-HT, Orexin decreases removing activation of REM OFF neurons: REM sleep begins

Suprachiasmatic Nucleus (SCN)

A nucleus situated atop the optic chiasm. It contains a biological clock that is responsible for organizing many of the body's circadian rhythms

lipid detectors

Brain: glucose Liver: glucose and fatty acids (if levels are low, this information is sent to the brain via the Vagus Nerve)

Allostatic factors

Need to stay awake to modify homeostatic factors: stressful circumstances; stays awake when tired because of some stressful even in the environment; hormones, neural response, or neuropeptides (like orexin)

chronic sleep deprivation

Not getting enough sleep over an extended period of time, long term sleep deprivation can be linked to fatal familial insomnia; animal studies show that chronic sleep deprivation is fatal

brain development

REM sleep helps promote brain development; adults still need REM sleep because of changes in neuron structure as a result of learning

Ibuka and Kawamaur (1975)

SCN's role in circadian rhythms; SCN lesions in rats- had normal amount of sleep but timing was disrupted

nocturnal enuresis

SWS disorder; "bed wetting" Treatments: behavioral intervention

pavor nocturnus

SWS disorder; "night terrors" - not a bad dream, no memory of it

sommambulism

SWS disorder; "sleep walking", sleep-eating disorder Treatment: DA agonists; topiramate

SWS

Slow wave sleep; a non-REM stage of sleep characterized by delta waveform activity in an EEG record; does not dream just experience thoughts, emotions, and images (non-narrative)

REM OFF

Stimulation of the REM-OFF region suppresses REM sleep, whereas damage to the area of infusions of GABA agonists dramatically increases REM sleep; (REM-OFF = suppresses REM sleep)

ventrolateral preoptic are (vlPOA)

a group of GABAergic neurons in the preoptic area whose activity suppresses alertness and behavioral arousal and promotes sleep

leptin

a hormone secreted by adipose tissue; decreases food intake and increases metabolic rate, primarily by inhibiting NPY-secreting neurons in the arcuate nucleus

circadian rhythms

a daily rhythmical change in behavior or physiological process; 24 hour cycle of sleep/wake patterns

binge-eating disorder criteria

a disorder that includes bouts of excessive eating

anorexia nervosa criteria

a disorder that most frequently affects young women; exaggerated concern with being overweight that leads to excessive dieting and often compulsive exercising; can lead to starvation; patients usually have an enlarges sulci, third ventricle, and lateral ventricle

glucoprivation

a dramatic fall in the level of glucose available to cells; can be caused by a fall in the blood level of glucose or by drugs that inhibit glucose metabolism

fatal familial insomnia

a fatal inherited disorder characterized by progressive insomnia

Narcolepsy

a sleep disorder characterized by periods of irresistible sleep, attacks of cataplexy, sleep paralysis, and hypnagogic hallucinations; increased emotion activates amygdala which activates REM-ON (SLD): results in cataplexy Caused by the loss of the orexin system; hereditary Treatments: Methylphenidate (Ritalin) for sleep attacks, antidepressants for cataplexy and sleep paralysis, Modafinil

Zeitgeber

a stimulus (usually the light of dawn) that resets the biological clock that is responsible for circadian rhythms

Ob mouse

a strain of mice whose obesity and low metabolic rate are caused by a mutation that prevents the production of leptin

glycerol

a substance (also called glycerine) derived from the breakdown of triglycerides, along with fatty acids; can be converted by the liver into glucose

fatty acids

a substance derived from the breakdown of triglycerides, along with glycerol; can be metabolized by most cells of the body except for the brain

"Ticking" of the clock

activity within neurons: 1. the time it takes individual neurons to produce, and then degrade, a set of proteins: PER/CRY 2. negative feedback loop

Long-Term Reservoir

adipose tissue; triglycerides: stored fats; the cells in adipose tissue convert nutrients (from the blood) into fat (triglycerides); used when short-term reservoir is depleted: fat cells convert triglycerides into fatty acids and glycerol and liver cells convert glycerol into glucose

Homeostatic factors

after a period of sleeplessness-increased sleep; mechanism: adenosine (induces drowsiness), accumulates during waking and decreases during SWS normal circumstances; goes to sleep when tired; accumulation of adenosine

Waking state

alpha waves (8-12 Hz): resting quietly beta waves (13-30 Hz): alert, focused, problem-solving

proteins

amino acids; protein synthesis; excess: long-term storage

Electroencephalogram (EEG)

an electrical brain potential recorded by placing electrodes on the scalp; brain activity

Electro-oculogram (EOG)

an electrical potential from the eyes, recorded by means of electrodes placed on the skin around them; detects eye movements; eye movements

Electromyogram (EMG)

an electrical potential recorded from an electrode placed on or in a muscle; muscles (facial)

seasonal rhythms

annual cycles; behaviors change as seasons change; the pathways: SCN, Paraventricular nucleus of the hypothalamus (PVN), spinal cord, sympathetic NS neurons, pineal gland, melatonin secretion (by pineal)

treatments (obesity)

bariatric surgery: -sleeve gastrectomy which removes most of the stomach -RYGB surgery which removes most of the stomach and attaches the rest of the stomach to the lower level of intestine *Benefits: feel less hungry (decrease in ghrelin so decrease in hunger) and increased PPY (increased satiety) *Risks: 1. Vitamin B12 and iron deficiencies. 2. deep vein thrombosis (blood clots), pulmonary embolism, non-discharge, death Pharmacological: -drug treatment: suppress appetite 1. targets for drug treatment under development: leptin, CCK, CART, and MC4 receptor -drug treatment: prevent digestion (decreased fat absorption) 1. Orlistat- helps maintain weight already lost - GI side effects -drug treatment: combination (of drugs) 1. Naltrexone (opioid antagonist) 2. Bupropion (agonist) Behavioral Intervention -exercise (burn calories and increases metabolic rate) -stress and overeating

non-declarative memory

become skilled in a particular activity and our abilities are demonstrated through the performance itself (ex: driving)

bulimia nervosa criteria

bouts of excessive hunger and eating, often followed by forced vomiting or purging with laxatives; sometimes seen in people with anorexia

Norepinephrine

catecholamine agonists produce arousal and sleeplessness; mediated primarily by the noradrenergic system of the locus coeruleus (LC), located in the dorsal pons. the firing of noradrenergic neurons was high during wakefulness (important for vigilance), low during SWS, and almost zero during REM sleep; within a few seconds of awakening, the rate of firing increases dramatically.

sleep apnea

cessation of breathing while sleeping; common cause: airway obstruction Treatment: surgery to remove obstruction or pressurized air forces airway to stay open (cPAP machine)

CCK

cholecystokinin; a hormone secreted by the duodenum that regulates gastric motility and causes the gallbladder (cholecyst) to contract; appears to provide a satiety signal transmitted to the brain via Vegus Nerve

Tucker et al (2006)

declarative learning task: list of paired words nondeclarative learning task: mirror tracing

Stage 3 sleep (SWS)

delta waves (<3.5 Hz); synchronous; the deepest stage of sleep; when awakened, the person will act groggy and confused

lipoprivation

depriving cells of lipids

health risks associated with obesity

diabetes, cardiovascular disease, stroke, arthritis, cancer

Prokineticin 2 (PK2)

diffuses through the ventricular system to activate SPZ

medulla

dorsal medial (AP/NST) and ventrolateral regions: vagus nerve input (stomach, liver, duodenum) and glucose detectors; activation of medulla signals need for food

environmental factors (obesity)

fast food restaurants, ease of access to snack foods, fructose: doesn't stimulate insulin or leptin (satiety signals), change in environment: college students, food deserts: low levels of fresh foods available so increased consumption of fast and processed foods

glucose

fuel for cells; transporter carries glucose across cell membranes; all cells except the NS requires insulin; NS does not require insulin because even when you don't eat, your brain still needs to have energy to function. Fuel for all cells except NS: glucose and fatty acids Fuel for NS: only glucose

Buchsbaum et al. (1989)

functions of SWS; focused on the brain; during SWS there is decreased metabolic activity in the brain (decreased neuron activity) - suggests the brain is resting during SWS; increased SWS-decreased metabolism

genetics (obesity)

genes can influence: metabolism, non-exercise activity (NEAT), and appetite level Efficient metabolism: more available for long-term reservoir Inefficient metabolism: less available for long-term reservoir twin studies: 40-70% of the differences in body fat are attributed to genetics mutations: MC4 receptor gene, FTO gene (enzyme that influences metabolism), leptin gene: normal levels but because of the blood brain barrier, the brain doesn't receive the leptin signals

Acetylcholine

important in arousal; two groups of acetylcholinergic neurons, one in the pons and one located in the basal forebrain, produce activation and cortical desynchrony when they are stimulated. A third group of acetylcholinergic neurons, located in the medial septum, controls the activity of the hippocampus; levels of ACh were high during both waking and REM sleep-periods in which the EEG displayed desynchronized activity - but low during SWS.

endocannabinoids

increases release of MCH and orexin; increases eating

Lucid dreams

individual is aware they are dreaming; May involve an active prefrontal cortex

excessive exercise related to eating disorders

is increase exercise intended to lose weight or a consequence of starvation? -Rats given limited access to food increase their running wheel activity (Smith et al 1989)

physical activity factors (obesity)

lifestyle (sedentary)

Short-Term Reservoir

liver cells; pancreatic hormones: insulin and glucagon

fat

long-term storage

PER/CRY

low level of PER/CRY: gene activation PER/CRY synthesis: proteins synthesized high level of PER/CRY: inhibition of gene activation

Synchronous

low level of brain activity

Retinohypothalamic Pathway

photochemical in retinal ganglion cells: melanopsin respond to the changes in light and the axons end in the SCN

Serotonin

plays a role in arousal; almost all of the brain's serotonergic neurons are found in the raphe nuclei; stimulation of the raphe nuclei causes locomotion and cortical arousal; acted just like the noradrenergic neurons: high during wakefulness, low during SWS, and virtually zero during REM sleep

Insomnia

primary: characterized by difficulty falling asleep or staying asleep during the night secondary: inability to sleep due to another mental or physical condition, such as pain, substance use, or a physiological or neurological condition Treatment: nonpharmacological- CBT, relaxation techniques, sleep hygiene; pharmacological- hypnotics (e.g., Ambien and Sonata), Benzodiazepines (enhance GABA), and Histamine antagonists

Flip-flop circuits

reciprical inhibition: only one component can be active at a time transition to sleep: sleep neurons of the hypothalamus- vlPAS, adenosine actavtes vlPOA, vlPOA inhibits the arousal systems (via GABA neurons), causes sleep Advantage: can quickly switch from one stat to another; disadvantage: can be unstable

Horne (1978)

study sleep deprivation with healthy participants; saw that physical exercise is not impaired while cognitive function is (difficulty concentrating and perception distortions); After sleep deprivation: more than 50% of SWS and REM sleep are made up in subsequent nights - this suggests that SWS and REM are more important stages of sleep

K complexes

sudden, sharp waveforms which unlike sleep spindles, are usually found only during stage 2 of sleep; they spontaneously occur at the rate of approximately one per minute but often can be triggered by unexpected noises; they occur before delta waves, which occur in the deepest form of sleep.

fasting phase of metabolism

the phase of metabolism during which nutrients are not available from the digestive system (tract is empty); glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase. -energy for the brain: glycogen conversion to glucose and triglyceride conversion to glycerol, then to glucose -energy for the rest of the body: triglyceride conversion to fatty acids -triglyceride conversion into fatty acids and glycerol requires the sympathetic NS: SNS activates adipose tissue, then pancreas to produce glucagon, then the adrenal gland to produce catecholamines

genetics (eating disorders)

theory: 1. unknown genetic or biological factors (distorted perception of body weight?) 2. starvation (restricted diet) 3. remaining symptoms

environmental factors (start a meal)

time of day, sight/smell of food, sight of others eating

free radicals

waste products produced during the waking state; they are highly reactive oxidizing agents that can bind with electrons from other molecules and damage the cells in which they are found through a process known as oxidative stress; during SWS the reduced rate of metabolism permits restorative mechanisms in the cells to destroy the free radicals and prevent their damaging effects

light cycle

when the sun rises and sets

internal clock

when to sleep and when to wake up

flip-flop impairment in narcolepsy

without orexin (which is what causes narcolepsy): 1. decreased activation of the other four arousal systems (causes daytime sleepiness) 2. decreased activation of the REM OFF region (vlPAG) (causes cataplexy)