S&F1
what are the first, second and third leading causes of death for adolescents
first: motor vehicle accidents - may be related to increased risk taking behaviors- i.e.: drugs and alcohol second: homocide *males are more at risk* third: suicide - males more likely to succeed, may be due to hopelessness/helplessness, alcoholism (American Indian/Alaskan Native), LGBTQ more at risk
what is special about C7 (ligamentum nuchae, bifid, foramen houses what?)
VERTEBRA PROMINENS 7th cervical vertebra is where the *first palpable spinous process* is this is because the thick LIGAMENTUM NUCHAE binds top 6 spinous processes C7 is where bi pronged processes end- C7 is NOT bifid also where foramen is smallest- while C1-C6 can house arteries, C7 only houses VEINS
self esteem at school age- depends on, what can be negative influences?
academic, social, physical/athletic COMPETENCIES personal appearance *romantic appeal, close relationships are added as they approach adolescence* culture can add GENDER STEREOTYPES, helicopter parents or negligence from parents can also be problematic
what is the function/structure/location of INTERVETEBRAL foramina, intervetebral discs and superior/inferior processes
foramina is a hole formed BETWEEN PEDICLES= house NERVES (foramina transversaria houses veins/arteries) superior and inferior processes stack upon each other and form JOINTS between vertebrae intervertebral discs JOIN the bodies of vertebrae *made up of gelatin core and collagen fibers*
how does driving force of Na/K change during AP
during rising phase the driving force for Na is large [conductance/permeability is large], small at the peak due to equilibrium during falling phase driving force and conductance for K is large
electrical vs chemical synapse
electrical= electrical signal transmission as a current thru GAP JUNCTIONS causes membrane potential change in neighboring cell- AP *direct connection between the two cytosols, PASSIVE diffusion, rapid communication, coordinated response* chemical= synaptic CLEFT between pre and postsynaptic membranes contains specialized structures to ensure quick delivery of signal via neurotransmission release and binding *high in mitochondria, vesicles and cytoskeletal proteins*
cognitive and motor development in toddlers (1-3 years) *problem areas?*
explore, search for hidden objects, deferred imitation make believe play, problem solving with more thinking, building, scribbling, develop more rhythmic motion problem areas= tantrums, sleep and feeding difficulties, developmental delays or language problems
problem areas for preschool children
fears/nightmares, temper tantrums, emotional regulation, masturbation
Erikson 7-8 stages (generativity/stagnation, ego integrity/despair)
generativity/stagnation= middle adulthood= work-life balance, giving to next generation, productive work ego integrity/despair= old age= reflection on life and worth, did I make the right decisions?
length constant *formula and depends on*
(λ) DECAY of the signal as it travels over a DISTANCE *want it to be HIGH so that the current travels a long ways* dependent on membrane resistance = ion channels that are open *want less channels open so there is MORE RESISTANCE, such as in a myelinated axon* and axial resistance= diameter *want larger diameter so current flows faster* axial resistance is principal way to INCREASE length constant/make current travel farther/faster
which way does the voltage sensor need to move to activate, what does it respond to and what is the sensor called?
*S4 voltage sensor* moves OUTWARD to pull the channel open in response to change in the MEMBRANE POTENTIAL
how is Ca removed from neuron
*excess Ca will cause more release of vesicles and exocytosis of vesicles* eventually need to slow this process uptake by mitochondria , proteins that bind Ca and Ca ATPase that pumps it out
other NTs (ATP and NO)
ATP can be released from vesicles as a NT degraded into adenosine, may accumulate adenosine if there is high metabolic activity *adenosine can be a singalong molecule for neuronal function* NO is made by Nitric Oxide Synthase- can diffuse out of cell- made when needed- quickly degraded major target= GUANYLYL CYCLASE that makes cGMP from GTP
Anorexia nervosa vs bulimia nervosa
Anorexia- Refusal/fear of maintain a body weight, body image is disorted, Amenorrhea May use restriction or binge eating/purging *always underweight* Bulimia Nervosa- binge eating, sense of lack of control May use vomiting, fasting, misuse of medications *could be overweight, average, underweight*
how do tetanus toxins and botulism infections affect NT release (which neurons and what is pathophys)
BOTH TARGET SNARE PROTEINS- prevent NT release Tetanus= prevents INHIBITION of excitatory signals- causes excessive excitation of *spinal cord MOTOR neurons*- uncontrolled muscle contraction and spasms *begins with the jaw, "lock jaw"* Botulism= affects NMJ- also cleave SNARE proteins- prevents release of Ach, LOSS of function causes *PARALYSIS*, may require ventilation
Egocentrism what ages/stages and how are they similar
Both adolescents (12 and up) feel a type of egocentrism where they feel that everyone is watching them *IMAGINARY AUDIENCE* , may create a personal fable (think they are "special") to rationalize their actions, should gradually decline. All of this contributes to TAKING RISKS- leads to accidents, drug/alcohol use, sexual activity Also occurs in Pre-operational thought in 2-7 year olds
C1 and C2 structure and function (what motion)
C1 is AXIS= no body, just a ring of bone. has tubercles on both arches permits YES motion, felxion/extension movements C2 is ATLAS= typical vertebrae with DENS (Odontoid process that sticks up into C1 ring) it is a PIVOTAL joint allows shaking head in "NO" motion, also allows hanging
what are demyelinated diseases of CNS and PNS and what are the typical effects on propogation
CNS= oligodendrocytes myelinate neurons= if defective= MS PNS= Schwann cells= if defective= Guillan Barre *slows the propogation exposes voltage gated and leak channels*, decreases the length constant because resistance DECREASES- therefore signal does not travel far
how can changing the extracellular concentration of Ca/Mg affect mem potential
Ca/Mg are NOT PERM- they interact with extracellular side of cell cell membrane typically is NEGATIVE along outside Ca/Mg divalent ions NEUTRALIZE these negative charges if they are missing *hypocalcemia/hypomagnesemia* then the negative charges are exposed- causes resting potential to be LESS NEGATIVE- now less K+ is leaving the cell [positive ion typically attracted to negative charge outside of cell]
enzymes and precursors for dopamine, norepinephrine and epinephrine (CATECHOLAMINES)
Catecholamine synthesis starts with TYROSINE then Tyrosine hyrdoxylase makes DOPA then Dopa decarboxylase makes Dopamine (DA) then dopamine betahydroxylase makes Norepinephrine (NE) then Phenylethanolamine N-methyltransferase (PNMT) makes Epinephrine
Eriksons Psychosocial Stages vs Freud
Erikson is more accepted- recognizes that development occurs over WHOLE LIFE *uses a crisis scenario at stage about every 1.5-3 years* also takes into account context of CULTURE
S/F neurotransmitter vesicles [what proteins for tethering and docking]
H+ATPase to maintain proton gradient- allows for transport of neurotransmitters into the vesicle tethered to cytoskeletal proteins with synapsin, synaptobrevin vSNARE protein for docking
enzyme and precursor for histamine
HIstidine converted by histidine decarboxylase to histamine
comparing current flow between Na and K, as it flows thru channel, which is faster and which lasts longer?
INa current appears MORE QUICKLY, but does not last even if membrane is depolarized still due to INACTIVATION K+ current appears SLOWLY, but will last as long as the membrane is depolarized if RECTIFIER channel
Identity development in adolescents- identity achievement, moratorium, identity foreclosure, identity diffusion
Identity achievement: explore choices, make an ACTIVE choice, feel comfortable Moratorium: in the process, has not determine values, PROGRESSION Identity foreclosure: COMMITMENT without EXPLORATION, accept an identity fully without exploring* Identity diffusion: LACKS clear DIRECTION and commitment. May find identity overwhelming, may WITHDRAW* Last two put them at risk for depression, suicide, vulnerarbility to manipulation
end result of NT release (re-uptake by what 2 things, recycling and effect on next cell)
NT bind to receptors on post synaptic membrane= causes depolarization of that neighboring cell and same cycle to occur reuptake of NT is thru high affinity transporter proteins and GLIAL cells *requires secondary active transport* also there are enzymes that specifically target degradation of NT such as AChesterase choline can be recycled into new NT and ENDOCYTOSIS of vesicles allows for release of vesicles and prevents membrane from expanding *clathrin for invagination and dynamin for pinching*
G-Protein metabotropic receptors S/F (slower or faster than ionotropic receptors)
NT binds receptor, causes conf change that leads to a CASCADE of G Protein activation/inactivation used for GABAb and muscarinic Ach may open OR close channels, signal secondary messengers, enzymes, etc. POSTSYNAPTIC potential resulting from NT binding is SLOWER than iontropic AP
Na/Ca vs K channel structure (where is inactivation particle)
Na channel has 4 repeats in ONE PROTEIN mlc contains an "inactivation particle" between *domains III and IV* Ca channel just like Na except inactivation particle is between I and II K channel is FOUR separate PROTEINS that assemble in a tetamer *think letter K has four points* may contain an inactivation particle in the N terminal
how does increasing Na extracellularly affect body
Na has a major role in OSMOTIC balance *rather than membrane potential* therefore changes in Na may cause EDEMA rather than problems with MEMBRANE potential changes (it does affect ACTION potential)
Nernst vs Goldman-Hodgins-Katzs equation
Nernst allows you to calculate value of RESTING membrane POTENTIAL for ONE ION [ie: -94mV] *mV where electrical gradient is equal to the chemical potential* Goldman-Hodgins-Katzs equation to determine membrane potential for MULTIPLE IONS where there is no net movement *provides ratio of how perm ions are relative to each other*
Major development changes upon adolescence
Secondary sex characteristics (earlier in girls than boys) includes all developed characteristics- breasts, hair, deep voice Develop INTIMATE relationships, independence and IDENTITY *can make formal operational thoughts- think about things they have not experienced* Can understand sarcasm, irony, abstract thoughts
Where is synovial fluid and what are synovial plane joints, spinal fusion?
Synovial fluid is in the connective tissue that makes up SYNOVIAL JOINTS between articulate processes in vertebrae Spinal fusion occurs to ELIMINATE movement, typically these joints can slide across Use surgery to insert screws between FACETS
why is there an undershoot in the action potential [voltage and leak]
after Na channels are closed K+ voltage AND leak channels allow for the most INFLUENTIAL MOVEMENT since there is NO GATING mechanism on voltage channels they will slowly inactivate= allows cells to get more negative than resting = HYPERPOLARIZATION eventually voltage "rectifier K+ channels" close and passive diffusion restores mem potential
Anterior vs posterior longitudinal ligament and ligaments flava and interspinous and supraspinous ligaments (what do they connect, which contains elastin?)
anterior= strong, gives stability by JOINING bodies on ANTERIOR side posterior= weaker, narrow, INSIDE vertebral CANAL, posterior to body but ANTERIOR in the canal ligamenta flava= yellow ELASTIC band that connects laminae between bodies inter/supraspinous ligaments= holds SPINOUS processes together on outside of vertebral column *thickened in cervical section*
what are factors that affect development of attachment and why important
attachment is important in FORMING future REALTIONSHIPS form attachment starting at 6 weeks can form a reciprocal relationship around 2 years *factors= responsiveness of caregiver, predictability of enviro, opportunity for attachment (social interactions)*
inactive vs deactivated Na channels
ball and stick binds upon max polarization which INactivates the channel "puts the ball into the channel" and blocks ion movement deactivated channels occur when voltage sensor sees that membrane potential is at equilibrium
how can toxins affect voltage gated Na channels or K channels during depolarization (MS treatment)
blocking Na channels with the use of drugs [local anesthetics, toxins TTX, STX] reduces cells ability to FIRE an ACTION potential at high rate- prevents rising phase/depolarization toxins are deadly, drugs can partially block and are tolerable *treatment for cardiac arrhythmias* blocking K+ channels with TEA, 4 aminopyridine increases the DURATION OF ACTION POTENTIAL [takes longer to make cell negative again] also shortens refractory period- can INTENSIFY the signal with more APs *can be used to treat MS*
what does the typical vertebrae look like
body is anterior, houses the MOST WEIGHT vertebral arch is posterior, surrounds vertebral canal that houses the spinal cord Pedicles project from body laminae line the ARCH processes extend posteriorly (spinous) and laterally (transverse)
what logical and motor development occurs in preschool
can sort things, hierarchy, but cannot understand CONSERVATION (preoperational) start to understand that make believe play is symbolic become more gender specific (phallic), ROLE PLAY, become less egocentric/ more social motor= can jump, run more smoothly, catch and throw
membrane capacitance [what properties of the cell allow increase]
capacity of the membrane to store charge keep ions inside/outside of the cell= LIPID bilayer *depends on THICKNESS and SA* if you increase thickness= decrease capacitance, more difficult to hold charge due to SEPARATION of charge if you increase SA= increase capacitance, think, more area to store the charge myelinated cells have LOWER capacitance
temperament
certain characteristics that a baby is BORN with- relatively stable, includes emotion, activity level, attention, self-regulation may contribute to personality development later *dificult babies are more likely to be victims of neglect/abuse*
sections of vertebral column and any defining characteristics
cervical C1-C7 (have foramen TRANSVERSARIUM for arteries and veins, bifid until C7, also have thickened Ligamentum Nuchae) throarcic T1-T12 (have costal facets for rib head and transverse process for tubercles) lumbar L1-L5 (sagittal plane for processes, not very mobile) sacral S1-S5* coccygeal Co1-Co3* bottom two are fused
what plane/tilt does each type of vertebrae have for their ARTICULAR processes and what type of motion
cervical is tilted SUPERIORLY and MEDIALLY *allows most movement*= flex/ext, lateral, rotation thoracic has CORONAL plane, has limited movement- only small rotations lumbar has SAGITTAL plane, has flex/ext motion
where are channels located on myelinated axons *how does this affect MS patients if de-myelination occurs*
channels are on AXON nodes of ranvier on myelinated axons contain voltage gated Na+ channels juxtaparanodal regions have K+ channels only [beneath myelin] where Na channels are determines where current travels- causes jumping of current to nodes *if there is demyelination then these K channels are EXPOSED, less resistance prevents propagation of signal= MS*
membrane conductance vs resistance and formula, what determines
conductance (gm) is measured in Siemens= membrane permeability of IONS resistance (Rm) is measured in ohms= difficulty of ions to pass thru membrane *inverse relationship* Rm=1/gm *BOTH ARE determined by number of ion channels*
current flow- anions vs cations
current flow is based on POSITIVELY charged ions= cations outward current makes the cell MORE NEGATIVE inward makes the cell MORE POSITIVE if you have anions must still use outward/inward to describe flux depending on the condition of the cell (more positive or negative) not the direction
membrane current [formula, requires 2 things]
current= RATE of charged ion flow across the membrane *requires membrane conductance=CHANNELS and driving force= electrical and concentration GRADIENTS, high to low and positive attracts negative charges and vice versa* I= driving force x conductance I = [Vm - Eion] x conductance or I = [Vm - Eion]/R
fusion of vesicle (synaptotagmin, how does it specifically allow fusion?)
depolarization/ Ca influx Ca BINDS to CALCIUM SENSOR= synaptotagmin increases lipid solubility and vesicle is able to fuse with membrane to form a PORE where NT can pass thru may be kiss and run or complete fusion model
frequency coding what and why
describes the frequency of action potentials- if there are more APs then the signal is stronger *allows cells to communicate the INTENSITY of the stimulus*
what determines the 'driving force' of an ion, formula?
determine by both membrane potential [electrical and concentration gradients] and the STRENGTH of the concentration gradient [determined by Nernst equation- permeability/ion channels] [driving force] ∆V= Vm - Eion [membrane potential-ion equilibirum potential] *if membrane potential is equal to Eion then there is no driving force! this is when the ion equilibrium is equal to the current membrane potential*
docking and priming of vesicle to presynaptic membrane (synaptobrevin, SNAP25, Syntaxin)
docking and priming must occur BEFORE Ca influx vSNAREs on the vesicle= synaptobrevin tSNAREs on target= SNAP25 and Syntaxin SNARES interact and zipper up so that vesicle is brought very close to membrane
glial vs neurons permeability (how do changes in perm affect mem potential)
glial cells ONLY perm to K+ *changes in concentration are generally NEGLIGIBLE b/c the amount of K+ required to establish the membrane potential is VERY LOW* neurons perm to both Na/K *if there is a change in permeability for neurons then there is a greater change in membrane potential because cell must ACTIVELY pump out Na/K to compensate*
AA transmitters (gly, glu and gaba)
glycine- INHIBITORY for SPINAL CORD glutamate- EXCITATORY GABA- INHIBITORY for BRAIN (made from Gluatamate by glutamic acid decarboxylase) *inhibitroy GABA made from excitatory Gluatamate in brain*
types of attachment (secure, avoidant, resistant, disorganized)
ideal= SECURE= parent is secure base that child uses to learn avoidant= child is UNRESPONSIVE to the parent, but not distressed resistant= child does not EXPLORE on its own, may appear mad or upset disorganized= child shows INSECURITY, appears confused, flat *may be due to inconsistent responses from parent in the past*
how does increasing/decreasing extracellular concentration of K+ affect resting membrane potential
if you increase PLASMA K+= potential becomes more POSITIVE because K+ is driven to move out of the cell where there is a lower concentration *hyperkalemia* if you decrease PLASMA K+= potential becomes more negative *hypokalemia*
school age children MAJOR development changes
increased INDEPENDENCE increase logical thought (conservation), can understand IRONY ability to FOCUS improved motor skills develop relationships with PEERS, school is important
MAJOR changes in preschool age (3-5)
increased independence, master toilet training by this stage, improved COORDINATION interest in PEERS, MAKE BELIEVE play, can form sentences, grasp conversation start to form GENDER identity have more FLUID motion
Erikson 4-6 stages (industry/inferiority, identity/identity diffusion, intimacy/isolation)
industry/inferiority= 6-11= pride and accomplishment, cooperation identity/identity diffusion= adolescence= who am I, who do I want to be? intimacy/isolation= young adulthood= develop your own family, intimate ties to others
concentration of ions in extra and intracellular fluid, how would solution be without channels
intracellular= protein molecules [A-], K+ NEGATIVE extracellular= blood plasma, CSF, *mostly Na+* and Cl- [sodium chloride solution] POSITIVE *Cl can be ignored both intracellular and extracellular fluid would be ELECTRONEUTRAL without leak channels- must have open diffusion to create typical resting membrane
ionotopic vs metabotropic receptors
ionotropic- receptor DRIECTLY gates the ion channel metabotropic- receptor INdirectly regulates an effector molecule could be a channel, enzyme, etc.
how is neuron suited to generate membrane potentials [excitability, conductance, charge]
it has an EXCITABLE membrane lipid bilayer makes it a good CONDUCTOR [can hold charge] polar heads hold negative charge along membrane- allows for a NET NEGATIVE charge inside the cell
abnormal curvatures= kyphosis, scoliosis, lordosis= which direction, which segment, what population/cause
kyphosis= concave ANTERIORLY in the thorax *may be due to osteoporosis in women, especially elderly* scoliosis= abnomoral LATERAL curvature, may be in thoracic, most common is LUMBAR *may be due to hemivertebrae when one half fails to develop* lordosis= exaggerated lumbar POSTERIOR curvature *may be due to pregnancy or obesity, shifts center of mass and causes back pain*
Freuds psychosexual AGE and SKILLS for stages- latency, genital (6-adult)
latency- 6-11 social values, friendships genital- 12 to adult romantic relationships/ sexual impulses
general strucuture of voltage gated ion channels- P loop, S4 segment and structure
made of a single TRANSMEMBRANE peptide chain that loops thru membrane with ALPHA subunits Pore- loop= P LOOP= between S5 and S6 forms a SELECTIVITY filter= determines what ions can flow thru S4 segment is a VOLTAGE sensor= contains positively charge AA, if it is pulled outward, channel is open *think S4, Sensor 4 voltage*
what makes up a intervetebral disc and what happens if it is HERNIATED
made up of nucleus pulposus (gelatin core) and anulus fibrosus (collagen) found in between BODIES of vetebrae serves as a SHOCK ABSORBER If back is strained, DEGENERATION allows HERNIATION of the nucleus pulposus in the POSTERO-LATERAL direction Pushes nucleus against nerve, compresses nerve and causes pain
channelopathies- pathophysiology and resulting sx- Na channel block
may be due to genetic mutation or autoimmune attack mutations of Na channel are well understood- may be specific to an organ and will cause ALTERED APs ex: periodic paralysis= mutated Na channel causes hyperkalemia- remains depolarized longer than normal= cannot trigger another AP *since channelopathies are specific to organs, can also use DRUGS that are SPECIFIC to organs/tissues channels*
what proteins and molecules are involved in tethering and release of synaptic vesicles
mobilization occurs when Ca triggers movement of vesicles from reserve pool to RELEASABLE pool synapsin is tethering vesicle to cytoskeleton and remains attached until PKA or cAM phosphorylates synapsin and allows vesicle to move to ACTIVE zone now vesicle is positioned near Ca channels (can feel depolarization immediately) and positioned for exocytosis
action potential= when occurs [what must it reach] and what happens [response and stages]
must have a DEPOLARIZING current that produces a large ACTIVE response due to the membrane potential reaching THRESHOLD *consists of rising phase- Na voltage activation, overshoot Na voltage INactivation, falling phase- K voltage activation and then undershoot K voltage slowly de-activates and Na voltage deactivates*
what property of lipid bilayer allows membrane to have a POTENTIAL and what two DRIVING FORCES act on this
need ion channels to create a gradient (permeability/conductance) net movement is driven by: 1. *electrical charge distribution*- positive charges are drawn to negative charges 2. *concentration gradient* high to low
how is the Na flow after an action potential exacerbated and how does the perm of Na compare to K
once the cell is depolarized [made more positive] it OPENS voltage gated channels this allows even more Na to enter the cell due to the GRADIENTS/CHARGE now cell is very positive Na is much more permeable than K+ until INactivation of Na by ball and chain
Freuds psychosexual AGE and SKILLS for stages - oral, anal, phalli (birth-6)
oral- birth to 1 year feeding anal- 1-3 toilet training phallic- 3-6 gender identity/ sex characteristics
membrane permeability vs ion membrane permeability vs membrane conductance
permeability= ease of movement *more perm if there are more channels* ion membrane perm= determined by number of OPEN ion channels membrane conductance= ease of movement of ELECTRICAL charge through membrane conductance=permeability *determined by number of channels*
peer relations in school age children (popular, rejected, controversial and neglected)
popular kids- everyone wants to be their friend either PROsocial (good kids) or ANTIsocial (cool kids) rejected- no one wants to be friends with them may be AGGRESSIVE or WITHDRAWN *puts them at risk to be victim or bully* controversial- mixed reviews, neglected- no one puts them on lists
what makes up pre and post synaptic density
pre= mitochondria, active zone filled with synaptic VESICLEs, cytoskeletal proteins (MTs, neurofilaments) electron dense material found in cleft in between post= plasma membrane proteins such as RECEPTORS, G Proteins, enzymes and structural proteins
when do babies develop senses (which develop after birth)
present at birth= touch, most of taste (except salty), smell, hearing vision is the LEAST mature sense at birth- will develop by 6 months, including color perception
how can you prolong the falling phase of AP
prevent Na DEactivation- cell stays positive longer or prevent ACtivation of K+ so positive cells do not leave the cell and cell stays polarized/positive
where is primary and secondary curvature formed
primary- FETAL position- everything curved concave ANTERIORLY *think, top and bottom curve towards front secondary- in early childhood CERVICAL (hold head) and LUMBAR curvature (support trunk) forms POSTERIORLY lateral curvature also forms OPPOSITE to handedness, helps to carry things
equilibrium potential vs membrane potential
resting charge of membrane when the fluids inside/outside of cell are at equilibrium *for a single ion* MEMBRANE POTENTIAL is the actual potential based on multiple ions-falls somewhere between where equilibrium for K and equilibrium for Na would be it is the SUM OF ALL electrical potentials across the membrane *since membrane is MORE PERM to K+ lies closer to EK* we can ignore Cl- for neurons
what is the resting equilibrium of K/Na ions [when does it occur, where is each ion mostly found, gradients present? how did it reach eq]
resting eq= mostly Na out of cell, mostly K+ in cell equilibrium occurs around -60mV when there is NO NET MOVEMENT because there is no concentration gradient nor electrical gradient only the ions CLOSEST to the membrane influence the potential= everything else is electroneutral
problem areas for school age children
school (learning disability, bullying, friends), attention (ADHD), aggression, depression/anxiety, bed wetting (if older than 7)
leak potassium channel [S/F]
selective membrane ion permeability= only perm to K+ transmembrane PORE filled with water- ALWAYS OPEN establishes resting membrane potential- there is a 20:1 ratio of K+ perm to Na+ perm
Piagets theory of development (Sensorimotor, Preoperational, Concretre Operational, Formal Operational)
sensorimotor- birth to 2 experience things with SENSES, reflexes, make intential behaviors preoperational- 2-7 make believe play, development of language, thing LACKS logic concrete operational- 7-11 LOGICAL thinking, *conservation* organize into hierarchies, not yet abstract formal operational- older than 11 ABSTRACT thinking, reason with symbols and think of multiple solutions to a problem
enzymes and precursors for serotonin
serotonin is synthesized from TRYPTOPHAN TRP converted by Trp hydroxylase to 5 HTP 5HTP converted by 5HTP decarboxylase to Serotonin (5-HT)
difference between small and large NT (where synthesized, give examples, what is co-expression
small NT are made and packaged into vesicles within the NERVE TERMINAL *Ach, GABA, NE, etc. large NT are made and packaged into vesicles in the CELL BODY, then transported ANTEROGRADELY down axon to terminal *Nueroactive peptides- Substance P most neurons MAKE BOTH *co-expression*
three major categories (+others) and characteristics of small molecule tranmitters
small NT have low MW, made within the nerve terminal - transferred into vesicle for storage amino acids= glycine, glutamate and GABA BIOGENIC amines= CATECHOLAMINES (NE, DA, Epi), Serotonin, HIstamine Ach others= ATP, NO
when do infants reach social smile, laughing and familiar smiles, multiple types of smiles
social = 1-2 months laughing= 3-4 months familiar people may get increased smiles at 6 months several different smiles at 10-12 months
synaptotagmin vs synaptobrevin vs synapsin vs syntaxin
synaptotagmin= Ca sensor- allows for FUSION of membranes synaptobrevin= vSNARE synapsin= tethers vesicle to cytoskeleton syntaxin= t SNARE (along with SNAP 25)
Curare and Barbiturates/Benzodiazepine drugs
targets postsynaptic NICOTINIC ACH receptor- ANTAGONIST- prevents activation of Ach receptors= paralysis/ muscle relaxant Barb/Benzos bind GABAa receptors as AGONists and ENHANCE the inhibitory effects of GABA depresses the CNS- used for SEDATION, preventing seizures, promote sleep, reduce anxiety
how does an AP travel, what is forward AP called
the AP is REGENERATED at each segment along the length of the axon due to traveling current of ions once next portion is DEPOLARIZED, Na channels open and propagate the polarization *previous segments are hyperpolarized and in refractory period so current does not travel backwards* ORTHDROMIC are forward, antidromic are backward
Dales law
the SAME transmitter is released from ALL SYNAPTIC terminals may be a co-expression of TWO transmitters in a single neuron= one small NT and one neuropeptide
membrane time constant [what properties of cell contribute, what factors determine each variable]
time constant= LAG between flow of current and change in membrane potential *determined by RESISTANCE [ion channels] and CAPACITANCE [surface area and thickness]* want the time constant to be low, therefore, need resistance and capacitance to be LOW [many channels and thick membrane]
MAJOR changes in toddlerhood (1-3 years)
toilet training (Freud, anal stage), independence (Erikson- autonomy), sensorimotor (Piaget) LANGUAGE EXPOLOSION- learn the "rules", form sentences, learn how to tell stories (pragmatics- appropriate communication) empathy appears, improved motor skills to EXPLORE, egocentrism (dont think of NEGATIVE consequences), have a SENSE of SELF
Erikson 1-3 stages (trust/mistrust, autonomy/doubt, initiative/guilt)
trust/mistrust= birth to 1= trust allows development of relationships autonomy/shame and doubt= 1 to 3= develop sense of self, *parental permission is important here* initiative/guilt= 3-6= role play, discover responsibility, what they can do
when do infants reach milestones of turning over, sit without support, teething, fear of strangers, crawling, first words, walking
turn over and transfer items from hand to hand around 4 months sit up without support and imitate at 6-7 months teething 6-8 months fear of strangers, crawling around 8-12 months first words, walking around 12-15 months
ball and chain Na channel
typically the ball is freely hanging upon activation of voltage gate the ball remains hanging eventually it can bind and PREVENTS further depolarization of the cell potential by BLOCKING more Na movement inactivates the channel so that membrane returns to resting potential, K perm takes over
unmyelinated vs myelinated axons [what determines how far AP signal can travel, which has a longer length constant?]
unmyelinated axons have less membrane surrounding them *LENGTH constant determines how far current goes- therefore depends on diameter and number of ion channels* a larger diameter will cause a FASTER CONDUCTION VELOCITY in both unmyelinated and myelinated neurons myelinated axons have widely dispersed ion channels [at nodes of Ranvier], decreased capacitance [thicker membrane does not allow cell to hold charge well] and MORE RESISTANCE [signal jumps from node to node] all of this increases the length constant *myelination in general allows for FASTER propagation than demyelinated axon singals*
Piagets assimilation vs accomodation
use schemas to organize info/construct knowledge assimilation- add information to current schema accomodation- alter schema to allow new information to be included
ionotropic receptors S/F where can drugs interfere
used for SMALL NT rapid gating, fast synaptic transmission may be perm to many cations- if driving force exists= ion movement once NT binds ions enter the cell and CHANGES the MEMBRANE POTENTIAL - inhibitory or excitory may have modulatory sites that alter how long channel opens *MODULATORY sites are important sites for DRUG ACTION*
components of Na channel [voltage sensor, ball and chain, pore] and role of each upon depolarization
voltage sensor (S4) - receives signal and once it reaches threshold [positive charge] it opens the gate ball and chain- is NOT bound when depolarization first occurs, binds once cell is very positive/depolarized pore (P loop) for Na ions- Na ions ENTER cell due to opening of gate *when voltage sensor moves OUTWARD*
why does the cell have a refractory period
while the cell is depolarized by Na voltage channels and then quickly the ball/chain binds- prevents a NEW POLARIZATION [absolute refractory] additionally, the hyperpolarization of the cell makes it more negative than resting so it is MORE DIFICULT to reach threshold [relative refractory]