Anatomy 2 Flashcards

1
Q

what’s in a neuronal circuit? exception?

A

stimulus –> *sensory neuron –> *spinal cord response/1+ interneuron –> *motor neuron –> effector muscle. stretch reflex (no interneurons –> monosynaptic)

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2
Q

Propriospinal fibers

A

fibers travel b/t levels of the spinal cord –> link limbs together for a single reflex; Part of white matter immediately adjacent to gray matter, present in all funiculi; Form fasciculi propri

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3
Q

innate vs acquired/conditioned reflexes

A

connections that form b/t neurons during development & are genetically programmed
o Ex: spinal reflex— occur w/o immediate conscious awareness –> sent to higher centers & conscious sensation may result (e.g., pain)
 Most are never consciously sensed
 Spinal reflexes can be suppressed by conscious thought arising from higher centers
vs
enhanced by repetition; more complex, learned (somatic) motor patterns

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4
Q

Effective spinal reflexes (in correcting & adjusting muscle movement) –> need very detailed motor output & very accurate sensory input describing fxnal status of ea muscle at ea instant. How?

A

2 sensory receptors in skel muscle provide subconscious, continuous feedback to the spinal cord –> cerebellum –> cortex: Golgi tendon organs for muscle tension, muscle spindle organs for muscle length. both = proprioceptors (conscious in post column, subconsc in spinocerebellar tracts)

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5
Q

muscle spindles. explain all their fibers

A

elongated, sac-like structures W/IN skel muscles. 8-12 modified intrafusal fibers in parallel w/ extrafusal fibers. 2 classes of intrafusal: nuclear bag (clustered nuclei, #2-4 per spindle) supplied by type Ia sensory nerve fibers/primary endings & dynamic y-motor neurons, nuclear chain (single-file, #6-8 per spindle) supplied by type II sensory nerve fibers/secondary endings & static y-motor neurons

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6
Q

how do muscle spindles receive SENSORY info about muscle length? why does CNS need to care?

A

intrafusal fibers in parallel w/ extrafusal –> when extrafusal stretches, intrafusal feels it too. muscle = always feeling some amt of stretch –> type Ia & II give info to CNS abt amt => static response; type Ia give info to CNS abt rate of change of stretch => dynamic response… CNS cares b/c stretching w/o correction can dmg muscle

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7
Q

how do muscle spindles receive MOTOR info about muscle length? –> primary vs secondary response? do alpha and y-motor neurons need to be coactivated & why?

A

sensory input –> activate alpha motor neurons –> extrafusal fibers ctx to counter stretch & potential injury vs activate y-motor neurons –> reg activity intrafusal fibers to report amt & rate of change. yes or else intrafusal = slack relative to extrafusal –> can’t efficiently report muscle length to CNS

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8
Q

what is myotatic/stretch reflex? what neurons = involved?
what’s reciprocal inhibition?

A

sudden stretch of muscle –> reflexive ctx of that muscle. single type Ia sensory neuron w/ homonymous alpha motor neuron
seen in patellar reflex: type Ia sensory neurons excite inhibitory interneurons that innervate motor neurons in flexors/hamstrings –> hamstrings relax –> quads ctx

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9
Q

dynamic/phasic vs static/tonic stretch reflex

A

type Ia sensory fibers oppose sudden changes in muscle length vs BOTH type Ia & II sensory fibers respond to slower/steady stretch –> make small instantaneous corrections –> prevent us from falling while standing and smooth ctx

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10
Q

when is stretch reflex strongest? can it be suppressed?

A

in gravity-opposing extensors. yes in higher centers b/c strength of reflex = low enough

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11
Q

golgi tendon organs. what happens to GTO w/ inc muscle tension?

A

encapsulated nerve endings of unmyelinated type Ib afferent fibers entwined in collagen of muscle, equalize contractile forces among groups of muscle fibers. nerve endings = compressed by collagen –> impulses sent in proportion to degree of compression

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12
Q

type Ib sensory fibers of GTO synapse on 2 types of interneurons in ant horn of gray matter:

A

inhibitory interneurons: inhibit alpha motor neurons of active muscle –> relaxes them to avoid tension overload
excitatory interneurons: activate alpha motor neurons of antagonist muscles –> ctx them to unload active muscle

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13
Q

what is inverse myotatic/stretch reflex? what’s lengthening rxn?

A

inc muscle tension –> GTO causing relaxation. spinal cord can mediate instant relaxation of entire muscles in extreme tension –> prevents tears or tendon avulsion

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14
Q

what’s flexor reflex? does it always involve flexor muscles? what’s crossed extensor reflex?

A

involves whole limb (stretch reflex and GTO reflex involve single muscle) –> quicker ctx of flexor muscles to w/draw from noxious stimuli detected by nociceptors to type II & III afferents. no. after flexor reflex –> contralat limb extends to support & push body away from stimulus (LE) and provide bal (UE)

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15
Q

hyperalgesia vs analgesia vs allodynia

A

inc pain from something that nmlly provokes pain vs no pain from something that nmlly provokes pain vs pain for something that doesn’t provoke pain

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16
Q

what are nociceptors? where are their free nerve endings?

A

sensory receptors detecting stimuli that elicit tissue dmg, or signals/chemicals from dmged tissue; free/bare nerve endings in skin, muscle, joints/bone, viscera

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17
Q

Aalpha/beta vs Adelta vs C fibers

A

myelinated, lg, proprioception/light touch vs lightly myelinated, medium, nociception vs unmyelinated, small, innocuous temp/itch/nociception, responds to inflam –> gives pain sensation after a cut

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18
Q

what is pain? acute vs chronic pain. mechanism for chronic pain?

A

submodality of somatic sensation –> unpleasant sensory & emotional experiences assoc w/ tissue dmg. activation of nociceptors for short time, no sig tissue dmg vs pain lasting mo+ from tissue injury, inflamm, nerve dmg, tumor/lesion, occluded blood vessels –> evoke chemical, fxnal, structural changes (like activating G proteins). noxious peripheral stimuli –> excitatory gluE and asp bind to NMDA receptors –> hyperalgesia, neuropathic pain

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19
Q

pain categories: fast pain/pinprick/sensory pain vs burning/soreness pain vs aching pain

A

sharp/stinging pain, well localized, on skin, neospinothalamic tract; Adelta vs inflamm secondary to tissue dmg, diffuse & lasts longer, on skin or muscle, paleospinothalamic & archispinothalamic tracts; C fibers vs poorly localized pain form deep structures like joints or viscera, paleospinothalamic & archispinothalamic tracts; C fibers

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20
Q

know how pain = transmitted

A

noxious stimulus from periphery –> primary afferent neurons (A or C fibers) –> DRG –> dorsal root projection neurons in spinal cord –> higher centers

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21
Q

somatic pain = classified into: superficial/cutaneous/peripheral pain vs deep pain

A

pain from skin, muscle, peripheral nerves; has initial response then later response vs pain form joint receptors, tendon, fascia; has autonomic response like sweating, nausea, change in bp & HR

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22
Q

visceral nociceptors. where are their free nerve endings?

A

contain mechanical pressure, temp, chemical and silent nociceptors. free nerve endings = scattered –> any stimulus that excites them cause visceral pain

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23
Q

cause vs s/s of visceral pain

A

GI lesions/tumors, artery thrombosis, tissue obstruction or stretching vs low grade diffuse pain, low HR and bp, cold sweats, nausea, hunger, thirst, electrolyte imbal, irreg circ/resp systems

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24
Q

referred pain vs phantom pain

A

pain from same myotome b/c innervated by same nerve, but not where pain actually originated from vs pain receptors = activated post amputation b/c brain can’t understand it

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25
Q

gate control theory

A

nonpainful input closes painful/noxious input –> prevent pain sensation from traveling to CNS; large sensory fibers w/ cutaneous sensory input activate inhibitory interneurons –> inhibit pain transmission by pain fibers

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26
Q

syringomyelia. s/s?

A

when fluid-filled cavity/cyst forms w/in spinal cord => syrinx; syrinx can expand over time –> destroy surrounding nerve tissue. pain in neck & shoulders, pain & stiffness in legs, muscle weakness, numbess/dec sensation, scoliosis, chiari malformation

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27
Q

mechanoreceptors: rapidly adapting vs slowly adapting

A

signal a change in stimulus; Meissner corpuscles (touch), Pacinian corpuscles (pressure, vibration); respond at beginning & end of stimulus vs signal continued presence and intensity of stimulus; Merkel discs (touch), Ruffini corpuscles (steady pressure); respond at beginning of stimulus then dec then stops when stimulus stops

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28
Q

what is a receptor potential?

A

when sesnsory receptors transduce physical stimulus ot electrical signal –> open/close ion channels

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29
Q

mechanoreceptors produce what type of RP? deformation of ion channels are?

A

depolarizing RPs. stretch-gated –> dendrite stretches –> ions flow in/out

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30
Q

short duration vs long duration stimuli

A

make constant RP and AP; proportion to duration vs time dependent decline in RP and AP; more robust NT release

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31
Q

what is receptive field?

A

area of sensory space = stimulated –> elicits neuronal responses

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32
Q

know DCML

A

primary neurons at DRG & ascend in dorsal funiculus –> secondary neurons in gracile/cuneate nucleus –> decussate as internal arcuate fibers –> ascend thru med lem –> thal –> postcentral gyrus

33
Q

2 point discrimination

A

most densely innervated body regions –> most sensitive –> have smallest 2pt discrim threshold, greatest somatosensory cortical representation

34
Q

what types of sensations are detected in anterolat system vs post column?

A

pain, temp vs vibration, joint position/proprioception

35
Q

midbrain vs pons vs medulla oblongata

A

from forebrain to pons w/in tentorial notch; has nuclei for CN3, 4; cerebral peduncles, interpeduncular fossa, optic tracts lat around midbrain vs from midbrain to med obl; CN5-8 at pontomedullary jxn; middle cerebellar peduncle-C5-basilar pons, rhomboid fossa vs from pons to spinal cord; CN10-12; pyramids, corticospinal tracts & DCML, inf olivary eminences

36
Q

brainstem: tectum vs tegmentum vs basis

A

in dorsal midbrain; 2 sup + 2 inf colliculi => corpora quadrigemina; sup colliculus + lat geniculate body => visuo/motor system via brachium of sup colliculus, inf colliculus + med geniculate body => auditory system via brachium of inf colliculus vs ventral to aqueduct in midbrain & ventral to 4th ventricle in pons; cranial nerves & most reticular formation vs most ventral; corticospinal and corticobulbar tracts

37
Q

medial medullary/Dejerine syndrome

A

disrupt ant spinal a –> medulla infarct; dmg corticospinal tract/pyramid –> contralat hemiparesis, medial lemniscus –> contralat loss of position/ vibration/discrim touch, CN12 –> tongue deviation to ipsi/tongue atrophy/fasciculations

38
Q

lateral medullary/Wallenburg syndrome

A

disrupt PICA; dmg spinothalamic tract –> contralat loss pain/temp on body, spinal trigeminal tract of V –> ipsi loss pain/temp on face, nucleus ambiguus (motor for CN9&10) –> dysphagia/palate paralysis/ hoarse/dec gag reflex, descending hypothal –> ipsi Horner syndrome, vestibular nuclei –> N/V/nystagmus/vertigo, inf cerebellar peduncle/spinocerebellar fibers –> ipsi ataxia

39
Q

medial pontine syndrome

A

disrupt paramedian branches of basilar a –> ipsi 6th nerve palsy; dmg corticospinal tract –> contralat hemiparesis, medial lemniscus –> contralat loss position/vibration/discrim touch, CN6 –> /esotropia

40
Q

locked in syndrome

A

occluded basilar a, bil pons lesion –> only movement in eyes & eyelids

41
Q

medial midbrain/Weber syndrome

A

disrupt paramedian branches of post cerebral a –> 3rd nerve palsy; dmg corticospinal tract –> contralat hemiparesis UE, corticobulbar tract –> contralat paresis of lower face, CN3 –> ipsi paralysis of ocular adduction/exotropia/mydriasis/ptosis

42
Q

know which eye muscles are innervated by what and conseq

A

“LR6, SO4, all others 3”. Lec 13-14, slide 61

43
Q

what does cerebellum do? know anatomic, phylogenetic, fxnal name of lobes

A

timing & force of ctx of voluntary muscles for smooth muscle ctx; fold in to folia. Lec 16, slide 4

44
Q

sup vs middle vs inf cerebellar peduncle

A

fibers decussate, cerebellum output vs pontocerebellar fibers from pontine nuclei & project to contralat cerebellum, cerebellum input vs lg part of restiform body in med & sm part of juxtrarestiform body in 4th ventricle, spinal cord fibers, cerebellum input

45
Q

what are cerebellar nuclei?

A

paired nuclear bodies in white matter near roof of 4th ventricle, influences motor activity

46
Q

cerebellar nuclei divisions: vermis vs intermediate/paravermal hemisphere vs lat hemisphere vs floccolonodular lobe. globose + emboliform make up what?. know what ea nuclei look like in section

A

head, trunk, prox limb; fastigial nuclei vs distal appendicular muscle; interposed nuclei vs motor planning in extremities & multi-joint motor programs; dentate nuclei vs bal & vestibulo-ocular reflexes. interposed nuclei. Lec 16, slide 10

47
Q

lesions to cerebellum or cerebellar peduncle cause what effects? know diagram on Lec 16, slide 16. spinal lvls of Clarke’s column

A

ipsi effects; ataxia (discoordination of agonist & antag muscles in multi-joint movements) –> unsteady trajectory, over/undershooting target => dysmetria, abnl timing => dysrrhythmia. Lec 16, slide 16. T1-L2

48
Q

cerebellar cortex: molec layer vs Purkinje cell layer vs granule cell layer

A

granule cell axons, purkinje dendrites, interneurons vs all cerebellar output in white matter vs excitatory neurons

49
Q

2 primary axonal inputs to cerebellum: mossy fibers vs climbing fibers

A

cerebellar cortex –> synapse w/ granule cells –> granule axons bifurcate to parallel fibers –> parallel fibers excitatory synapse w/ Purkinje cells –> Purkinje axons inhibitory synapse w/ cerebellar nuclei vs contralat inf olivary complex excitatory wrap around Purkinje cells –> desensitize Purkinje from parallel fibers (parallel fibers stellate cells & basket cells laterally inhib neighboring Purkinje)

50
Q

know AICA, PICA, SCA territories

A

Lec 16, slide 20

51
Q

cerebellar lesions: ant lobe vs post lobe vs flocculonodular lobe syndrome

A

from alc, malnutrition; Purkinje cells first affected; lose coordination in LE and progress to UE if not txed vs from CVA, tumor, accidents, degen dz; intention tremor w/ volitional movement vs truncal ataxia (wide stance to bal); common in children w/ tumors in roof of 4th ventricle

52
Q

basal nuclei/ganglia. dorsal vs ventral divisions?

A

gray matter masses in cerebral hemispheres influencing motor activity. caudate & putamen ( => striatum –> primary input), globus pallidus (interna –> output); fxnally related to dorsal: substantia nigra, subthal nucleus, pedunculopontine tegmental nucleus vs nucleus accumbens, substantia innominate, basal nucleus of Meynert, olfactory tubercle

53
Q

4 loops of basal ganglia: motor vs executive vs motivational vs visuomotor loop

A

influence motor activity vs cog mechanisms to multitask vs having drive, pleasure, want, emotion vs sup colliculus influencing extraocular movement

54
Q

3 NT and their pathways: gluE vs GABA vs dopamine

A

excitatory influence on striatum vs inhibitory output from striatum to substantia nigra & globus pallidus interna vs faciliatory effects w/ D1 receptors & depressant effects w/ D2 receptors from substantia nigra to nigrostriatal pathway. can modulate both in/direct but DRIVES DIRECT

55
Q

direct/globus pallidus medial vs indirect/globus pallidus lateral pathway BG motor circuit

A

premotor cortex –> striatum –> substantia nigra pars reticulata & GPi –> inhib output nuclei on thal –> cortex –> spinal cord vs premotor cortex –> striatum to GPe –> to subthal nucleus –> excite output nuclei on thal –> cortex –> spinal cord

56
Q

dyskinesia vs bradykinesia vs akinesia vs hypokinetic vs hyperkinetic vs dystonia vs ballismus vs chorea vs athetosis vs rigidity. know ranking movement d/o by speed

A

abnl movement from BG d/o vs dec vel & amp in movements vs unable to initiate voluntary movements vs dec movement vs inc movement vs slow, repetitive, sustained, twisting movements vs unctrlled flinging and/or rotaory movements vs rapid, irreg, involuntary, dance-like movements flowing from 1 region to another vs continuous writhing of distal portions of 1+ extremities esp UE vs inc resistance to passive movement. Lec 17, slide 13

57
Q

Huntington’s chorea vs Sydenham chorea

A

caudate > putamen in indirect pathway degenerate –> choreiform movements, cog & speech deteriorate –> bedridden; auto dom vs beta hemolytic streptococci –> ab against bacteria attack epitopes of BG => autoimmune dz –> rapid irreg movements of limb, face, trunk

58
Q

hemiballismus

A

vasc lesion, infarct, dmg to contralat subthal nucleus –> more ballismus

59
Q

Parkinson’s

A

degen melanin in granule-containing dopaminergic cells from substantia nigra pars compacta –> pill roll tremors, shuffling gait, stooped posture, mask-like facial expression, lose “arm swing” during gait

60
Q

deep brain stimulation

A

electrodes placed on various nuclear structures esp subthal nucleus –> connect to subq electrical stimulator; replaced ablation procedures

61
Q

Wilson dz/hepatolenticular degen

A

auto rec mutation in gene for copper-transporting protein –> copper accumulates in liver, lenticular nucleus, eye –> hyperkinetic d/o, Kayser-Fleischer rings around iris

62
Q

hypothal has 3 sites of fxnal influence: ant pit vs post pit vs non-pit of hypothal. know which site does HEAL

A

f/light, stress, sex/reprod, growth, metab vs body fluid bal, maternal behavior vs temp, circadian rhythem, immunity, appetite, autonomic nervous system. Lec 18, slide 8

63
Q

know Lec 18, slide 11

A

yep

64
Q

medial vs ant preoptic nucleus vs suprachiasmatic nucleus

A

neuronal maturation –> sexual dimorphism, high GnRH make neurons produce lg peptides to target cells in ant pit vs maintain body temp vs direct retinal input, circadian rhythm

65
Q

paraventricular vs supraoptic nuclei

A

both of their axons project to post pit that store their NT in terminals; circumventricular organs esp OVLT give systemic feedback to hypothal. secrete oxytocin vs secrete vasopressin

66
Q

dorso/ventromedial nuclei vs ant nuclei of hypothal; what happens if there is a lesion?

A

feed, reprod, parenting, thermoreg vs appetite; medial (satiety center) –> obesity, lateral (hunger center) –> anorexia

67
Q

post hypothal vs mammillary body

A

respond to temp changes –> sweat/shiver, lesion –> hypothermia; arousal, shift of attn, behavior vs limbic forebrain & midbrain fxnal integration –> emotions

68
Q

epithal vs thal. thal blood supply

A

periventricular nuclei, habenular nuclei, stria medullaris, post commissure, pineal gland vs 2 ovoid grey matter masses making lat borders of 3rd ventricle, connected by interthalamic adhesion, have internally medullary lamina, separated in 3 groups: ant, med, lat. ant: thalamoperforating branches of P1; post: thalamogeniculate branches of P2; caudomedial area: medial post choroidal a (P2)

69
Q

know thal nuclei

A

Lec 19, slide 14

70
Q

relay nuclei vs association nuclei vs reticular nuclei

A

receive specific info and relay it to precise cortical target vs receive input from diverse regions & project to mult cortical regions; dorsomedial nucleus: receive afferents from olf, amygdala –> projects efferents to frontal lobe (dmg –> Wernicke-Korsakoff syndrome); pulvinar: process secondary visual info –> reciprocal projection relationship w/ sup colliculus, visual cortex, frontal & temp cortices (dmg –> visual attn d/o); centromedian: arousal, attn vs receive collateral afferents & to thal

71
Q

internal capsule: ant limb vs genu vs post limb

A

b/w head of caudate nucleus & tentiform nucleus. frontopontine fibers: from frontal lobe to pontine nuclei for cerebellar involvement, thal radiations: connect thal to cortex, FEF fibers: from front eye field to CN nuclei vs closest to ant tubercle of thal; corticobulbar fibers: project to motor nuclei of CN vs b/w thal & lentiform nucleus; corticospinal tract: projects to ventral horn, thal radiations

72
Q

what are the 4 limbic fxns? HOME

A

homeostasis (autonomic, neuroendocrine), olf, mem, emotion/drive

73
Q

hippocampus fxns. what are its 3 parts?

A

mem, learning. dentate gyrus, hippocampus proper, subiculum

74
Q

Papez circuit. Wernicke’s encephalopathy vs Wernicke-Korsakoff syndrome

A

transfer short term mem to long term mem; hippo emits signals to reverberate circuit –> store permanently in cerebral cortex for long term mem. hippo –> fornix –> mamillary nuclei/bodies –> mamillothalamic tract –> ant thalamic nucleus –> thalamogeniculate radiation –> cingulate gyrus –> cingulum –> hippo. thiamine defic exac by alc –> atxia, ophthalmoplegia, confusion –> thiamine supplements, stop alc vs advanced Wern’s encephalopathy –> dmg Papez circuit –> ant/retrograde amnesia, confabulation, apathy; dmg dorsomedial thal nuclei

75
Q

Alzheimer’s

A

irreversible senile dementia; assoc w/ reduced cholinergic activation, degen neurons in entorhinal cortex & subiculum of hippo

76
Q

dopaminergic pathways = in midbrain: mesolimbic vs mesocortical vs mesostriatal/nigrostriatal vs tuberoinfundibular pathways

A

ventral tegmental area –> limbic structures vs VTA –> prefrontal cortex vs substantia nigra pars compacta –> caudate/putamen vs hypothal –> pituitary

77
Q

nucleus accumbens. what happens if excess dopamine?

A

primary mesolimbic DA target –> motivation/drive/reward. euphoria related to psychostimulants, schizo

78
Q

amygdala. know pathway. Kluver-Bucy syndrome

A

in uncus of med temporal lobe. experience consequences, fear, f/light, anxiety, aggression. Lec 20, slide 32. bil destruction of amygdala –> no fear, hypersexuality, docile, overly attentive to all sensory stimuli

79
Q

hypothal reg for water bal

A

dec plasma vol –> renin –> angiotensin II –> hyperosmolality –> hypothal-hypophyseal tract –> circumventricular organs –> paraventricular & preoptic nuclei activated by OVLT –> release vasopressin/ADH –> renal receptors –> H2O & electrolyte reabsorption from urine –> restore nml osmolality