Biological Basis of Behavior Flashcards

(51 cards)

1
Q

Describe the synapse between a motor neuron & a muscular junction

A
  • Synapse btw moror neuron & muscular junction
    • AP propogates wave of depolarization (opens Nav)
    • Cav that causes flux of Ca at the presynaptic terminal - leads to fusion of vesicles that contain neurotransmitters (ACh)
      • ACh diffuses into the synapse - binds to nicotinic AChR (Na channels)
      • causes depolarization - AP on muscle membrane
        • propogates to sarcoplasmic T-tubules which creates calclium flux -> muscle contraction
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2
Q

Nicotinic ACh receptors are what type of receptor?

Describe their composition & binding sites.

A

ligand-gated ion channel

5 subunits in a donut shape looking into plane of membrane w/ ion channel in middle ; 2 agonist binidng sites on alpha subunits -> conformational change

leads to Na influx and depolarization

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3
Q

Muscarinic ACh receptors are what type of receptor?

A

G protein coupled recptors

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4
Q

What are the 5 subunits of the nicotinic AChR?

A

a2Byd

alpha(2), beta, gamma, delta

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5
Q

What is the function of agrin?

A

triggers the clustering of acetylcholine receptors (AChR)

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6
Q

How does agrin trigger the clustering of AChR?

A

binds to receptor & co-receptor -> activates muscle specific tyrosine (MuSK) -> phosphorylates other kinasea & leads to clustering

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7
Q

What two proteins are required for clustering?

A

Agrin

Rapsyn

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8
Q

What is the goal of ACHR regulation with regards to location?

A

upregulate AChR syntheis at NMJ

down regulated AChR synthesis distant from NMJ

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9
Q

How is synthesis of AChR downregulated?

Where would you want this to occur?

A

Electrical activity

down regulated AChR synthesis distant from NMJ

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10
Q

Describe the pathophysiology of MG & how this might relate to AChR expression at the NMJ

A
  • Presentation
    • muscle weakness that worsens after periods of activity & improves after periods of rest
  • d/t autoAb for AChR -> decreased signaling & degradation of NMJ
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11
Q

Symptomatic Acute treatment for MG?

A

pyridostigmine

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12
Q

Chronic treatment MG?

A

immunosupression / thymmectomy

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13
Q

Pyridostigmine

MOA

AE

A

Pyridostigmine

  • MOA
    • ACh esterase inhibitor
    • does not cross BBB
  • AE
    • sweating
    • diarrhea, nausea, vomiting, abdominal cramps, increased salivation
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14
Q

What word describes:

physiological responses that occur more or less unconsciously when the brain detects situations

A

emotions

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15
Q

What word describes:

the conscious experience resulting from the emotions

A

feelings

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16
Q

What word describes:

some stimuli evoke emotions automatically

A

emotional competence

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17
Q

Describe the pathway of emotional stimuli

A
  • Emotional stimuli -> thalamus -> hypothalamus & sensory cortex
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18
Q

What is the role of the hypothalamus in the emotional response?

Descending & ascending connections?

A
  • evaluates the emotional quality &
    • descending connections give rise to emotional response
    • asecnding connections to hippocampus & anterior thalamus give rise to feelings
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19
Q

How is synthesis of AChR up regulated?

A

Neuregulin activation of ErbB tyrosine kinase - HER2 receptor

Induces AChR synthesis

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20
Q

What is the function of the Cingulate Cortex?

How does it communicate wihth the hypothalamus?

A

creating feelings

hypothalamus -> anterior thalamus -> cingulate cortex

cingulate cortex -> hippocampus -> hypothalamus

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21
Q

What are the roles of the limbic system?

A
  • emotional behavior
  • memory
  • integration of homeostatic responses
    • preservation of the species
    • securign food
    • fight or flight response
  • sexual behavior
  • motivation
22
Q

What is the major function of the hippocampal formation?

A

learning & memory formation

23
Q

What is the major function of the cingulate gyrus?

A

emotional behavior & pain

24
Q

What is the major function of the amygdala?

A

v. important site for emotion & fear

25
What is the major function of the nucleus accumbens?
pleasure & _addiction_
26
What is the major function of the pre frontal cortex?
social interaction
27
The amygdalal receives information from what afferents? Role with theses stimuli?
olfactory, somatosensory, auditory, visual (most are reciprocal) integration of stimuli & actions
28
What is the term for: learn to associate predictive stimuli with danger, harm, or pain
conditioned fear
29
What is the term for : inborn avoidance
innate fear
30
Fear conditioning can be blocked by damage to what structure?
amygdala
31
Describe the pathway for processing through the amygdala of a stimuli recognized to be a threat
* Cortex / Hippocampus / Talamus * -\> Lateral Nuclear Complex of Amygdala * -\> Central Nucleus * -\> Hypothalamus * (sympathetic activation of CRF release)
32
The hypothalamus releases what substance in response to fear? This leads to what physiologic responses?
* Corticotropin releaseing factor (CRF) * -\> release of cortisol from adrenals * suppress inflammation * catabolic state * heighten arousal * survival resoponse
33
The amygdala controls the release of what stress hormones?
CRF epinephrine norepinephrine cortisol
34
Why does the amygdala communicate with the hippocampus?
enhances the memory of the stressful event
35
What are the subcategories of implicit & explicit memory?
* Implicit (non-declarative) * unconscious * perception & motor skills * Explicit (declarative) * conscious recall * people, places, objects
36
What were the impact on memory for patient H.M. who had bilateral medial temporal lobes removed?
* Long-term memory (some retrograde amnesia) & short-term memory in tact * dramatic lack of transfer of short-term to long term * Learning motor skills in tact
37
Lesions where will have no impact on implicit memory but will impact explicit declarative memory?
medial temporal lobe
38
Damage to the hippocampus can cause problems with what type of memory?
impair **explicit** memory storage explicity memory (episodic & semantic)
39
What is the functional significance that hte septum & amygdala are involved in informaiton modulation?
things learned ina happy state are better recalled during a happy state than during a sad state things learned during a sad state are better recaled when feeling sad
40
What are the 3 cellular mechanisms of implicit memory?
**habituation** (decrease in transmitter release upon repeated stimulation) sensitization facilitation
41
What is the cellular mechanisms of explicity memory?
long term potentiation (activity dependent increased synaptic efficacy)
42
What is the term for: the inabilityto move information from short-term to long-term memory?
anterograde amnesia
43
What site is most heavily damaged in Alzheimer's disease & is also the site of early onset?
entorhinal cortex
44
What is Wernicke-Korsakoff syndrome? Cause?
memory disruption d/t loss of neurons in the mamillary nuclei (amnesia & confabulation) cause: prolonged thiamin (vit B1) deficiency (chronic alcoholics)
45
What is the relationship between the hippocampus & seizures?
low threshold for seizure activity -\> does not become generalized
46
What is the earliest clinical sign of a subfrontal meningioma?
anosmia
47
What is the significance of Alzheimer pathology occurring at the entorhinal cortex?
isolates hippocampal formation from rest of cerebral cortex
48
Characterization of temporal lobe epilepsy?
psychological & motor manifestations
49
Where is the likely neuropathology seen in schizophrenia?
cortical & subcortical limbic structures
50
What are the symptoms of herpes simplex encephalitis?
* focal seizures, focal neurologic signs, progressive deterioration of consciousness * necrotizing process with a predilection of the limbic system
51
What is the clinical impact of diazepam?
anxiolytic (benzodiadepam) increased the time mice spent on the "open arms" ledge - decreasing innate fear response