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Neuro > Autonomic Nervous System B&B > Flashcards

Autonomic Nervous System B&B Flashcards

1
Q

what is the indirect method by which the parasympathetic system causes vasodilation?

A

induces endothelium to release NO (nitric oxide) —> lowers BP

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2
Q

what is the neurotransmitter and receptor type at the first and second synapse of the parasympathetic nervous system, respectively?

A

1st: acetylcholine (ACh) binds nicotinic receptors

2nd: acetylcholine (ACh) binds muscarinic receptors

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3
Q

what is the neurotransmitter and receptor type used at the first synapse in the sympathetic nervous system?

A

acetylcholine binds nicotinic receptor (same as parasympathetic)

[this also applies to synapsing directly on the adrenal medulla to simulate nor/epinephrine release]

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4
Q

what is the neurotransmitter and receptor type used at the second synapse of the sympathetic nervous system at the following targets:
a. sweat glands
b. cardiac and smooth muscle, gland cells
c. renal vasculature, smooth muscle

A

a. sweat glands: acetylcholine binds muscarinic receptors

b. cardiac and smooth muscle, gland cells: norepinephrine binds alpha/beta adrenergic receptors

c. renal vasculature, smooth muscle: dopamine binds dopamine receptors

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5
Q

what is the neurotransmitter and receptor type used to stimulate somatic skeletal muscle?

A

acetylcholine binds nicotinic receptors

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6
Q

what is the main neurotransmitter for the sympathetic, parasympathetic, and somatic muscle systems, respectively?

A

SNS uses norepinephrine mostly

PNS uses acetylcholine on muscarinic receptors

somatic muscle uses acetylcholine on nicotinic receptors

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7
Q

describe the process by which acetylcholine is released into the synaptic cleft (4)

A
  1. choline enters presynaptic neuron and combines with acetyl-CoA to form acetylcholine
  2. acetylcholine is packaged into vesicles by choline-acetyl-transferase (ChAT)
  3. depolarization causes calcium influx
  4. Ca2+ triggers ACh vesicles to fuse with neuron membrane/ exocytosis occurs
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8
Q

what is the effect of the following drugs on acetylcholine release into the synaptic cleft?
a. hemicholinium
b. vesamicol
c. botulism

A

a. HEMIcholinium - blocks choline from entering presynaptic neuron (cannot combine with acetyl-CoA, left with only half or HEMI product)

b. Vesamicol - blocks choline-acetyl-transferase (cannot package ACh into Vesicles)

c. botulism - blocks ACh release into synaptic cleft

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9
Q

what are the risk factors for adult exposure to botulism? (3)

A
  1. undercooked food
  2. canned food (anaerobic environment promotes growth)
  3. wound

remember exposure is via spores!

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10
Q

what are the 3 D’s of botulism presentation? why do these occur?

A
  1. diplopia
  2. dysphagia
  3. dysphonia

this is due to botulism toxin blocking acetylcholine release, preventing it from binding to nicotinic receptors

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11
Q

describe the process by which norepinephrine is released into the synapse (5)

A
  1. tyrosine enters presynaptic neuron
  2. tyrosine is converted to dopa —> dopamine
  3. dopamine is packaged inside a vesicle, THEN converted to norepinephrine
  4. depolarization causes Ca2+ influx, which triggers vesicle release/ exocytosis of NE into synapse
  5. NE binds alpha or beta adrenergic receptor
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12
Q

what are 3 sources of feedback to norepinephrine release from the presynaptic neuron?

A
  1. muscarinic 2 receptors give negative feedback to allow PNS to regulate SNS
  2. angiotensin II can induce NE release
  3. alpha2 adrenergic receptors give negative feedback to modulate SNS activity
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13
Q

what is the effect of the following drugs on norepinephrine release into the synapse?
a. metyrosine
b. resirpine
c. guanethidine
d. bretylium
e. amphetamine
f. cocaine
g. tricyclic antidepressants (TCAs)

A

a. metyrosine: inhibits tyrosine hydroxylase (converts tyrosine to dopa), treats pheochromocytoma

b. resirpine: blocks dopamine packaging

c/d. guanethidine, bretylium: blocks NE release

e. amphetamine: promote NE release and block reuptake

f/g. cocaine, tricyclic antidepressants (TCAs): block NE reuptake

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14
Q

describe the presentation of cocaine intoxication (5)

A

recall cocaine blocks reuptake of NE, dopamine, and serotonin

  1. agitation
  2. HTN
  3. dilated pupils
  4. chest pain (coronary vasoconstriction)
  5. abnormal nasal mucosa/septum

[separately, cocaine blocks Na+ channels and can be used as local anesthetic]

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15
Q

where are alpha1 vs alpha2 adrenergic receptors found, and what do they do?

A

alpha1: located in peripheral vessels to induce vasoconstriction (raise BP) + eyes to induce mydriasis (dilation)

alpha2: located on presynaptic neuron to give negative feedback after NE release + pancreas to inhibit insulin release

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16
Q

where are beta1 vs beta2 adrenergic receptors found, and what do they do?

A

beta1: located in heart to raise HR and contractility + kidneys to stimulate renin release at JG apparatus

beta2: located in lungs to bronchodilate, liver/muscle to vasodilate, GI to decrease motility, and bladder for relaxation

17
Q

which adrenergic receptors are responsible for the following effects?
a. vasodilation
b. vasoconstriction
c. heart rate

A

vasoconstriction = alpha1

vasodilation= alpha2 + beta2

heart rate (increase) = beta1

stimulation of ALL receptors = increase HR and BP

18
Q

what type of receptors are the following receptors?
a. nicotinic
b. muscarinic
c. adrenergic

A

a. nicotinic = ligand-gated ion channels (NT binds and causes influx of ions)

b/c. muscarinic, adrenergic = GPCR

19
Q

what occurs following Gs activation on GPCR of cardiac muscle? (5)

A
  1. Gs stimulates formation of adenylyl cyclase (AC)
  2. AC induces formation of cAMP from ATP
  3. cAMP activates protein kinase A (PKA)
  4. PKA promotes entry of calcium into cell
  5. calcium enters sarcoplasmic reticulum (SR) and induces more calcium release to cause contraction
20
Q

what occurs following Gs activation on GPCR of smooth muscle? (3)

A
  1. Gs stimulates formation of adenylyl cyclase (AC)
  2. AC induces formation of cAMP from ATP
  3. cAMP INHIBITS myosin light chain kinase (MLCK), thereby INHIBITING contraction
21
Q

what is the effect of Gs stimulation in cardiac vs smooth muscle, and why does this make sense?

A

cardiac Gs —> contraction

smooth Gs —> relaxation

this makes sense because if the body wants to increase blood flow with more contraction, the blood vessels will need to be more relaxed to handle all that blood pressure!

[recall Gq proteins induce contraction of vascular smooth muscle]

22
Q

where are Gq proteins found, and what occurs after they are stimulated? (3)

A

only in vascular smooth muscle

  1. Gq activates phospholipase C (PLC)
  2. PLC hydrolyzes PIP2 to inositol triphosphate (IP3)
  3. IP3 induces the sarcoplasmic reticulum (SR) to release calcium to cause contraction
23
Q

in which type of receptors are Gs, Gi, and Gq proteins found? [hint: memory trick!]

A

Gq: HAVe 1 M&M: H1, alpha1, V1, M1, M3

Gi: MAD2: M2, alpha2, D2

Gs: all others: beta1, beta2, D1, H2, V2

Neuro (50 decks)

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