L1 Intro to ANS (Exam #1) Flashcards

1
Q

In parasympathetic, ____ preganglionic fibers release ____, acting on ____ receptors

A

PARASYMPATHETIC

Long preganglionic release ACh onto N receptors

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2
Q

In parasympathetic, ____ postganglionic fibers release ____, acting on ____ receptors

A

PARASYMPATHETIC

Short postganglionic release ACh on M receptors

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3
Q

In sympathetic, ____ preganglionic fibers release ____, acting on ____ receptors

A

SYMPATHETIC

Short preganglionic release ACh on N receptors

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4
Q

In sympathetic, ____ postganglionic fibers release ____, acting on ____ receptors

A

SYMPATHETIC
Long postganglionic release NE onto a1 or b1 receptors

  • Sometimes DA or ACh
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5
Q

What is released from the adrenal medulla, and to where?

A

Epi or NE are released from the adrenal medulla directly into circulation

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6
Q

What is released from sympathetic neurons innervating sweat glands? What type of receptor do they act on?

A

ACh onto M receptors

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7
Q

What is released from sympathetic neurons innervating renal vasculature? What type of receptor do they act on?

A

DA onto D1 receptors

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8
Q

Which two receptor types are the ONLY inhibitory?

A
  • a2

- M2

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9
Q

With cholinergic transmission, after ACh is released from its storage vesicle by an AP, what two receptor types can it bind to, and what is the response of each?

A
  • Presynaptic receptors (N): inhibits release of more ACh (negative feedback)
  • Postsynaptic receptors (M): cholinergic response
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10
Q

During cholinergic transmission, what is the enzyme that synthesizes ACh? What is the enzyme that degrades ACh?

A
  • Synthesized by ChAT (choline acetyltransferase)

- Degraded by AChE (acetyl-cholinesterase)

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11
Q

How does Botox affect cholinergic transmission?

A

Inhibits cholinergic vesicle release, resulting in low ACh levels

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12
Q

How do muscarinic antagonists affect cholinergic transmission?

A

Inhibit activation of muscarinic receptors on postganglionic terminal

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13
Q

How do cholinesterase inhibitors affect cholinergic transmission?

A

Inhibits AChE, resulting in high ACh levels in synaptic cleft

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14
Q

With adrenergic transmission, what is the rate limiting step?

A

After tyrosine enters the nerve terminal, it is converted to L-DOPA by tyrosine hydroxylase

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15
Q

With adrenergic transmission, after tyrosine is converted to L-DOPA by tyrosine hydroxylase, what two neurotransmitters can it be converted into?

A
  1. L-DOPA to DA

2. L-DOPA to DA to NE

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16
Q

With adrenergic transmission, what type of transporter is used to reuptake NE? What two drugs act on this transporter, inhibiting the reuptake of NE - what is the result?

A

NET

- Cocaine and antidepressants block NET, resulting in high NE levels in synaptic cleft

17
Q

How do Amphetamines affect adrenergic transmission?

A

Displaces/increases levels of NE in nerve terminal, so more NE is released, resulting in high NE levels in synaptic cleft

18
Q

Which three drugs require an INTACT nerve terminal to work?

What drug type is an exception to this, and why?

A
  • Cocaine
  • Antidepressants
  • Amphetamines

Adrenergic antagonists inhibit activation of adrenergic receptors

19
Q

In which two systems does sympathetic NS dominate?

A
  • Blood vessels

- Skin/sweat glands

20
Q

Which receptors are activated by NE? Which receptors are activated by Epi?

A
  • NE: a1, b1

- Epi: a1, b1, b2

21
Q

For sympathetic stimulation of blood vessels, what neurotransmitter and receptor type is often used, and what is the result?

A

NE acts on a1 receptors

- Vasoconstriction

22
Q

For sympathetic stimulation of blood vessels, when Epi is released in low doses, what receptor does it act on and what is the result? In high doses?

With what type of blood vessels is this an exception, where Epi = NE?

A

Low Epi acts on b2 receptors
- Vasodilation

High Epi acts on a1 receptors
- Vasoconstriction

In skin and reservoir veins, Epi = NE so it acts mostly on a1 receptors to vasoconstrict

23
Q

On what type of blood vessels does DA act? When DA is released in low doses, what receptor does it act on and what is the result? In high doses?

A

Renal vasculature

Low DA acts on D1 receptors
- Vasodilation

High DA acts on a1 receptors
- Vasoconstriction

24
Q

What is mydriasis?

A

Pupil dilation

25
Q

What is miosis?

A

Pupil constriction