L1 Intro to ANS (Exam #1) Flashcards
In parasympathetic, ____ preganglionic fibers release ____, acting on ____ receptors
PARASYMPATHETIC
Long preganglionic release ACh onto N receptors
In parasympathetic, ____ postganglionic fibers release ____, acting on ____ receptors
PARASYMPATHETIC
Short postganglionic release ACh on M receptors
In sympathetic, ____ preganglionic fibers release ____, acting on ____ receptors
SYMPATHETIC
Short preganglionic release ACh on N receptors
In sympathetic, ____ postganglionic fibers release ____, acting on ____ receptors
SYMPATHETIC
Long postganglionic release NE onto a1 or b1 receptors
- Sometimes DA or ACh
What is released from the adrenal medulla, and to where?
Epi or NE are released from the adrenal medulla directly into circulation
What is released from sympathetic neurons innervating sweat glands? What type of receptor do they act on?
ACh onto M receptors
What is released from sympathetic neurons innervating renal vasculature? What type of receptor do they act on?
DA onto D1 receptors
Which two receptor types are the ONLY inhibitory?
- a2
- M2
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?
- Presynaptic receptors (N): inhibits release of more ACh (negative feedback)
- Postsynaptic receptors (M): cholinergic response
During cholinergic transmission, what is the enzyme that synthesizes ACh? What is the enzyme that degrades ACh?
- Synthesized by ChAT (choline acetyltransferase)
- Degraded by AChE (acetyl-cholinesterase)
How does Botox affect cholinergic transmission?
Inhibits cholinergic vesicle release, resulting in low ACh levels
How do muscarinic antagonists affect cholinergic transmission?
Inhibit activation of muscarinic receptors on postganglionic terminal
How do cholinesterase inhibitors affect cholinergic transmission?
Inhibits AChE, resulting in high ACh levels in synaptic cleft
With adrenergic transmission, what is the rate limiting step?
After tyrosine enters the nerve terminal, it is converted to L-DOPA by tyrosine hydroxylase
With adrenergic transmission, after tyrosine is converted to L-DOPA by tyrosine hydroxylase, what two neurotransmitters can it be converted into?
- L-DOPA to DA
2. L-DOPA to DA to NE
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?
NET
- Cocaine and antidepressants block NET, resulting in high NE levels in synaptic cleft
How do Amphetamines affect adrenergic transmission?
Displaces/increases levels of NE in nerve terminal, so more NE is released, resulting in high NE levels in synaptic cleft
Which three drugs require an INTACT nerve terminal to work?
What drug type is an exception to this, and why?
- Cocaine
- Antidepressants
- Amphetamines
Adrenergic antagonists inhibit activation of adrenergic receptors
In which two systems does sympathetic NS dominate?
- Blood vessels
- Skin/sweat glands
Which receptors are activated by NE? Which receptors are activated by Epi?
- NE: a1, b1
- Epi: a1, b1, b2
For sympathetic stimulation of blood vessels, what neurotransmitter and receptor type is often used, and what is the result?
NE acts on a1 receptors
- Vasoconstriction
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?
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
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?
Renal vasculature
Low DA acts on D1 receptors
- Vasodilation
High DA acts on a1 receptors
- Vasoconstriction
What is mydriasis?
Pupil dilation
