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SANS v PANS energy SANS: not essential for life PANS:anabolic, esential for life
SANS v PANS dominant? PANS dominant at rest
PANS efferent fiber origin? craniosacral (CN 3,7, 9, 10) and sacral segs (2-4)
preganglionic PANS fibers? long
postgang PANS fibers? short
preganglionic fibers? SANS: paravertebral ganglia on either side of SC PANS: ganglion cells distributed in networks or near organs
postganglionic fibers? SANS: paravertebral ganglia on sides of SC to tissue innervated PANS: located on effector organs
PANS activity? discrete and localized discharge
PANS princple neurotransmitter? Ach
what systems lack duel innervation? blood vessels
what neurotransmitter stimulates the nicotinic receptor at the adrenal medulla to release catacholamines? Ach
what neurotransmiters do the adrenal medulla release? NE (15%) and EPI (80%)
what drugs block NA channel? local anasthetics, tetrodotoxin (puffer fish poison) and saxitoxin (shellfish poison)
what drugs increase permiability of Na channel to cause persistant depolarization? batrachotoxin (s. american frog), and scorpion toxins
where does Ach work? preganglionic PANS and SANS to nicotinic receptors. PANS postganglionic to muscarinic effector organ and few SANS effector cells. All somatic fibers use Ach.
hemicholinium and triethylcholine? inhibit Ach synthesisby competing for choline uptake into presynaptic terminal
botulinum toxin? block Ach release
black widow spider venom? promote Ach release
Atropine? blocks Ach activity at postsynaptic muscarinic receptors
Physostigmine? inhibit enzymatic metabolism (Ache inhibitor)
where do catacholamines work? NE work in SANS postganglionic to adrenergic receptors. EPI released from the adrenal medulla. DA is a CNS neurotransmitter.
catacholamine synthesis? tyrosine to DOPA by tyrosine hydroxylase (RLS). DOPA to dopamine by aromatic aminoacid decarboxylase, then into storage granule. dopamine to NE by dopamine beta hydroxylase (nonspecific). NE to EPI by phenyl-N-methyltransferase in the AM cytoplasm.
what is catacholamine Uptake-1? localized to presynaptic adrenergic terminal back into storage.
catacholamine uptake-2? localized to non-neuronal tissues
enzymatic degredation of catacholamines? MAO A and B ain the cytoplasm of the neuron. COMT for NT released from the adrenals that escapes the uptake-1 process. metabolites (MHPG, VMA, NMN)
destruction of Ach? AchE to choline and acetate. Choline taken up by presynaptic terminal to reuse. Ach diffuses away. Butyrylcholinesterase can also hydrolyze Ach.
what is DA? precursor of NE. NT in the CNS basal ganglia
what is 5HT? CNS NT. regulate smoth muscle in cardiovascular and GI systems, platlet function
5HT synthesis? tryptophan to 5-hydroxytryptophan by tryptophan hydroxylase. then to 5HT by dopa decarboxylase
how is 5HT metabolized? MAO A and aldehyde dehydrogenase
alpha methyldopa, alpha methyltyrosine? compete with enzymes to make false NT to inhibit storage of active NT.
reserpine, guanethidine? inhibit, deplete storage of NE and DA.
guanethidine, bretylium? reuptake-1, cause transient release of catecholamin followed by long lasting decrease in adrenergic activity.
clonidine? acts at presynaptic adrenergic receptor to decrease NE release
imipramine, cocaine? block uptake-1, reuptake of NE and DA
Created by: lmh9p4