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57 Cards in this Set
- Front
- Back
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How is ACh synthesized?
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AcCoA + Choline -> (Choline Acetyltransferase) -> ACh + CoA
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What is ChAT?
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ChAT is Choline Acetyltransferase, a cytosolic enzyme found in specific nerve terminals & may be loosely bound to the outside of synaptic vesicles
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Where does AcCoA come from?
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AcCoA comes from mitochondrial metabolism of pyruvate (from glucose)
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Where does Choline come from?
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Choline comes from the diet and 50% of ACh production uses recycled choline following high affinity reuptake
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What helps terminate cholinergic transmission by degrading ACh to choline and acetate?
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Choline Esterases such as Acetylcholine Esterase
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What is made in the liver and circulate in plasma, scavenging any ACh which washes out of the PNS synapse?
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Choline Esterases
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Where is AChE found
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AChE is found localized at ACh synapses, either bound to the cell membrane or basal lamina within the synapse
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What kind of effect does Bungarotoxin and Black Widow Spider Venom have on a neuron?
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Stimulates the terminal end to release vesicles, depleting the number for future use
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What kind of effect does Botulinum Toxin have?
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Inhibitory effect few vesicles are released due to synaptic vessicles being unable to bind to membrane for exocytosis
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What effect does neostigmine & physostigmine have and are they medically useful?
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Inhibits Prolongs ACh Transmission...OVERSTIMULATED
It is a cholinesterase inhibitor, which interferes with the breakdown of acetylcholine Yes because they are reversible |
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What medications prolong ACh transmission resulting in overstimulation of the neuron, via cholinesterase inhibitors, Irreversibly?
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Malathion
Nerve gas (deadly, but some medical uses at low concentration) |
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What medications prolong ACh transmission resulting in overstimulation of the neuron, via cholinesterase inhibitors, Reversibly?
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Neostigmine**
Physostigmine (attack ACh Esterase so ACh is not broken down in the synapse) |
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What are agonists for nicotinic receptors? (enhance transmission)
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Nicotinic Receptor Agonists
1. Carbachol 2. ACh 3. Nicotine |
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What are agonists for muscarinic receptors? (enhance transmission)
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Muscarinic Receptor Agonists
1. ACh 2. Muscarine 3. Pilocarpine (treats xerostomia) 4. Oxotremorine |
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What are antagonists for muscarinic receptors? (inhibit transmission)
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Muscarinic Receptor Antagonists
1. Atropine 2. Scopolamine |
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What are the antagonists for nicotinic receptors?
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Nicotinic Receptor Antagonists
1. Curare 2. Succinylcholine 3. Rabies virus |
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What is the main thing to remember about post synaptic mechanisms?
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When you see nicotinic, think ion channels
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What are the catecholamines?
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Catecholamines
1. Dopamine 2. Norepinephrine 3. Epinephrine |
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What determines which neurotransmitter is released by a neuron?
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Which neurotransmitter released by a neuron is determined by which enzymes it expresses
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Where are neurotransmitters stored?
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Neurotransmitters are stored in vesicles until released by elevated intracellular Ca++
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Where does tyrosine come from in the body?
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From diet or phenylalanine
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What converts tyrosine to DOPA (DiOhPhenylAlanine)?
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Tyrosine hydroxylase (cytosolic; inhibited by alpha-methyl-tyrosine)
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What converts L-DOPA to DOPAMINE?
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DOPA decarboxylase removes CO2
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What inhibits DOPA decarboxylase?
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alpha-methyl DOPA inhibits DOPA Decarboxylase
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What converts Dopamine to Norepinephrine?
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Dopamine-Beta-hydroxylase, which is inside vesicles of cells which release NE or EPI
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What converts Norepinephrine to Epinephrine?
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Phenylethanolamine-N-methyl Transferase (PNMT) -found in the cytosol of cells which release EPI
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What stimulates Phenylethanolamine-N-methyl Transferase (PNMT)?
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PNMT are stimulated by corticosteroids
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When vesicles are released from the terminal end of a neuron what drugs affect this step?
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Amphetamines- displace NT from vesicles, causing initial release but long-term depletion
inhibits gamma-OH-Butyrate for DA |
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What affects High affinity reuptake of norepinephrine?
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Cocaine (inhibitory) - increases NE in cleft, but long term NE depletion
Desipramine (inhibitory) & other tricyclic antidepressants - enhance NE in cleft 6-OH-Dopamine (inhibitory)- a toxic compound taken up and which destroys the terminal |
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What affects recycling of Norepinephrine?
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Reserpine (inhibitory)- long lasting NE depletion in vesicles
(prevents NE from reentering vesicles) |
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What is also used to produce parkinsonism?
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6-OH-Dopamine (inhibitory)- a toxic compound taken up and which destroys the terminal
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About 80% of released NE (for instance) is taken back into the terminal by what method?
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High-affinity reuptake
(the remaining 20% is catabolized) |
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What 2 enzymes act sequentially to produce the final product of catecholamine catabolism excreted in the urine?
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Monoamine Oxidase (MAO)
Catechol-O-methyl transferase (COMT) |
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What is the end product of catecholamine catabolism?
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Vanillylmandelic acid (VMA) is the catabolite for NE & EPI
Homovanillic acid (HVA) is the catabolite for DA |
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What is bound to the outer mitochondrial membrane and is important in catabolizing NE which is not contained in vesicles?
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MAO
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What are the primary enzymes in catecholamine catabolism?
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MAO & COMT
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Would it be of value to produce drugs that affect COMT?
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No COMT is found in nearly all cells and will act on all molecules with catechol group. (It is widely distributed and fairly non-specific) It's activity would produce many effects and would have little value
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What is a COMT inhibitor?
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Tropolone is a COMT inhibitor
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What do MAOI's do to catecholamine transmission?
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MAOIs (Pargyline) stimulate catecholamine transmission
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How do MAO's impact catecholamine terminals?
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MAO's impact the storage of NT which has been through reuptake.
Specifically, MAO Inhibitors (MAOIs) will tend to increase DA, NE and EPI in nerve terminals allowing for more incorporation into vesicles |
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What are 2 medical problems MAOI's are used for?
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Antidepressants & Blood Pressure Regulators
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What happens when MAO is inhibited?
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Inhibited MAO leads to NE entering vesicles resulting in more NE released
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NE is also a CNS NT and the cell bodies are located in the _______ ________
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Locus Ceruleus
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Where are most dopaminergic cell bodies located?
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In the Substantia Nigra of the midbrain
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Where do most dopaminergic axons go to?
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the Corpus Striatum (caudate & putamen) via the Niagrostriatal Tract
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Which Dopamine receptor increases cAMP?***
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D1 family receptors
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Which Dopamine receptor decreases cAMP?
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D2 family receptors
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What are the agonists for adrenergic receptors?
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EPI > NE ephedrine
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What is an antagonist for alpha receptors?
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Phenoxybenzamine**
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What is an agonist for beta receptors?
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Isoproterenol
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What is a beta receptor antagonist?
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Propranolol
(treats hypertension) |
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What is a Beta 1 agonist?
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Dobutamine
{increases contractility & heart output} |
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What is a Beta 2 agonist?
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Albuterol
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What is a beta 1 antagonist?
(REMEMBER -OL USUALLY MEANS BETA RECEPTOR) |
Atenolol
(slows down the heart & reduces its workload) |
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T/F The majority of sympathetic neurons will synapse w/other nervous systems
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True
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How long are preganglionic sympathetic neurons?
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They are short
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What kind of synapse does the adrenal medulla have?
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The Adrenal Medulla does not have a synapse
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