General Flashcards
Five steps of neurotransmission
1) NT synthesis
2) Vesicular Storage
3) Synaptic Release
4) Binding to receptor
5) Termination of transmission
Botulinum Toxin
Degrades SNARES of the cholinergic NMJ.
skeletal muscle paralysis due to loss of Ach release
amphetamine or ephedrine
Bind indirectly to the receptor
stimulates NT release in a Ca independent manner
can reverse the direction of NT transport, resulting in the release of endogenous NT back out of the extracellular side of the membrane without membrane voltage change or Ca influx
reverses monamine uptake transporters. used in the treatment of narcolepsy and ADHD
Monamines
Seratonin, NE, Epi, Histamine, serotonin
Rate limiting step of catecholamine production
tyrosine hydroxylase
Metyrosine
Binds to tyrosine hydroxylase, can’t be transformed into L-DOPA. Decreases dopamine production
used to treat HTN-reduces NE production
Carbidopa
blocks the conversion of L-DOPA to dopamine
Does not cross BBB, so protects peripheral adrenergic neurons from producing too much dopamine and NE
used to reduce cardiovascular side effects of L-DOPA
Also used to treat Parkinson’s disease
Dopamine-ß-Hydroxylase
Converts Dopamine to NE
Prevents destruction of NE in cytosol
Reserpine
Blocks the vesicular monamine transporter (VMAT) uptake of monamines
Results in depletion of monamines DA, NE, serotonin
Crosses BBB and can block vesicular monamine uptake in the CNS
Bretylium
inhibits excitability (AP generation) of the nerve temrinal membrane and Ca dependent fusion of the synaptic vessicle with the plasma membrane. causes reduction of NT release.
Has specific effects on adrenergic neurotransmission. taken up by transport proteins that usually take up NE
used to reduce ventricular arrythmia
influences neuropeptide release
catecholamine-O-methyltransferase (COMT)
termination of NE
degredation of catecholamines
Monoamine oxidase (MAO)
in cell cytoplasm. oxidizes NE and DA
degrades catecholamines
Termination of monamines
mediated mainly by reuptake
Cocaine
Inhibits re-uptake of monamines NE, DA, serotonin
anelgesic durign surgery
Phenylephrine
activates adrenergic receptors. reistant to degradation by COMT, so has a longr half life.
Tyramine
When combines with an MAO inhibitor increases NE.
Normally gets metabolized by MAO in the liver, but when MAO is inhibited tyramine accumulates and gets transported into noradrenergic cells where it competes with NE for transport into synaptic vessicles. This raises levels of NE in the cytoplasm.
This can reverse the NE reuptake transporter, causing increased NE in the synapse and can lead to hypertensive crisis sue to excess vasoconstriction.
MAO-A
Specifically breaks down serotonin, NE, DA in the brain
MAO-B
degrades tyramine in the gut
Naloxone
small lipophillic (nonpeptide) opiod receptor antagonist
crosses the BBB, acts in CNS
used to reverse opiod overdose/ dependency
Naltrexone
Nonpeptide opiod receptor blocker in CNS. long duration of action
used in treatment of opiate addiction and alcoholism
SSRIs
selective inhibition of serotonin reuptake transporter
used to treat depression/anxiety
ACE inhibitors
(ex. lisinopril) inhibit peptide cleavage of angiotensin I to angiotensin II.
used to treat hypertension
MAO inhibitors
block cytoplasmic metabolism of monoamines
used to treat depression
L-DOPA
precursor of dopamine, stimulates dopamine production
Used in Parkinson’s disease
