Neurotransmitter P1 & P2 Flashcards
What does dopamine start as
tyrosine
What monoamine is dopamine
catecholamine
What turns tyrosine into l-Dopa (dihydroxyphenyl amine)
tyrosine hydroxylase
what turns dopa into dopamine
dopa decarboxylase
what works at full potential always
tyrosine hydroxylase
Dopa decarboxylase’s more general term
l-aromatic amino acid decarboxylase
dopamine can be broken down by what and then what (works vise versa)
MAO & COMT
intra and extra neuronal, has two forms A + B
MAO (monoamine oxidase)
This form of MAO is more important for dopamine breakdown in human brains
MAO-B
extra neuronal only
COMT (catechol-o-methyl-transferase)
either dopamine route leads to this, this is also needed to determine how much dopamine is in a persons brain
HVA
in the middle of MAO and COMT breakdown
DOPAC and 3 methyltyramine
Main dopamine pathways
nigrostriatal, mesolimbic (most important), and mesocortical
all of these are slow, g-protein coupled
dopamine receptors
result of activation is EPSP due to Na+ inflow
D1-like receptors
prevalent in basal ganglia, frontal lobe, and limbic regions
D1 receptors
prevalent in hippocampus
D5 receptors
result of activation is IPSP due to K+ outflow
D2-like receptors
widespread as inhibitory auto receptors on dopamine neurons
D2 short
prevalent in hippocampus
D2 long
prevalent in nucleus accumbens, l-dopa can’t pass through blood brain barriers
D3 receptors
prevalent in frontal lobe
D4
Metyrosine inhibits, l-dopa increases
dopamine synthesis
reserpine and tetrabenazine block this
dopamine storage
amphetamines promote
dopamine release
cocaine, methylphenidate (ritalin) block
dopamine reuptake
MAO-B and COMT can be blocked
dopamine metabolism
many antipsychotics antagonize
blocks dopamine receptors
bromocriptine, pergolide, apomorphine, agonize various receptors
stimulate dopamine receptors
need a decarboxylase inhibitor for this disease so l-dopa doesn’t turn into dopamine and so it can get through blood brain barrier
Parkinsons Disease
tolcapone and entacapone
COMT-I
l-dopa and carbidopa
sinemet
originally used for Parkinsons, FDA approved for treating CCI (doggie dementia)
selegitine and rasagiline
What does dopamine need to turn into norepinephrine
Dopamine- B hydroxylase
What does Norepinephrine start out as
Dopamine
metabolism is same as dopamines
norepinephrine
all are also slow, g-protein coupled
norepinephrine receptors
a1 is usually excitatory, a2 inhibitory
alpha-adrenergic types
widespread as presynaptic autoreceptors on norepinephrine neurons (inhibitory)
a2
important in CNS and PNS
a1 and a2
usual result of activation is EPSP for norepinephrine receptors
beta-adrenergic types
more important in PNS than CNS
B1 B2 B3
fusaric acid blocks dopamine-B-hydroxylase
norepinephrine synthesis
reserpine blocks
norepinephrine storage
amphetamines promote
norepinephrine release
same as da and atomoxine and various anti-depressants block
norepinephrine re-uptake
MAO-I’s promote
norepinephrine metabolism
alpha and beta blockers
block norepinephrine receptors
clonodine and xylazine act on a2 autoreceptors
stimulates norepinephrine receptors
what does serotonin start as
tryptophan
what does tryptophan need to turn into 5-hydroxy-tryptophan
tryptophan hydroxylase
5-HT is not a catecholamine, but
an indolamine
what does 5-hydroxy-tryptophan need to turn into serotonin
dopa decarboxylase
acted on mainly by MAO-A followed by AD, to produce 5-HIAA
5-HT metabolism
serotonin is not acted on by this due to it being an indolamine
COMT
