Corso Stuff
Biogenic Amines
dopamine, norepinephrine, 5-HT, ACh, histamine, melatonin
all of the basic ones
amino acids (AAs)
glutamate, glycine, GABA
ALL START WITH G
purigenic
adenosine, ATP
ALL START WITH A
peptide
encephalins, endorphins
START WITH E
retrograde transmitters
nitric oxide, endocannabinoids
WEIRD ONES
endocannabinoids regulate glutamate and GABA release
I THINK HE’LL ASK ABOUT ENDOCANNABINOID BEING A RETROGRADE TRANSMITTER
STRUCTURES
acetylcholine: NO RINGS, 7 C’s
dopamine: 1 ring, one amine
norepinephrine: 1 ring, one amine, one hydroxyl
epinephrine: 1 ring, one amine, one hydroxyl, additional methyl
SO REMEMBER: DA —> NE —> EPI
each step adds an additional group
5-HT: 2 rings, one amine
melatonin: 2 rings, carboxylic acid added on
SO REMEMBER: 5-HT —> melatonin
so the step is an additional group
histamine: 1 ring with 2 N’s in it
I ALSO think of histamine looking like a chiller melatonin
glutamate: 5 C’s
GABA: 4 C’s
4 LETTERS —> 4 C’S
glycine: 2 C’s
serine —> glycine
REMOVES A CARBON
adenosine: looks like a purine
endocannabinoids: arachidonic acid derivatives, 20 C’s
ATP: 3 phosphate groups
don’t overthink it, you know what it looks like
SEROTONIN
structure: 2 rings, one amine
found: raphe
synthesis: tryptophan —> 5-HTP —> 5-HT
precursors:
tryptophan
5-hydroxytryptophan
degradation: serotonin broken down by MAO-A —> 5-hydroxyindoleacetaldehyde —> 5-hydroxyindole acetic acid
drug targets: MAOIs
inhibits degradation of serotonin (depression and anxiety)
VMAT2: inhibited by reserpine
receptors:
inward sodium channels
5HT3
trimeric Gi —> decr. cAMP, decr. PKA
5HT1
trimeric Gq —> DAG, IP3, Calcium, PKC
5HT2
trimeric Gs —> cAMP, PKA
5HT3 inhibitors are used for nausea caused by chemo
MELATONIN
structure: 2 rings, one amine, carboxylic acid
found: pineal gland
synthesis: tryptophan —> 5-HTP —> 5-HT —> N-acetyl serotonin —> melatonin
precursors:
tryptophan
5-HTP
5-HT
N-acetyl serotonin
HISTAMINE
structure: 1 ring with 2 N’s
found: hypothalamus
THINK H GOES WITH H
function: alertness
synthesis: histidine (histidine decarboxylase) —> histamine
precursor: histidine
degradation: histamine (SAM) —> methylhistamine (MAO-B) —> methylimidazole acetic acid
VMAT2: inhibited by reserpine
receptors:
trimeric Gs —> cAMP, PKA
H2
trimeric Gq —> DAG, IP3, Calcium, PKC
H1
H1: EXCITATORY: DAG, IP3, calcium, PKC
H2: EXCITATORY: incr. cAMP
H3, 4: INHIBITORY
AcetylCholine
structure: NO RINGS, 7 C’s
found: nucleus basalis/basal ganglia
pre-ganglionic autonomic cells
Alzheimer’s: causes depletion
treatment: acetylcholinesterase inhibitors
synthesis: acetyl coA + choline
enzyme: choline acetyltransferase
degradation: acetylcholinesterase (results in acetyl coA and choline)
drug target for myasthenia gravis and alzheimer’s
botulinum toxin blocks release
receptors:
inward sodium channels
N1, N2 (5 subunits) (nicotinic)
trimeric Gi —> decr. cAMP, decr. PKA
m2 (muscarinic)
trimeric Gq —> DAG, IP3, Calcium, PKC
m1 (muscarinic)
nicotinic receptors
FAST
N1: muscles
N2: neurons
muscarinic receptors
SLOWER
odd numbers: 1, 3, 5: EXCITATORY Gq
even numbers: 2, 4: INHIBITORY Gi
myasthenia gravis:
serum antibodies against N1 receptors
typical: alpha 1 subunit
acquired slow channel: epsilon subunit
neonatal: gamma subunit
ACETYL CHOLINESTERASE INHIBITORS
LEMS (lambert-eaton myasthenic syndrome)
immune disorder against voltage gated calcium channelscc
DOPAMINE
structure: 1 ring, 1 amine
found: substantia nigra
flow: substantia nigra —> striatum
too little: Parkinson’s
side effect of D2 antagonists: Parkinsonian tremors
too much: schizophrenia, hallucinations
synthesis: phenylalanine —> L-tyrosine (hydroxylation) —> L-dopa (decarboxylation) —> dopamine
precursors:
phenylalanine
tyrosine
degradation: MAO-B and COMT
drug targets: MAOIs and COMTIs
prevent degradation —> increase dopamine levels (Parkinson’s)
metabolites:
DOPAL
DOPET
DOPAC
3-Me-DOPET
3-Me-DOPAL
3-MT
HVA
Parkinson’s treatment: L-dopa + carbidopa
L-dopa can cross the BBB, dopamine can NOT
carbidopa can NOT cross the BBB, prevents L-dopa from converting in the periphery —> minimizes ADRs
VMAT2: inhibited by reserpine
receptors:
trimeric Gs —> cAMP, PKA
D1
trimeric Gi —> decr. cAMP, decr. PKA
D2
D1 and D5: EXCITATORY
think as the ones on the ends
D2, D3, and D4: INHIBITORY
the middle ones
NOREPINEPHRINE
structure: 1 ring, one amine, one hydroxyl
found: locus ceruleus
post-ganglionic sympathetic cells
synthesis: phenylalanine —> L-tyrosine (hydroxylation) —> L-dopa (decarboxylation) —> dopamine (hydroxylation) —> norepinephrine
precursors:
phenylalanine
tyrosine
dopamine
degradation: MAO and COMT
drug targets: MAOIs and COMTIs
prevent degradation —> increase dopamine levels (DEPRESSION)
VMAT2: inhibited by reserpine
receptors:
trimeric Gs —> cAMP, PKA
beta 1,2,3
trimeric Gi —> decr. cAMP, decr. PKA
alpha 2
trimeric Gq —> DAG, IP3, Calcium, PKC
alpha 1
alpha 1: EXCITATORY: DAG, IP3, calcium, PKC
alpha 2: INHIBITORY
beta 1,2,3: EXCITATORY: cAMP, PKA
EPINEPHRINE
structure: 1 ring, one amine, one hydroxyl, additional methyl
found: adrenal gland
synthesis: phenylalanine —> L-tyrosine (hydroxylation) —> L-dopa (decarboxylation) —> dopamine (hydroxylation) —> norepinephrine (SAM) —> epinephrine
precursors:
phenylalanine
tyrosine
dopamine
norepinephrine
degradation: MAO and COMT
drug targets: MAOIs and COMTIs
prevent degradation —> increase dopamine levels (DEPRESSION)
receptors:
trimeric Gs —> cAMP, PKA
beta 1,2,3
trimeric Gi —> decr. cAMP, decr. PKA
alpha 2
trimeric Gq —> DAG, IP3, Calcium, PKC
alpha 1
GLUTAMATE
structure: 5 C's
most abundant NT in the brain and spinal cord
receptors:
inward sodium channels
AMPA
fast sodium
kainate
fast sodium
NMDA (glutamate/glycine) —> memory!!!
slow
trimeric Gi —> decr. cAMP, decr. PKA
mGluR2
trimeric Gq —> DAG, IP3, Calcium, PKC
mGluR1
NMDA, AMPA, kainate: EXCITATORY: inward sodium channels
mGluR1: EXCITATORY: DAG, IP3, calcium, PKC
mGluR2: INHIBITORY
transporter: VGLUT
drugs that block glutamate release: riluzole, lamotrigine, topiramate, levetiracetam, gabapentin, pregabalin
decreases amount of glutamate in synapse —> treats overactivity —> anticonvulsants, epilepsy, anxiety, etc.
drugs that enhance reuptake: riluzole, tianeptine
decreases amount of glutamate in synapse
glutamate receptor agonist (AMPA/Kainate): domoic acid
toxin in contaminated shellfish (from algae)
glutamate receptor antagonist (AMPA): perampanel, halothane
treat seizures / anesthetic
glutamate receptor inhibitor (NMDA): memantine
treat’s alzheimer’s
GABA
structure: 4 C’s
THINK 4 LETTERS, 4 C’S
most common INHIBITORY NT in brain
synthesis: glutamate —> GABA (removes a CO2)
degradation: converted back to glutamate
receptors:
inward chloride channels (inhibitory)
GABA-A, C
outward potassium (inhibitory)
GABA-B
benzos bind to the GABA site and open the chloride channel —> alleves anxiety
GLYCINE
structure: 2 C’s
most common INHIBITORY NT in the spinal cord
synthesis: serine —> glycine (removes carbon)
THF removes the carbon
receptors:
inward sodium channels
NMDA (glutamate/glycine)
inward chloride channels (inhibitory)
glycine
ATP
structure: 3 phosphate groups
“co-transmitter”: common to find purigenics copackaged with ACh or catecholamines
receptors:
inward sodium channels
P2X1-7
found both pre and postsynaptic
ENKEPHALINS
structure: peptide
receptors:
outward potassium channels
mu
delta
ENDORPHINS
structure:
receptors:
outward potassium channels
mu
ENDOCANNABINOIDS
structure: arachidonic acid derivatives, 20 C’s
receptors:
trimeric Gi —> decr. cAMP, decr. PKA
CB1, 2
*note: nerve growth factor is an insulin-like receptor
SO IN TERMS OF THE RECEPTORS
good rule of thumb is that the even numbers are inhibitory Gi (m2, D2, alpha 2, mGluR2)
the main exception is serotonin, where 5HT1 is inhibitory (think of it like there’s another number in there so it’s opposite)
other exceptions are things like beta 1-3 and N 1-2 which all do the same thing
other exception is H1 and H2, both are excitatory but H1 is Gq, H2 is Gs (2 looks like s)