neuropharm DRUG definitions

a-methyl NA

gets into NA nerve & vesicles, cotransmission

carbidopa

inhibits dopa decarboxylase in PNS, allows L-DOPA in CNS

L-DOPA

precursor for DA synthesis

a-methylDA

gets into DA nerve & vesicles, cotransmission

LSD

similar structure to 5-HT, binds

ACh esterase inhibitors

prolongs ACh in cleft

benzodiazepines

positive allosteric modulator of GABAA at allosteric site, increases frequency of channel opening

barbiturates

positive allosteric modulator of GABAA at transmembrane site, increases duration of channel opening

GHB

binds allosteric site of GHB-R & GABAB, increases channel opening

D-serine

co-agonist at GlyR & NMDAR

guanethidine

binds VGCC, blocks exocytosis, reduces ATP & NA release

6-Hydroxydopamine

makes intracellular toxic metabolite, blocks NA re-uptake, destroys vesicle membranes

resperine

blocks NA synthesis, maintains ATP & NPY release

botox

prevents ACh exocytosis, binds SNARE proteins

Ketamine

blocks NMDA on GABAergic interneurons, disinhibition, increase Glu release, synaptogenesis

NO

retrograde messenger, makes NO that diffuses across cleft, increases Ca2+ entry and NT release

tyramine

displaces NA in vesicles, NA released independent of nerve stimulation

entacapone

inhibits COMT, increases DA in cleft

selegiline

inhibits MAO-B, increases DA in cleft

xanomeline

M1 agonist, crosses BBB, reduces DA signaling in brain

trospium

M1 antagonist, doesn’t cross BBB

TCAs

block NA re-uptake

TCA example

doxepin

SSRIs

block 5-HT reuptake

SSRI example

fluoxetine

MAOIs

block NT breakdown

MAOI example

selegiline, moclobemide

Atypical AD example

esketamine

Ketamine/Esketamine

NMDA receptor antagonist on GABAergic inhibitory interneurons

riluzole

glutamate receptor antagonist, stops excitotoxicity in MND

edaravone

antioxidant, deals w/ ROS in MND

tofersen

antisense oligonucleotide, suppresses mutant SOD1 expression in MND

amphetamine medication

thought to normalize pre-existing DA deficit in ADHD

alcohol

activates GABAA on GABAergic VTA interneurons, increase Cl- influx, decrease GABA, increase DA

cannabis

activates CB1R on GABAergic VTA interneurons, inhibits GABA release, increase DA

hallucinogens

5HT2A agonist

opiods

activates MOR on GABAergic VTA interneurons, inhibits GABA release, increase DA

stimulants

block monoamine reuptake transporters

AMPH

inhibits VMAT, reverse efflux

MDMA

blocks 5-HT reputake

tobacco

nicotinic a4b2 nACh agonist, increase DA

naltrexone

MOR antagonist, reduces craving of drug

NRT

nicotine replacement therapy, change route of administration

methadone

MOR agonist but also addictive, change route of administration and substitute drug

memantine

uncompetitive NMDA antagonist, reduce excitotoxicity, reduce neuroinflammation

aducanumab

removes amyloid plaque in alzheimers

MPTP

converted to MPP+ in astrocytes, taken up into DA neurons, depletes energy, DA cell death

taxol

stabilises microtubules in polymerised state, blocks neuronal transport

colchicine

stabilises microtubules in depolymerised state, blocks neuronal transport

Hm1a infusion

removes fast inactivation of VGNC on GABAergic interneurons in Dravet syndrome, restores AP firing, no seizures

organon

allosteric inhibitor of mutated HCN channel, restores AP firing threshold

gabapentanoids

binds pre-synaptic VGCC, decrease Ca2+ influx and NT release, decrease pain signal

local anaesthetic

blocks VGNC, decrease Na+ influx and NT release, decrease pain signal

codeine

opioid, must be metabolised by CYP2D6 in liver to morphine

tramadol

atypical opioid, must be metabolised by CYP2D6 in liver to morphine

tapentadol

atypical opioid, also blocks NA reuptake

racetams

positive allosteric modulator at AMPA & N-type VGCC, increase cell membrane fluidity, cognitive enhancer