NEUROTRANSMITTERS

Neurotransmitter Function Receptor Action Related drugs/illnesses

Acetylcholine Excitatory Nicotinic ACh-R Ionotropic channels  incr gNa, gK, Curare (N1), hexamethonium (N2)
(N1-neuromusc, N2- gCa
NT for many post ganglionic ANS) nd Atropine (M)
Muscarinic ACh-R Metabotropic channels 2
parasympathetics mssrs, phos of channels,
(M1-CNS, GI; M2-
conductance changes
heart)
Norepinephrine (many postgang symp) 1 Tyrosine  Dopa  Lack of NE may cause manic-depression: Tricyclics
(ie desipramine) inhibit reuptake (by
1- contracts sm musc, bv 2 dopamine  NE
autoreceptors); MAO (monoamine oxidase)
2 – autorec of NE (inhibits release) 1 inhibitors increase presynaptic concentration
1 – incr HR, contractility 2 (prevent NE degradation)
2 – relax GI sm musc, some vasc sm
Dopamine Pleasure and reward D1 Gsincr Cocaine, amphetamines – inhibit reuptake (can
Involved in memory D2 cAMPphosphor. have long-term effect-dcr receptors)
BIOGENIC AMINES

Gidecr cAMP Parkinson’s-decr in DA treat with DOPA

Schizophrenia: excess D4  treat with blockers of
receptors (ie phenothiazines)
Serotonin (pleasure) All GPCR except Made from Trp-5-HT SSRIs = selective serotonin reuptake inhibitors ie
5-HT3 (ionotropic) Prozac (fluoxetine) – targets Na-coupled transport
– treat depression, esp anxiety
OCDs – use Paxil (SSRI)
LSD – activates 5-HD2 receptor
MDMA (ecstasy)- elev 5-HT, then decr
Histamine Mediates allergic response; H1-H3= GPCRs in Benadryl (antihistamine) drowsiness
arousal hypothalamus -Can block H1 to decr motion sickness (blocks
vestibular function)
-Block H2 (gastric acid synthesis) to control peptic
ulcers
Glutamate (and Main excitatory NT in the brain 11 metabotropic *NMDA is ligand- and if Glu  too much Ca  kills cell
Aspartate) Synaptic plasticity – learning receptors voltage-gated: Mg blocking Excitoxin achieves this
*mGluR4 = basis of umami Ionotropic: pore is only moved when V >
kainite, AMPA, -60mV
AMINO ACIDS

NMDA but necessary for Ca influx

GABA (and glycine) Main inhibitory NT in the brain
(20% of CNS synapses)
GABAA-ionotropic GABAA incr gCl – opposes depol
GABAB- GABAB  Gi decr gCa, inc gK
Gly – incr gCl mainly in SC
metabotrop
Activation by GABA alone 
hyperpol; GABA+enhancer more
sustained inhibitory response
Barbiturates and benzodiazepines (ie Valium) –
enhance effects of GABA on gCl reduce anxiety,
muscle relaxants
Strychnine – blocks Gly receptors convulsions,
hyperactivity – used by athletes to boost
performance
 NEUROTRANSMITTERS

Oxytocin and Uterine contractions, nursing;

vasopressin water reabsorption in kidney
Substance P Mediates pain (found in Can block in depressed patients who
intestine) don’t respond to SSRIs
PEPTIDES

Vasoactive intestinal GI function

peptide (VIP) and
cholecystokinin
Opioid peptides analgesics Same as opiates POMC (pro- May be involved in athletic “high”
opiomelanocortin) - Receptors can also bind morphine,
endorphin and enkephalin codeine
(analgesics)
NO Relaxes smooth muscle NOSGC  synth cGMP cGMP hydrolyzed by PDE – block with
Interneuronal messenger in -- phos smooth musc protein Viagra etc.
GASES

brain
CO -- Made from heme-oxygenase
H2S Cardioprotective effect during
--
ischemia