Neurotransmitter Class

NT Name

General Function



movement control, cognition

Monoamines - Catecholamines


affect, reward, movement


affect, alertness


alertness mood, arousal, modulation of pain, sleep

Monoamines - Indoleamine

Serotonin (5-HT)



waking state

Amino Acids - Excitatory

Glutamic Acid (GLU)

general excitation, sensation

Aspartic Acid (ASP)

Amino Acids - Inhibitory

Glycine (GLY)

general inhibition

signaling Hunger Substance P SP Pain Opioid peptides Enkephalin Control of Pain .GABA general inhibition Nitric Oxide Endocannabinoids NO Vasodilation.

Enzymes TH. but not PNMT " (also.produced solely in tuberomammillary nucleus when the astrocyte takes up GLU. it activates Na-K pump that signals neuron to take up more glucose for energy (positive feedback) Tyrosine hydroxylase Unclear High-affinity Uptake High-affinity Uptake High-affinity Uptake . and acetate. Dopa only (High-affinity uptake) is main expresses TH.Synthesis Degradation/Recycling Rate-limiting step Requires Choline Acetyl Transferase (ChAT). or EPI. COMT is the breakdown pathway for lowaffinity uptake) " Reuptake and MAO Tyrosine hydroxylase Express TH. choline. DBH and PNMT synthesized by tryptophan hydroxylase synthesized from histidine by histidine decarboxylase . means of removal (blocked by cocaine) Tyrosine hydroxylase Express TH and DBH enzymes. Reuptake whether the NT is dopa. NE. Acetylcholinesterase Choline availability Monoamine Oxidase (MAO) Synthesis starts with AA tyrosine. DBH and COMT and PNMT and the level of expression determines (postsynaptically).

transmitter for primary sensory nociceptors 5 AA peptide.made from glutamate using Glutamic Acid Decarboxylase (enzyme only in cells that actually high-affinity uptake removes use GABA). intracellular degradation by GABA-T it from cleft region generates more precursor (GLU) formed on demand by NOS (stimulated by Ca++) in postsynaptic neuron thought to be released via cleavage of the membrane and trafficked by a carrier protein 11 AA peptide. smallest member of opioid peptides (analgesic properties) release inhibited by enkephalin (presynaptic inhibition) diffusion .

receptor Strychnine is receptor like GABA. Antagonist (Atropine) Location of Neurons Muscarinic or Nicotinic widely distributed: throughout PNS. Excitotoxicity: neurons can be stimulated to death by excitatory AAs Coupled to a Cl. Antagonist (tubocurarine) Muscarinic: Agonist (Muscarine. Locus ceruleus and lateral tegmental system " In affective disorders (depression/mania). brainstem reticular core. Pilocarpine). D1 increase cAMP while D2 decrease cAMP Increasing dopamine causes psychosis (decreases gives opposite effect) originates in the midbrain. (LSD is a partial agonist) tuberomammillary nucleus G-protein coupled receptors non-sedating histamines (H1. Substantia nigra (pathology: Parkinson's). involved with abuse) and Arcuate nucleus (site of prolactin inhibition) alpha or beta adrenergic receptors. Alpha-2 is the autoreceptor " receptor markers include high-uptake of 5-HT and tryptophan hydroxylase Interneurons have lots of receptors for drugs of abuse (amphetamines increase DA and NE release) NE transmission associated with affective disorders (depression/mania).Receptor type/marker Other Nicotinic: Agonist (Nicotine). Ionotropic/metabotropic receptors Receptor marker is highaffinity ASP transport PCP binds in the NMDA channel. 5HT plays permissive role cell groups are located in the raphe nuclei (in brainstem) and travel throughout CNS. hypothalamus and retina. Ventral tegmental area (major pleasure pathway. H3) don’t cross BBB Receptor marker is highaffinity GLU transport. Receptor marker antagonist (convulsant is high-affinity GLY poison) transport Renshaw cells of spinal cord . H2. basal forebrain D1 or D2.

GABA is associated with Cl. SP fibers synapse in the dorsal horn opiate receptors (morphine binds these) block substance P by presynaptic inhibition descending 5-HT fibers from medullary raphe nuclei stimulate enkephalin . reflex (skin injury causes causes ascending transmission of pain message to local vasodilation) CNS. major drug target receptor markers include (ethanol. benzos and high affinity uptake and bicucline act as GAD that is a Coupled to Cl. picrotoxin acts as antagonist) resistant to autonomic pathways neurotoxicity take 2-3 weeks for CB1 is the most abundant Geffects since they act protein receptor in the brain through g-proteins discrete neuronal populations (interneurons of cerebrum. hippocampus and striatum) mediates the local axon released from the spinal cord substantia gelatinosa.receptor.