Neurotransmitter Class

NT Name

General Function

Acetylcholine

ACh

movement control, cognition

Monoamines - Catecholamines

Dopamine

affect, reward, movement

Norepinephrine

affect, alertness

Epinephrine

alertness mood, arousal, modulation of pain, sleep

Monoamines - Indoleamine

Serotonin (5-HT)

Histamine

Histamine

waking state

Amino Acids - Excitatory

Glutamic Acid (GLU)

general excitation, sensation

Aspartic Acid (ASP)

Amino Acids - Inhibitory

Glycine (GLY)

general inhibition

GABA

general inhibition

Nitric Oxide Endocannabinoids

NO

Vasodilation, signaling Hunger

Substance P

SP

Pain

Opioid peptides

Enkephalin

Control of Pain

Synthesis

Degradation/Recycling

Rate-limiting step

Requires Choline Acetyl Transferase (ChAT), choline, and acetate.

Acetylcholinesterase

Choline availability

Monoamine Oxidase (MAO) Synthesis starts with AA tyrosine. Enzymes TH, DBH and COMT and PNMT and the level of expression determines (postsynaptically). Reuptake whether the NT is dopa, NE, or EPI. Dopa only (High-affinity uptake) is main expresses TH. means of removal (blocked by cocaine)

Tyrosine hydroxylase

Express TH and DBH enzymes, but not PNMT

" (also, COMT is the breakdown pathway for lowaffinity uptake) " Reuptake and MAO

Tyrosine hydroxylase

Express TH, DBH and PNMT synthesized by tryptophan hydroxylase synthesized from histidine by histidine decarboxylase - 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

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, transmitter for primary sensory nociceptors 5 AA peptide, smallest member of opioid peptides (analgesic properties) release inhibited by enkephalin (presynaptic inhibition)

diffusion

Receptor type/marker

Other Nicotinic: Agonist (Nicotine), Antagonist (tubocurarine) Muscarinic: Agonist (Muscarine, Pilocarpine), Antagonist (Atropine)

Location of Neurons

Muscarinic or Nicotinic

widely distributed: throughout PNS, brainstem reticular core, basal forebrain

D1 or D2. D1 increase cAMP while D2 decrease cAMP

Increasing dopamine causes psychosis (decreases gives opposite effect)

originates in the midbrain, hypothalamus and retina. Substantia nigra (pathology: Parkinson's), Ventral tegmental area (major pleasure pathway, 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). Locus ceruleus and lateral tegmental system "

In affective disorders (depression/mania), 5HT plays permissive role

cell groups are located in the raphe nuclei (in brainstem) and travel throughout CNS. (LSD is a partial agonist) tuberomammillary nucleus

G-protein coupled receptors non-sedating histamines (H1, H2, H3) dont cross BBB Receptor marker is highaffinity GLU transport. Ionotropic/metabotropic receptors Receptor marker is highaffinity ASP transport PCP binds in the NMDA channel. Excitotoxicity: neurons can be stimulated to death by excitatory AAs

Coupled to a Cl- receptor Strychnine is receptor like GABA. Receptor marker antagonist (convulsant is high-affinity GLY poison) transport

Renshaw cells of spinal cord

GABA is associated with Cl- channel that is a Coupled to Cl- receptor. major drug target receptor markers include (ethanol, benzos and high affinity uptake and bicucline act as GAD agonists; 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, reflex (skin injury causes causes ascending transmission of pain message to local vasodilation) CNS. 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