Pathway: Nucleus basalis of meynert and septum to cerebral cortex and hippocampus, this degenerates in (alzheimers); balance DA in corpus striatum (parkinsons)

Metabolism: AcCoA is broght in through nerve, choline is taken up by CHT, inside the nerve terminal ChAT combines the two to make AcH, which is taken up by VAT into vessicles and will later be released; AcH will be taken up again via AcH autoreceptor

Receptors: Muscarinic receptors or nicotinic; M1 - widespread, increase IP3 and DAG; M2 - hippocampus and cortex, decrease cAMP, increase K+ so are inhibit neurons; M4 - may help in scizophrenia

Pathway: locus coeruleus and reticular formation, project throughout the brain

Metabolism: Synthesized from Dopamine, which is synthesized from Tyrosine hydroxylase action on tyrosine; stored in vessicles via VMAT; taken up via NET

Receptor: A1, A2, B1, B2

A1 - activate PLC, increases IP3 and DAG

A2 - decreases Ca influx (presynaptic); increases K conductance to decrease cAMP (postsynaptic)

B1 - Wide distribution, increase cAMP, decrease K conductance

B2 - Cerebellum, increases cAMP

Amphetamines cause NE release, cocaine and some antidepressants inhibit the NE transporter (NET)

Pathway: Mesolimbic system; Nigro striatal pathway, degenerates in parkinson's disease causing movment disorders; ventral tegmental area to nucleus accumbens and prefrontal cortex involved in addiction

Metabolism: tyrosine is converted to l-dopa via tyrosine hydroxylase, l-dopa is then converted to dopamine

Receptors: D and D subtypes

D1 - increases cAMP

D2 - presynaptic D2r decreases Ca influx; postsynaptic D2r decreases cAMP and increase K conductance via Gi

Amphetamine and cocaine inhibit reuptake

Pathway: Raphe nucleus to the limbic system and cerebral cortex

Metabolism: Tryptophan-> tryptophan hydroxylase -> 5-hydroxytryptophan -> aromatic L amino acid decarboxylase -> serotonin

Receptors: 5-HT and subtypes

5-HT1A = increases K conductance and causes hyperopolarization, like GABA

5-HT2A = Increase IP3 and DAG, decrease K conductance, important in schizophrenia

5-HT3 = ligand gated ion channel, increase cation conductance, involved in nausea

Main inhibitory NT in brain

Receptors: 

GABA-A = ionotropic, increased Cl- conductance, neuronal inhibition

GABA-B = GPCRs, decrease Ca conductance or increase K conductance

Major excitatory AA NT; important in memory and learning and LTP

Metabolism: NMDAr is permeable to Ca, Na and K, requires binding of glycine to a modulatory site in order to function

Receptors: NMDAr - in all neurons; increases Na and Ca influx

AMPA - in almost all neurons; involved in seizures

Kainic (kainate) acid receptor- in hippocampus, cerebellum and spinal cord; involved in seizures