In what ways do different neurotransmitters affect postsynaptic cells?
Sanjay Manohar, Cambridge 2001
Intro: difficulty in defining classical NT
presynaptic localisation, synthesis, release
postsynaptic effect
Biochemically
Amines (from a.a.)
glutamate, aspartate
GABA, glycine
Monoamines
Catecholamines
dopamine
NA
5HT
histamine
Modulators
Peptides
SP
enkephalins, endorphins
CCK, gastrin, VIP
Others
ACh
adenosine, ATP
NO, CO
D-serine
Effects
Short term (ion channels, can be metabotropic or ionotropic)
Depolarisation (EPSP/IPSP) -> AP generation
Contraction (muscle)
Long term (metabolic)
synaptic growth -- number, size, location
Receptor modification
Desensitisation
phosphorylation
bARK
b-arrestin
Receptor Down-/Upregulation
synthesis
breakdown
internalisation
Other
splice variants eg. AMPA
post-transcriptional modification
Mention: retrograde transmission eg. NO
presynaptic autoreceptor inhibition
Receptor mechanism
Ionotropic [give examples...]
Na, Ca -> depol, EPSP
K -> hyperpol, IPSP
Cl -> stabilise membrane
Metabotropic [give examples...]
G proteins -- diagram, Gi, Gq, Gs
Second messengers
IP3
PLC
Ca channels
cAMP
PKA
Na channels
Ca
Activation of multiple enzymes
time & location dependent