Neurotransmitter systems Flashcards
Ach central location
Pons/Midbrain (arousal and REM sleep)
Caudate and Putamen neurons in Striatum of basal ganglia (motor control)
Ach f(x)
wakefulness/motor control
Ach receptor
ionotropic - nicotinic
metabotropic - muscarinic
GABA central location
CNS, more in higher CNS
GABA f(x)
major inhibitory - motor control, consciousness
GABA receptor
ionotropic - GABAa (Cl conductance)
metabotropic - GABAb (GiGo –> GIRK –> inhib. Ca
channel)
Pre-synaptic - regulate NT release
Post-synaptic - inhib. of post-synaptic cell
Glycine central location
spinal cord and lower CNS
Glycine f(x) (how? what blocks?)
general inhibition
influx of Cl leads to ipsp
Stychnine binds to and blocks
Glycine receptor
ionotropic - GlyR
Purines central location
widespread
Purines f(x)
adenosine - sleep, inhibition;
atp
Purines receptor
2 major classes: P1, P2
ionotropic - P2X
metabotropic - P1(A), P2Y
Opiods central location
Basal ganglia; hypothalamus; pons/medulla
Opiods f(x)
analgesia (nociceptive modification)
mood/effect (sedative)
Opiods receptor
metabotropic - Mu (increase K efflux & hyperpolarization) , delta, kappa (GiGo) (decrease Ca influx)
Endocannabinoids central location
Basal ganglia; cortex, spinal cord
Endocannabinoids f(x)
Neuroprotection
mood
nociception
Endocannabinoids receptor
metabotropic - CB-1 (Gi) (reduces EAA and GABA release)
CB-2 is anti-inflammatory
which muscarinic receptors use Gq pathway
M1, 3, 5
increase IP3 and DAG –> increased Ca
which muscarinic receptors use Gi pathway
M2, 4
decreased cAMP –> increased K
GABA removal from synapse
GATs (Gly uses this too)
GAT1 - presynaptic terminals; repackaged into vesicals
as is
GAT2 - glial cells surrounding synapse; broken down
into glutamate in ECF, taken up by presynaptic
terminal, recycled into GABA
P1 purine receptor (A receptors)
ligand = adenosine post-synaptic: sleep induction general inhib. of neural function pre-synaptic: regulation of NT release
P2 purine receptor
P2X: ATP
P2Y: ATP, ADP, UTP, UDP
(GsGq coupled)
learning and memory
modification of locomotor pathways