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Regulation of GABA signaling by Nicotine acetylcholine receptors
Nicotinic acetylcholine receptors (nAChR ) are cholinergic
receptors that form ligand-gated ion channels in the plasma membranes of certain neurons
and on the postsynaptic side of the neuromuscular junctions. As ionotropic receptors,
nAChR are directly linked to ion channels and do not use
second messengers. nAChR are activated by the binding of the
neurotransmitter Acetylcholine and can be opened by
Nicotine [1 ].
nAChR are composed of different subunits including:
alpha- (Cholinergic receptor, nicotinic, alpha 1, 3, 4, 5, 7 (nAChR
alpha-1 , nAChR alpha-3 , nAChR
alpha-4 , nAChR alpha-5 , nAChR
alpha-7) ), beta-( Cholinergic receptor, nicotinic, beta 1, 2
(nAChR beta-1 , nAChR beta-2 ))
and nAChR gamma/epsilon .
nAChR activate transport of Ca('2+)
extracellular region into the presynaptic neuron and thereby promote
Gamma-aminobutyric acid (GABA ) release [2 ], [3 ], [4 ], [5 ], [6 ], [7 ].
GABA activates a wide variety of GABA receptors
(GABA-A receptor ) on postsynaptic membrane, which are
composed of different alpha, beta and gamma subunits including: GABA-A
receptor alpha-1/beta-1/gamma-2 ; GABA-A receptor
alpha-2/beta-3/gamma-2 ; GABA-A receptor
alpha-4/beta-3/gamma-2 , and GABA-A receptor
alpha-6/beta-2/gamma-2 [8 ], [9 ], [10 ].
Activation of GABA-A receptor leads to increased
Cl('-) extracellular region import into the cell and
promotes hyperpolarization of postsynaptic neurons [11 ], [12 ].
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