Evidences a(MESH:Nicotine) to complex(p(HGNC:CHRNA4), p(HGNC:CHRNB2))

α4β2* subtypes, in which the presence of different accessory subunits changes their pharmacological and biophysical properties, and their sensitivity to allosteric modulators and up-regulation by nicotine

By activating the α4β2 receptors on inhibitory GABAergic inputs to the VTA or GABAergic interneurons, smoked concentrations of nicotine transiently increase the release of GABA and subse- quently depress it for about one hour

Chronic nicotine treatment also activates the α7 receptors expressed on glutamatergic terminals, increases the release of glutamate (which facilitates the burst firing of VTA DA neurons), increases NMDA receptor activity, and LTP [79], but simultaneosusly induces the desensitisation of the α4β2 receptors on GABAergic terminals. Overall, these effects decrease the inhibition onto DA neurons, and increase DA release in the NAc [82].

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