Evidences a(MESH:Nicotine) to p(HGNC:CHRNA7)

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].

These alterations are very similar to those observed in cul- tured human airway cells or in ex vivo human lung explants treated with the selective α7 antagonist αBgtx, or epithelial cell cultures chronically exposed to nicotine in which nico- tine-induced desensitisation of α7 receptors mimics the ab- sence of α7 nAChR

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