Presynaptic Terminals
Simultaneously, nicotine activates presynaptic α7∗ nAChRs, boosting glutamatergic synaptic transmission onto DA neurons (23, 88, 123, 134). PubMed:17009926
This effect of preterminal nAChRs is inhibited by tetrodotoxin, which blocks sodium channels and, thus, prevents the regenerative voltage-dependent activation of calcium channels in the presynaptic bouton. PubMed:17009926
In addition, nAChR activity produces a depolarization that activates voltage-gated calcium channels in the presynaptic terminal (87). PubMed:17009926
Postsynaptic β2∗ nAChRs initially depolarize DA neurons, causing them to fire action potentials while presynaptic α7∗ nAChRs boost glutamate release. PubMed:17009926
Presynaptic and preterminal nicotinic receptors enhance neurotransmitter release, and postsynaptic and nonsynaptic nAChRs mediate excitation as well as activity-dependent modulation of circuits and intracellular enzymatic processes. PubMed:17009926
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.