Nicotine Enhances Firing Activity of Layer 5 Pyramidal Neurons in the Medial Prefrontal Cortex through Inhibition of Kv7 Channels

Nicotine enhances attention, working memory and recognition. One of the brain regions associated with these effects nicotine is medial prefrontal cortex (mPFC). However, cellular mechanisms that induce enhancing remain unclear. To address this issue, we performed whole-cell patch-clamp recordings from mPFC layer 5 pyramidal neurons in slices C57BL/6J mice. Shortly (approx. 2 min) after bath application nicotine, number action potentials, which were elicited by depolarizing current injection, was increased, increase persisted for over min. The effect blocked α4β2 nicotinic acetylcholine receptor (nAChR) antagonist dihydro-β-erythroidine, α7 nAChR methyllycaconitine, or intracellular perfusion Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA). Additionally, voltage-dependent potassium 7 (Kv7) channel blocker, 10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone dihydrochloride (XE-991), as well shortened spike threshold latency increased numbers. By contrast, Kv7 opener, retigabine reduced firings, addition did not These results indicate induces long-lasting enhancement firing activity neurons, mediated stimulation nAChRs subsequent levels followed suppression channels. novel might underlie nicotine-induced