Distributed network actions by nicotine increase the threshold for spike-timing-dependent plasticity in prefrontal cortex

J.J. Couey, R.M. Meredith, S. Spijker, R.B. Poorthuis, A.B. Smit, A.B. Brussaard, H.D. Mansvelder

Research output: Contribution to JournalArticleAcademicpeer-review

Abstract

Nicotine enhances attention and working memory by activating nicotinic acetylcholine receptors (nAChRs). The prefrontal cortex (PFC) is critical for these cognitive functions and is also rich in nAChR expression. Specific cellular and synaptic mechanisms underlying nicotine's effects on cognition remain elusive. Here we show that nicotine exposure increases the threshold for synaptic spike-timing-dependent potentiation (STDP) in layer V pyramidal neurons of the mouse PFC. During coincident presynaptic and postsynaptic activity, nicotine reduces dendritic calcium signals associated with action potential propagation by enhancing GABAergic transmission. This results from a series of presynaptic actions involving different PFC interneurons and multiple nAChR subtypes. Pharmacological block of nAChRs or GABA
Original languageEnglish
Pages (from-to)73-87
JournalNeuron
Volume54
Issue number1
DOIs
Publication statusPublished - 2007

Fingerprint

Dive into the research topics of 'Distributed network actions by nicotine increase the threshold for spike-timing-dependent plasticity in prefrontal cortex'. Together they form a unique fingerprint.

Cite this