Nicotine and Synaptic Plasticity in Prefrontal Cortex

Sci. STKE, 14 August 2007
Vol. 2007, Issue 399, p. pe44
DOI: 10.1126/stke.3992007pe44

Nicotine and Synaptic Plasticity in Prefrontal Cortex

  1. Daniel S. McGehee*
  1. Department of Anesthesia and Critical Care, Committee on Neurobiology, Committee on Cell Physiology, University of Chicago, 5841 South Maryland Avenue, MC4028, Chicago, IL 60637, USA.
  1. *Corresponding author. E-mail:dmcgehee{at}uchicago.edu

Abstract

Nicotinic receptor activation enhances working memory and attention. The prefrontal cortex is a key brain area involved in working memory, and plasticity of excitatory synaptic transmission within the cortex is likely an important cellular mechanism of memory. A recent study has explored the cellular and synaptic basis of nicotine’s effects on excitability within the prefrontal cortex. The findings suggest that nicotine enhances inhibitory synaptic inputs to layer V pyramidal cells, which suppresses induction of long-term potentiation (LTP). This inhibitory effect can be overcome by stimulating the pyramidal cells in bursts, which suggests a modification in the signal-to-noise ratio for synaptic input. Thus, the impact of strong stimuli on working memory would be enhanced when combined with nicotinic receptor activity. These findings may lead to novel and more effective treatments for memory disorders.

Citation:

D. S. McGehee, Nicotine and Synaptic Plasticity in Prefrontal Cortex. Sci. STKE 2007, pe44 (2007).
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