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The Role of Acetylcholine in Barrel Cortex

  • Chapter
The Barrel Cortex of Rodents

Part of the book series: Cerebral Cortex ((CECO,volume 11))

Abstract

Over the past several decades, acetylcholine (ACh) has been recognized as an important factor in neocortical function. The neocortical source of ACh arises from the basal forebrain, where specific nuclear groups supply the entire cortical mantle with this ubiquitous neurotransmitter (Mesulam et al., 1983; Rye et al., 1984; Wainer and Mesulam, 1990). Although numerous actions have been identified with ACh, in the cerebral cortex it appears to primarily enhance neural activity (for review see McCormick, 1992). ACh acts on both muscarinic and nicotinic receptors; however, the excitatory effect of ACh in the cerebral cortex is predominantly muscarinic and mediated by mechanisms that block K+ conductance (Krnjevic and Phillis, 1963; Krnjevic et al., 1971; Halliwell and Adams, 1982; Brown, 1983; McCormick and Prince, 1985). In the neocortex, ACh appears to work through several mechanisms; one of these blocks a voltage-dependent K+ current, which leads to a long-lasting increase in neural excitability (Brown and Adams, 1980; Madison and Nicoll, 1984; McCormick and Prince, 1987). It also impedes a Ca2+-activated potassium current, which is not substantially dependent on voltage (McCormick and Williamson, 1989). Additional contributions of a Na+-activated K+ current block and a slow afterdepolarization of unknown origin have also been implicated as potential mechanisms of ACh action in neocortex (McCormick and Prince, 1986; Schwindt et al., 1989).

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Juliano, S.L., Jacobs, S.E. (1995). The Role of Acetylcholine in Barrel Cortex. In: Jones, E.G., Diamond, I.T. (eds) The Barrel Cortex of Rodents. Cerebral Cortex, vol 11. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9616-2_10

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