作者: Sharon L. Juliano , S. Essie Jacobs
DOI: 10.1007/978-1-4757-9616-2_10
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摘要: Over the past several decades, acetylcholine (ACh) has been recognized as an important factor in neocortical function. The source of ACh arises from basal forebrain, where specific nuclear groups supply entire cortical mantle with this ubiquitous neurotransmitter (Mesulam et al., 1983; Rye 1984; Wainer and Mesulam, 1990). Although numerous actions have identified ACh, cerebral cortex it appears to primarily enhance neural activity (for review see McCormick, 1992). acts on both muscarinic nicotinic receptors; however, excitatory effect is predominantly mediated by mechanisms that block K+ conductance (Krnjevic Phillis, 1963; Krnjevic 1971; Halliwell Adams, 1982; Brown, McCormick Prince, 1985). In neocortex, work through mechanisms; one these blocks a voltage-dependent current, which leads long-lasting increase excitability (Brown 1980; Madison Nicoll, 1987). It also impedes Ca2+-activated potassium not substantially dependent voltage (McCormick Williamson, 1989). Additional contributions Na+-activated current slow afterdepolarization unknown origin implicated potential action neocortex 1986; Schwindt