抄録
Mammalian cortex receives dense cholinergic innervation from basal forebrain cholinergic neurons, but how acetylcholine (ACh) regulates cortical circuits is still unclear. Recent experiments favor the hypothesis that instead of producing simple facilitation or inhibition, ACh serves to shift the cortical circuits into a condition where cortical neurons are influenced predominantly by afferent inputs from thalamus rather than other cortical inputs. This is achieved by muscarinic suppression of intracortical connections and nicotinic facilitation of thalamocortical inputs, both presynaptically. Indeed, excitatory postsynaptic potentials (EPSPs) in layer 4 neurons elicited by thalamic stimulation were enhanced or in some cases "unsilenced" in the presence of a nicotinic agonist. Optical recordings further supported facilitatory effect of ACh, but it also revealed that this facilitation was followed by suppression only in layer 4. By comparing the sensitivity to a nicotinic agonist between excitatory and inhibitory cells, we found that inhibitory neurons were more susceptible to nicotine. Incidentally, we also found that thalamic activation of GABAergic neurons preceded that of excitatory neurons in a given barrel, which effectively works to produce a feedforward inhibition on excitatory relay cells. Thus, exploiting such intrinsic network property, ACh not only facilitate thalamic input to cortex, but also restrict the excitation of postsynaptic cells to a narrow window of time by selectively enhancing thalamic innervation to inhibitory neurons in the cortex. [J Physiol Sci. 2006;56 Suppl:S33]
