Metherate R, Ashe J H, Weinberger N M
Center for the Neurobiology of Learning and Memory, University of California, Irvine.
Synapse. 1990;6(4):364-8. doi: 10.1002/syn.890060409.
Cholinergic modification of neuronal responsiveness in auditory cortex includes alteration of spontaneous and tone-evoked neuronal discharge. Previously it was suggested that the effects of acetylcholine (ACh) and muscarinic agonists on neuronal discharge resembled those due to increases in the intensity of acoustic stimuli (Ashe et al. 1989). To determine the relationship between neuronal modifications due to ACh acting at muscarinic receptors and those due to changes in stimulus intensity, we determined acoustic rate-level functions for neurons in the auditory cortex of barbiturate-anesthetized guinea pigs before, during and after administration of ACh. ACh facilitated acoustic rate-level functions in 82% of the cells tested. In addition, during ACh administration 66% of neurons responded to stimuli that were previously subthreshold, that is, ACh decreased the response threshold. Cholinergic facilitation of rate-level functions was attenuated by the general muscarinic antagonist atropine. The nature of the muscarinic receptors involved in the actions of ACh was further examined by presenting single tones before, during, and after administration of ACh and specific muscarinic receptor subtype antagonists, either pirenzepine (M1) or gallamine (M2). ACh-induced facilitation of spontaneous and tone evoked neuronal discharge was antagonized by pirenzepine, but not by gallamine, suggesting the involvement of the M1 muscarinic receptor subtype. These data indicate that ACh can facilitate stimulus-evoked responses and decrease response thresholds for neurons in auditory cortex, possibly via activation of M1 muscarinic receptors. Such effects of ACh acting at muscarinic receptors could underly cholinergic regulation of information processing in the auditory cortex.
胆碱能对听觉皮层神经元反应性的调节包括对自发和音调诱发神经元放电的改变。此前有研究表明，乙酰胆碱（ACh）和毒蕈碱激动剂对神经元放电的影响类似于声学刺激强度增加所产生的影响（阿什等人，1989年）。为了确定毒蕈碱受体介导的ACh引起的神经元变化与刺激强度变化引起的神经元变化之间的关系，我们在给ACh之前、期间和之后，测定了巴比妥麻醉的豚鼠听觉皮层神经元的声学频率-强度函数。ACh使82%的受试细胞的声学频率-强度函数得到促进。此外，在给予ACh期间，66%的神经元对先前阈下的刺激有反应，即ACh降低了反应阈值。毒蕈碱拮抗剂阿托品减弱了胆碱能对频率-强度函数的促进作用。通过在给予ACh和特定毒蕈碱受体亚型拮抗剂（哌仑西平（M1）或加拉明（M2））之前、期间和之后呈现单音，进一步研究了参与ACh作用的毒蕈碱受体的性质。哌仑西平而非加拉明拮抗了ACh诱导的自发和音调诱发神经元放电的促进作用，提示M1毒蕈碱受体亚型参与其中。这些数据表明，ACh可能通过激活M1毒蕈碱受体，促进听觉皮层神经元的刺激诱发反应并降低反应阈值。ACh作用于毒蕈碱受体的这种效应可能是听觉皮层信息处理胆碱能调节的基础。
