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Separate activation of fast and slow inhibitory postsynaptic potentials in rat neocortex in vitro.

机译:在大鼠新皮层中快速和缓慢抑制突触后电位的独立激活。

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摘要

Synaptic inhibition was investigated by stimulating inhibitory neurones with focal microapplications of glutamate, while recording from layer V pyramidal neurones of rat somatosensory cortical slices. One class of inhibitory postsynaptic potentials (IPSPs) thus elicited was characterized as a fast, chloride-mediated, GABAA IPSP in part by its fast time-to-peak (mean 2.5 ms) and brief duration, but primarily on the basis of its reversal potential at -68 mV, and its blockade by picrotoxin. The average peak amplitude for these fast IPSPs was -1.5 mV, measured at -60 mV. The peak conductance calculated for these events was about 10 nS. The conductance change associated with the maximal fast inhibitory postsynaptic potential resulting from electrical stimulation of afferent pathways ranged up to 116 nS. A second class of IPSP was encountered much less frequently. These glutamate-triggered events were characterized as slow, potassium-mediated GABAB IPSPs partly because of their longer times-to-peak (mean, 45 ms) and duration, but especially because of their extrapolated equilibrium potential at about -89 mV and blockade by 2-hydroxysaclofen. The average peak amplitude for these slow IPSPs was -2.3 mV, measured at -60 mV. The peak conductance for these events was about 8 nS. IPSPs resulting from the excitation of individual inhibitory interneurones were elicited by glutamate microapplication at particular locations relative to recording sites. Both fast and slow IPSPs were generated, but these occurred as separate events, and mixed responses were never seen. Thus, the two mechanistically distinct types of IPSPs which result from GABA interaction at GABAA and GABAB receptors on neocortical neurones may be mediated by separate classes of inhibitory neurones.
机译:通过用谷氨酸的局部微量刺激刺激抑制性神经元,同时从大鼠体感皮层切片的V层锥体神经元记录,来研究突触抑制。由此引发的一类抑制性突触后电位(IPSP)被表征为快速的,氯化物介导的GABAA IPSP,部分原因是其快速达到峰值时间(平均2.5 ms)和短暂的持续时间,但主要是基于其反转电位在-68 mV,并且被微毒素阻断。这些快速IPSP的平均峰值幅度为-1.5 mV,在-60 mV处测得。计算出的这些事件的峰值电导约为10 nS。与传入途径电刺激导致的最大快速抑制突触后电位相关的电导变化范围高达116 nS。第二类IPSP的遇到频率要低得多。这些谷氨酸触发的事件被表征为钾介导的GABAB IPSPs缓慢,部分原因是其到达峰值的时间(均值,45 ms)和持续时间更长,但尤其是因为它们在-89 mV时外推平衡电位并被2-羟基沙氯芬。这些慢速IPSP的平均峰值幅度为-2.3 mV,在-60 mV处测得。这些事件的峰值电导约为8 nS。通过在相对于记录位点的特定位置通过谷氨酸微施用来激发由单个抑制性中间神经元的激发产生的IPSP。生成了快速和慢速IPSP,但是这些事件是作为单独的事件发生的,而且从未看到过混合的响应。因此,在新皮层神经元的GABAA和GABAB受体上的GABA相互作用产生的两种机理上截然不同的IPSPs可能由不同种类的抑制性神经元介导。

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