Responses of cortical neurons to stimulation of corpus callosum in vitro.
Responses of cortical neurons to stimulation of corpus callosum in vitro.
复制标题
皮质神经元对体外胼胝体刺激的反应。
DOI：
10.1152/jn.1982.48.6.1257
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发表时间：
1982
影响因子：
2.5
通讯作者：
A. Gorman
中科院分区：
文献类型：
--
作者：
B. Vogt;A. Gorman
1.采用大鼠扣带回皮质脑片的体外制备方法，分析了V层神经元对电刺激穹隆体区的反应。此外，我们还在电子显微镜下观察了与V层神经元的突触终止，为解释一些观察到的反应序列提供了结构基础。2.V层神经元静息膜电位(RMP)为60+/-0.68 mV，输入电阻为47+/-4.74M omega，膜时间常数为4.37+/-0.51ms，电紧张性长度常数为1.38+/-0.25，自发动作电位幅值为50+/-0.3 mV。细胞内去极化电流脉冲诱发尖峰，有时与低幅度(2-5 mV)去极化(持续5-10ms)和超极化(持续10-20ms)后电位有关。3.对CC的单一刺激产生下列反应序列之一：a)反向峰电位和兴奋性突触后电位(EPSP)，引发一个或多个峰电位；b)逆行峰电位、EPSP诱发的动作电位和超极化，它们可能代表固有的细胞特性或抑制突触活动；c)EPSP和诱发的棘波；d)高幅度的EPSP，有或没有动作电位爆发。4.逆行激活(AA)神经元总是在CC刺激下产生EPSP。与非逆行激活的神经元相比，AA细胞具有更负的RMP，更大的电紧张性长度常数(LN)，更高的树突/体细胞电导(Rho)比率，并形成持续时间较短的膝状体诱发的EPSP。5.前扣带回神经元产生EPSPS的持续时间比后扣带回神经元长(分别为50±3.57和26±1.56 ms)。前神经元EPSP的最大波幅(20.5+/-1.0 mV比11.5+/-0.79 mV)和达峰时间(11.6+/-2.2和8.2+/-0.8ms)也较高。6.对侧损毁后的高尔基体神经元的电子显微镜观察显示，锥体神经元和非锥体神经元均接受直接的穹隆传入。与前锥体细胞顶端树突的突触终末是后锥体神经元突触终末的6倍。7.前后部神经元EPSP形态的差异可能部分是由这两个皮质的穹隆传入神经的密度和分布所致。
1. An in vitro slice preparation of rat cingulate cortex was used to analyze the responses of layer V neurons to electrical stimulation of the corpus callosum (CC). In addition, synaptic termination of callosal afferents with layer V neurons was evaluated electron microscopically to provide a structural basis for interpreting some of the observed response sequences. 2. Layer V neurons had a resting membrane potential (RMP) of 60 +/- 0.68 (SE) mV, an input resistance of 47 +/- 4.74 M omega, a membrane time constant of 4.37 +/- 0.51 ms, an electrotonic length constant of 1.38 +/- 0.25, and produced spontaneous action potentials that were 50 +/- 0.3 mV in amplitude. Intracellular depolarizing current pulses evoked spikes that were sometimes associated with low-amplitude (2-5 mV) depolarizing (5-10 ms in duration) and hyperpolarizing (10-20 ms in duration) afterpotentials. 3. A single stimulus of increasing intensities to the CC produced one of the following response sequences: a) antidromic spike and an excitatory postsynaptic potential (EPSP), which initiated one or more spikes; b) antidromic spike, EPSP-evoked action potentials, and a hyperpolarization, which may have represented an intrinsic cell property or inhibitory synaptic activity; c) EPSP and evoked spikes only; d) high-amplitude EPSP with an all-or-none burst of action potentials. 4. Antidromically activated (AA) neurons always produced EPSPs in response to CC stimulation. When compared with nonantidromically activated neurons, AA cells had a more negative RMP, greater electrotonic length constant (LN), higher ratio of dendritic to somatic conductance (rho), and formed shorter duration, callosal-evoked EPSPs. 5. Neurons in anterior cingulate cortex produced EPSPs of longer duration than did those in posterior cortex (50 +/- 3.57 versus 26 +/- 1.56 ms, respectively). EPSPs in anterior neurons also had a higher maximum amplitude (20.5 +/- 1.0 versus 11.5 +/- 0.79 mV) and longer time to peak (11.6 +/- 2.2 versus 8.2 +/- 0.8 ms). 6. Electron microscopy of Golgi-impregnated neurons following contralateral lesions demonstrated that both pyramidal and nonpyramidal neurons received direct callosal afferents. Synaptic termination of callosal axons with the apical dendritic trees of anterior pyramidal cells was 6 times greater than it was with posterior pyramidal neurons. 7. EPSP shape differences in anterior and posterior neurons may be partially accounted for by the density and distribution of callosal afferents to these two cortices.