Abstract

The responses of 155 neurones and 91 glial cells to the electrical stimulation of the cortex were recorded in the suprasylvian gyrus of 20 cats under pentobarbital anaesthesia. Glial cells were identified by electrophysiological criteria: absence of action potentials and postsynaptic potentials; high membrane potential; slow depolarization during the electrical stimulation of the cortex. 50 glial cells showed membrane potentials between 80 and 100 mV. Stimuli of low intensity which evoked only excitatory postsynaptic potentials of apical dendrites, the so-called dendritic potentials, failed to evoke glial depolarization. However, glial depolarization could be elicited at high-frequency stimulation. Stimuli, which evoked not only the dendritic potential but also subsequent slow negativity, could usually bring about glial depolarization too. The amplitude of glial depolarization in response to one stimulus did not exceed 2 mV, the latency being 3–5 ms. A phenomenon of decrementai summation of glial depolarization was observed. The stronger and more frequent the stimulation, the larger was glial depolarization. However, at frequencies over 50/s glial depolarization decay was observed already during the stimulation and in some cases, membrane potential was drastically reduced to zero. After cessation of stimulation, glial depolarization decayed exponentially in 3–4 s; in some cases the decay was prolonged up to 10s and slow irregular fluctuations of the membrane potential were recorded; at the same time, spikes of the neighbouring neurone could be recorded from the glial cell. With a decrease of the membrane potential glial depolarization was attenuated, but it could be elicited even at membrane potential below 20 mV. The results are interpreted in relation to the potassium ion hypothesis. It is suggested that glial depolarization is determined by release of K +, which is associated with excitation of non-myelinated fibres and with excitatory postsynaptic potentials generated in the cortical neuropile. Significant increases in the concentration of extracellular potassium ions could provoke actual movement of glial cells. It is supposed that glial depolarization of small magnitude which is recorded occasionally at the membrane potential below 30 mV is the result of electronic spread of glial depolarization from the neighbouring glial cells.

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