<p>A comparative study of the electrophysiological characteristics of pyramidal (PC) neurons of the dorsal and ventral parts of the CA1 zone of the hippocampus of mice was conducted using the patch-clamp method in the “whole cell” configuration. The potassium load was used as a parameter for cell type discrimination (an increase in [K<sup>+</sup>]<sub>o</sub> from 3.0 to 8.5 mM in the medium). It has been established that two types of cells with different sensitivities to potassium are found in both parts of the CA1 zone. In PC-A type cells, the burst firing evoked by a step of current <i>I</i> (from 10 to 200 pA) is potentiated by potassium with an increase in [K<sup>+</sup>]<sub>o</sub> to 8.5 mM, whereas in PC-I type cells at currents <i>I</i> &lt; 100 pA there is no effect of potassium load and at currents ≥125 pA suppression of bursting is observed. The ratios of the number of PC-A/PC-I cells in the ventral and dorsal regions are 16&#xa0;:&#xa0;5 and 8&#xa0;:&#xa0;8, respectively. Potassium potentiation of burst firing is higher in ventral PC-A cells than in dorsal cells. The threshold current (<i>I</i><sub>th</sub>) decreases by 2.5 times and a spontaneous burst firing (pacemaker-like activity) is manifested only in PC-A cells with potassium loading. The Sag potential and the adaptation index of induced impulse activity are higher in the ventral PC-A cells than in the dorsal cells. The potassium load reduces the Sag potential. An analysis of the steady-state current-voltage relationships shows that inward and outward (predominantly) slow potassium currents are activated under a potassium load. The currents in the ventral neurons of both types are 1.5–2.0 times lower than in the dorsal neurons (at –100 and +20 mV). Taken together, these data suggest that <InlineEquation ID="IEq1"> <EquationSource Format="TEX">\({\text{K}}_{{\text{o}}}^{ + }\)</EquationSource> <!--BioPhys2570064Galashin-m1--> </InlineEquation>-sensitive ventral PC-A cells can play an important role in hyperexcitation of neural networks and induction of epileptogenesis.</p>

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Heterogeneity of Responses to Potassium Loading of Glutamatergic Neurons in the Ventral and Dorsal Parts of the Hippocampal CA1 Zone

  • A. S. Galashin,
  • M. V. Konakov,
  • V. V. Dynnik

摘要

A comparative study of the electrophysiological characteristics of pyramidal (PC) neurons of the dorsal and ventral parts of the CA1 zone of the hippocampus of mice was conducted using the patch-clamp method in the “whole cell” configuration. The potassium load was used as a parameter for cell type discrimination (an increase in [K+]o from 3.0 to 8.5 mM in the medium). It has been established that two types of cells with different sensitivities to potassium are found in both parts of the CA1 zone. In PC-A type cells, the burst firing evoked by a step of current I (from 10 to 200 pA) is potentiated by potassium with an increase in [K+]o to 8.5 mM, whereas in PC-I type cells at currents I < 100 pA there is no effect of potassium load and at currents ≥125 pA suppression of bursting is observed. The ratios of the number of PC-A/PC-I cells in the ventral and dorsal regions are 16 : 5 and 8 : 8, respectively. Potassium potentiation of burst firing is higher in ventral PC-A cells than in dorsal cells. The threshold current (Ith) decreases by 2.5 times and a spontaneous burst firing (pacemaker-like activity) is manifested only in PC-A cells with potassium loading. The Sag potential and the adaptation index of induced impulse activity are higher in the ventral PC-A cells than in the dorsal cells. The potassium load reduces the Sag potential. An analysis of the steady-state current-voltage relationships shows that inward and outward (predominantly) slow potassium currents are activated under a potassium load. The currents in the ventral neurons of both types are 1.5–2.0 times lower than in the dorsal neurons (at –100 and +20 mV). Taken together, these data suggest that \({\text{K}}_{{\text{o}}}^{ + }\) -sensitive ventral PC-A cells can play an important role in hyperexcitation of neural networks and induction of epileptogenesis.