Abstract

Effects of cryopreservation of male Wistar rat brain slices with different duration (4, 8, 10, 23, and 90 days) on changes in their electrical activity was investigated. The amplitudes of AMPA- and NMDA-dependent glutamatergic ionotropic mechanisms were measured, as well as the action potential of the lateral olfactory tract (AP LOT) at a temperature of –20°C and subsequent warming to +37°C. After cryopreservation, these mechanisms were preserved and restored. We used the method of electrophysiological registration of the AMPA and NMDA potentials and the total AP LOT. After cryopreservation, the AMPA-dependent mechanisms and the activity of conductive LOT fi bers were restored to normothermal values. On the contrary, the recovery of NMDA-dependent mechanisms was incomplete and averaged 34% compared with the normothermal values. The results indicate that, after cryopreservation, the activity of basic ionotropic glutamatergic mechanisms in rat brain slices is restored.

Highlights

  • Исследовали влияние криосохранения переживающих срезов мозга крыс-самцов популяции линий Wistar с различной длительностью (4, 8, 10, 23 и 90 сут) на изменения электрической активности

  • The AMPA-dependent mechanisms and the activity of conductive LOT fibers were restored to normothermal values

  • The recovery of NMDA-dependent mechanisms was incomplete and averaged 34% compared with the normothermal values

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Summary

Introduction

Исследовали влияние криосохранения переживающих срезов мозга крыс-самцов популяции линий Wistar с различной длительностью (4, 8, 10, 23 и 90 сут) на изменения электрической активности. Результаты свидетельствуют, что после криоконсервации срезов мозга крыс активности базовых ионотропных глутаматергических механизмов восстанавливаются. Целью исследования явилось определение влияния криосохранения срезов мозга при температуре –20°C с различной длительностью (недели, месяцы) на восстановление электрической активности в виде ионотропных глутаматергических рецепторных АМПА- (α-амино-3-гидрокси-5-метилизоксазол-4-пропионовая кислота) и НМДА-зависимых (N-метилD-аспартат) механизмов.

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