Effects of pentylenetetrazol on respiration and bulbar respiratory neurones and its interaction with K + ions and citrate

Abstract

Interactions between pentylenetetrazol (PTZ) and the metabolic modifier citrate and also with K + ions were examined. When superfused onto the bulb, at low concentrations PTZ increased tidal volume and slowed down respiration; the opposite was true for higher concentrations. Addition of citrate or K + ions did not essentially alter PTZ effects. Applied microelectrophoretically, PTZ influenced the spike density of three-quarters, and K + ions and citrate of two-thirds of all cells tested. When effective, PTZ excited the majority of the inspiratory (I) and inspiratory-expiratory neurones (IE), both excited and inhibited expiratory units (E) and inhibited the majority of the non-respiratory neurones. Citrate inhibited the majority of IE and E neurones; when combined with PTZ, effects of PTZ were abolished in most respiratory but not in unspecific cells. K + ions predominantly excited IE and E units. When combined with PTZ, inhibition exerted by PTZ on unspecific neurones was reversed into activation. This was not true for respiratory cells. Since activation of respiratory cells mediated by PTZ was neutralized by the metabolic inhibitor citrate and was mimicked by K + ions, PTZ may well act as modifier of the oxidative metabolism of glucose and of the passive efflux of K + ions.