POTENTIATING EFFECTS OF PROSTAGLANDIN E₂ ON BRADYKININ AND CAPSAICIN RESPONSES IN MEDIAL THALAMIC NOCICEPTIVE NEURONS

Abstract

Potentiating effects of prostaglandin E₂ (PGE₂) on bradykinin and capsaicin responses were studied in 34 gallamine triethiodide immobilized cats. Single neurons were recorded from the medial thalamus by using stainless steel microelectrodes. The animals were given agents into the femoral artery through a retrogradely inserted cannula. Of the 22 neurons responding to bradykinin, 13 were potentiated by the injection of PGE₂, and the remaining 9 neurons were ineffective. Nine of the 17 neurons responding to capsaicin were also potentiated by PGE₂. PGE₂ significantly shortened the mean latency of bradykinin to fire the neuronal activity without changing the duration, but with the injection of capsaicin, there was no change in latency and duration in the presence of PGE₂. Aspirin suppressed the increased activity of the medial thalamic neurons produced by bradykinin, and this suppression was antagonized by arterial infusion of PGE₂. However, the activity of medial thalamic neurons with capsaicin was scarecely affected by aspirin. These results suggest that the bradykinin-induced activity of medial thalamic neurons may be mediated by PGE₂ and that the mechanism of activation of nociceptive neurons produced by capsaicin is different from that of bradykinin.