Effect of glutamate stimulation of the cuneiform nucleus on cardiovascular regulation in anesthetized rats: Role of the pontine Kolliker–Fuse nucleus

Abstract

Cuneiform nucleus (CnF) is a reticular nucleus of the midbrain involved in cardiovascular function and stress. There is no report on the cardiovascular effects of the glutamatergic system in the CnF. In the present study, we investigated the cardiovascular effects of glutamate and its NMDA and AMPA/kainate receptors in the CnF. In addition, the possible mediation of Kolliker–Fuse (KF) nucleus in the cardiovascular effects of the CnF was explored. l-glutamate, AP5 (an NMDA receptor antagonist), and CNQX (an AMPA/kainate receptor antagonist) (50–100nl) were microinjected into the CnF of anesthetized rats. Also, the KF was blocked by cobalt chloride (CoCl2) then l-glutamate was microinjected into the CnF. The maximum changes of blood pressure and heart rate were compared with the pre-injection (paired t-test) and control (independent t-test) values. Microinjection of glutamate (25nmol/100nl) into the CnF produced either a short pressor and bradycardic or a long pressor and tachycardic responses. Microinjection of AP5 or CNQX alone did not affect the basal arterial pressure and heart rate. However, co-injection of glutamate with AP5 strongly attenuated the short and moderately attenuated the long cardiovascular responses elicited by glutamate. Co-injection of glutamate with CNQX did not attenuate the short and weakly attenuated the long cardiovascular responses elicited by glutamate. These data suggest that the responses are mediated mainly through NMDA receptors. Blockade of the KF nucleus strongly attenuated the short response and weakly attenuated the long response to glutamate microinjection, suggesting that the cardiovascular effects of glutamate in the CnF, especially the short responses, were mediated by the KF nucleus.