Parabrachial complex glutamate receptors modulate the cardiorespiratory response evoked from hypothalamic defense area

Abstract

To characterize the possible role of glutamate in the interaction between Hypothalamic Defense Area (HDA) and Parabrachial complex (PBc) nuclei, cardiorespiratory changes were analyzed in response to electrical stimulation of the HDA (1 ms pulses, 30–50 μA given at 100 Hz for 5 s) before and after the microinjection of the nonspecific glutamate receptor antagonist kynurenic acid (50 nl, 5 nmol), NMDA receptor antagonist MK-801 (50 nl, 50 nmol), non-NMDA receptor antagonist CNQX (50 nl, 50 nmol) or metabotropic glutamate receptor antagonist MCPG (50 nl, 5 nmol) within the PBc. HDA stimulation evoked an inspiratory facilitatory response, consisting of an increase in respiratory rate (pb0.001) due to a decrease in expiratory time (pb0.01). The respiratory response was accompanied by a pressor (pb0.001) and a tachycardic response (pb0.001). Kynurenic acid within the lateral parabrachial region (lPB) abolished the tachycardia (pb0.001) and decreased the magnitude of blood pressure response (pb0.001) to HDA stimulation. Similarly, the magnitude of the tachycardia and the pressor response was decreased after the microinjection of MK-801 (pb0.01 and pb0.001, respectively) and CNQX (pb0.05 in both cases) into the lPB. Kynurenic acid microinjection in this region produced an inhibition of the tachypnea (pb0.001) to HDA stimulation but the respiratory response persisted unchanged after MK-801 or CNQX microinjection into the lPB. Kynurenic acid within the medial parabrachial region (mPB) abolished the tachycardia (pb0.01) and decreased the magnitude of the pressor response (pb0.001) to HDA stimulation. MK-801 and CNQX microinjection in this region decreased the magnitude of the tachycardia (pb0.05, in both cases) and pressor response (pb0.05, in both cases). The respiratory response evoked by HDA stimulation was not changed after the microinjection of kynurenic acid, MK-801 or CNQX within the mPB.