NMDA AND GABA(A) RECEPTORS IN THE RAT KOLLIKER-FUSE AREA CONTROL CARDIORESPIRATORY RESPONSES EVOKED BY TRIGEMINAL ETHMOIDAL NERVE-STIMULATION

1. Electrical stimulation (10 s) of the ethmoidal nerve (EN5) evokes t he nasotrigeminal reflex responses, including apnoea, bradycardia and rise in arterial blood pressure. In the present study, we examined the involvement of N-methyl-D-aspartate (NMDA), AMPA/kainate, (gamma-amin obutyric acid(A) (GBBA(A)) and glycine receptors in the Kolliker-Fuse (KP) nucleus in the mediation of the nasotrigeminal reflex responses. 2. Unilateral injections (n = 6) of 50-100 nl of the NMDA receptor ant agonist AP5 into the KF area led to a significant blockade of the EN5- evoked respiratory depression and bradycardia. Injections placed into the midlevel of the KP area were most effective (80-90% blockade). The rise in arterial blood pressure remained unaffected. 3. Unilateral in jections (n = 6) of the AMPA/kainate receptor antagonist CNQX into the KP area failed to block EN5-evoked autonomic responses significantly. 4. Unilateral injections (n = 5) of the GABA(A) receptor antagonist bi cuculline enhanced the EN5-evoked respiratory depression and bradycard ia. The effect persisted for up to 30 s after stimulation. Bicuculline injections into the midlevel of the KF area were most effective. The increase in arterial blood pressure remained unaffected. 5. Unilateral injections (n = 5) of the glycine receptor antagonist strychnine into the KF area did not produce any significant effects on EN5-evoked aut onomic responses. 6. Our results suggest that the KF area represents a mandatory relay for the nasotrigeminally induced apnoea and bradycard ia which are predominantly mediated by NMDA receptors in the KF. Furth ermore, it appears that IIB neurons are under a potent GABAergic inhib itory control. The EN5-evoked rise in arterial blood pressure was not altered by any of the drugs and, therefore, appears not to be mediated via the KF.