ADENOSINE SUPPRESSES EXCITATORY GLUTAMATERGIC INPUTS TO RAT HYPOGLOSSAL MOTONEURONS IN-VITRO

Short-latency excitatory postsynaptic potentials (EPSPs), evoked by electrical stimulation lateral to the hypoglossal motor nucleus, were recorded from rat hypoglossal motoneurons (HMs) in brainstem slices. EPSPs were markedly suppressed or abolished by kynurenic acid (1 mM), showing that they were glutamatergic. The adenosine receptor agonist 2-chloro-N-6-cyclopentyladenosine (CCPA, 100 nM) reduced EPSP amplitude to 42% of control, while the agonist 2-chloroadenosine (2-CA, 0.5-50 mu M) caused a dose-dependent reduction of the EPSP. The adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 0.1-1 mu M) increased the EPSP amplitude to 124% of control, and blocked EPSP reduction by CCPA or 2-CA. CCPA, 2-CA and DPCPX did not significantly alter HM input resistance or membrane potential. These data indicate that excitatory glutamatergic inputs to rat HMs are modulated by adenosine A, receptors, most probably at a presynaptic site. This modulation may be especially significant in hypoxic responses of HMs.