APV-sensitive dorsal root afferent transmission to neonate rat sympathetic preganglionic neurons in vitro.

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices from neonate (12- to 22-day-old) rats. 2. Electrical stimulation of dorsal roots or dorsal root entry zone elicited in SPNs an excitatory postsynaptic potential (EPSP) or multiple EPSPs of varying latencies. The EPSP could be graded by varying the stimulus intensity and, on reaching the threshold, discharged an action potential. 3. The dorsal root-evoked EPSPs had a mean synaptic latency of 2.6 ms (range: 1.2-11 ms), suggesting a polysynaptic pathway. The EPSPs were characteristically slow in onset with a mean rise time and half-decay time of 8.3 and 23 ms, respectively. 4. At the resting membrane potential of -50 to -60 mV, the amplitude of EPSPs recorded in normal (1.3 mM Mg2+) Krebs solution was reduced by membrane hyperpolarization or depolarization. In Mg2(+)-free solution, EPSPs were potentiated and reached threshold for spike discharge. 5. The EPSPs were suppressed by the nonselective glutamate receptor antagonist kynurenic acid (0.1-0.5 mM) and by the N-methyl-D-aspartate (NMDA) receptor antagonists D-2-amino-5-phosphonovaleric acid (APV; 1-10 microM) and ketamine (5-10 microM), but not by the quisqualate (QA)/kainate (KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1-10 microM). The latter depressed the EPSPs elicited by stimulation of lateral funiculus in the same SPNs. 6. NMDA applied by pressure elicited a depolarization in the SPNs. In normal Krebs solution the response was voltage dependent with the peak amplitude occurring around -60 mV; conditioning depolarization or hyperpolarization diminished the response.(ABSTRACT TRUNCATED AT 250 WORDS)