FAST INHIBITORY POSTSYNAPTIC POTENTIALS AND RESPONSES TO INHIBITORY AMINO-ACIDS OF SYMPATHETIC PREGANGLIONIC NEURONS IN THE ADULT CAT

Intracellular recordings were obtained from sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus (IML) in slices of upper thoracic spinal cord of the anesthetized cat. A total of 44 neurons was studied. Single shock stimulation of an area of white matter dorsolateral to the IML, close to the recording electrode ( < 0.5 mm), evoked fast IPSPs with rise time of 3.8 ms and 1/2 decay time of 14.7 ms (n = 12). In 17 other cells only fast EPSPs were recorded but, after suppression of the EPSPs by the excitatory aminoacid receptor antagonists CNOX (20 muM) and APV (100-250 muM), fast IPSPs were unmasked. The IPSP reversed polarity at -63 mV (-67 mV in the presence of CNQX and APV). The reversal potential shifted to a less negative value when the extracellular chloride concentration was reduced. The IPSP was reversibly abolished by the GABA(A) receptor antagonist bicuculline in 32% of the cells, by the glycine receptor antagonist strychnine in 47% of the cells and by the combination of the two in 21% of the cells. The IPSP was abolished by TTX (0.5 muM), had constant latency and showed no failures during high frequency stimulation. The IPSP presumably resulted from the excitation of inhibitory axons-and/or inhibitory neuron somata with monosynaptic connections to the SPN. Glycine and GABA (1-3 mM) produced hyperpolarization associated with decreased membrane resistance. Sixty-nine percent of cells responded to both agonists, 19% to glycine only and 12% to GABA only. The GABA(B) agonist baclofen (5 muM) had no effect. The glycine- and GABA-evoked hyperpolarizations reversed at -65 mV at the normal Cl concentration and at less negative values of membrane potential when the extracellular chloride concentration was reduced. These responses were reversibly abolished by strychnine and bicuculline, respectively. These data suggest that inhibitory axons releasing glycine and GABA make monosynaptic connections with the SPN. The majority of neurons receive either glycine or GABA input from the stimulated area although they express both glycine and GABA receptors.