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Rats chronically implanted with intrathecal catheters displayed a dose-dependent increase in the hot-plate and tail-flick response latencies following the injection of human beta-endorphin into the lumbar spinal subarachnoid space through the indwelling catheter. beta-Endorphin was approximately 25 times more potent than morphine on a molar basis. Matching morphine and beta-endorphin doses such that approximately equal submaximal submaximal effects occurred, it was observed that the antinociception produced by beta-endorphin lasted approximately three times longer than that produced by morphine. Experiments with intrathecal injection of beta-endorphin into the spinal subarachnoid space of cats fitted with intrathecal catheters also revealed a potent antinociceptive effect which was completely antagonized by naloxone. In the rats, naloxone administered systemically in doses of 10--100 microgram/kg produced a parallel shift in the dose-response curves of both nociceptive measures suggesting a competitive antagonism. Using a dose ratio analysis, an in vivo pA2 of 7.1 for naloxone was obtained. These data and those derived from previous work based on the pA2 suggest that the interaction of morphine, certain pentapeptides, and beta-endorphin is the same with regard to the spinal opiate receptor population mediating behaviorally defined analgesia.

Extracellular spikes were recorded from cell bodies of sympathetic preganglionic neurones in spinal segments T1-T3 of the cat. Each neurone was identified by its antidromic response to electrical stimulation of the sympathetic chain and was found in histological sections to lie within the intermediolateral nucleus. Physiological properties studied in detail included basal activity, spike configuration, and latency of antidromic activation. Also studied, in tests with paired stimuli, were the threshold interstimulus interval evoking two responses, as well as changes in amplitude and latency of the second spike which occurred at intervals near this threshold. Approximately 60% of the units studied were spontaneously active, the rest were silent. Spontaneous activity was characterized by a slow (mean = 3.1 +/- 2.6 (SD) spikes/s), irregular pattern of discharge. With approximately one-third of the cases there was a periodic pattern of discharge in phase with oscillations in blood pressure. This correlation of phasic activity suggests that many of the units studied were involved specifically in cardiovascular function. Silent and spontaneously active units could not be differentiated on the basis of latency of antidromic activation or threshold interstimulus interval; mean latency for the two groups was 7.2 +/- 4.9 ms, mean threshold interval was 6.4 +/- 4.7 ms. Thus, with the exception of basal activity, the physiological properties studied failed to indicate more than a single population of neurones. These results therefore suggest that the sympathetic preganglionic neurones in the intermediolateral nucleus subserving varied autonomic functions share overlapping physiological properties, and that functional differentiation of these neurones may be based on differences in synaptic inputs.