PHENTOLAMINE I.V. CAUSES REDUCTION IN THE SIZE OF RECEPTIVE FIELDS OF LOW THRESHOLD SPINAL NEURONS

Intravenous (i.v.) phentolamine sometimes alleviates sensory abnormalities in patients with sympathetically-maintained pain. Alternation in activity of the central neurons may underlie the phenomenon. We hypothesized changes in the receptive fields (RF) of spinal neurons occur after i.v.phentolamine in physiological conditions as well as in the painful pathological conditions. To test this hypothesis in part, we investigated the effect of i.v. phentolamine on the size of RF of low threshold (LT) spinal neurons in intact rats under halothane anesthesia supplemented with ketamine. After confirmation of the phentolamine-induced reduction in the size of RF in LT neurons, we studied the degree of phentolamine-induced maximal reduction in the size of RF, reversibility of the change, and effect of yohimbine on the reduction in 12 rats. Those rats were divided into two groups. Following recovery of the RF size to their baseline levels on the first phentolamine (lmg/kg) i.v., the same dose of i.v. phentolamine was repeated 20 min after i.v. administration of either saline (saline group: n=5) or yohimbine (0.5mg/kg, yohimbine group: n=7). Results showed that i.v. phentolamine significantly reduced the size of RF at the first i.v. phentolamine, where the means of maximum reductions were 62.5% and 66.6% (mean % vs control) in the saline and yohimbine groups, respectively. The phentolamine-induced maximum reduction in RF size occurred 10 to 30 min after phentolamine administration, where the RF recovered to their baseline levels 10 to 30 min after the maximum reduction in most of the cases. The second phentolamine-induced reduction in RF size was 10.3% after yohimbine pretreatment, whereas it was 66.8% after saline treatment. We provided here the first evidence that i.v. phentolamine produced a yohimbine-reversible reduction in LT neuron RF size. Our results could indicate that sympathetic blockade with i.v. phentolamine results in inhibitory modulation of spinal neuronal activity.