JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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Response of neurons in the thalamic nucleus submedius (Sm) to noxious stimulation and electrophysiological identification of on- and off-cells in rats.

Pain 2002 September
Previous studies have indicated that thalamic nucleus submedius (Sm) is involved in nociceptive modulation and plays an important role in an endogenous analgesic system (a feedback loop) consisting of spinal cord (Sc)-Sm-ventrolateral orbital cortex-periaqueductal gray-Sc. However, the function of different types of Sm neurons in nociceptive modulation is unclear. For this reason, on the basis of further studies of properties of the Sm neurons responding to noxious stimuli, the different effects of systemic morphine on the Sm neurons were examined and two classes of nociceptive modulatory neurons, named as off- and on-cells, in this region were identified in lightly anesthetized rats. The results showed that (1) most (84%, 132/157) of the Sm neurons responded to peripheral noxious stimuli. Of these neurons, 66% (n = 87) were inhibited, 34% (n = 45) excited. All neurons had very large and bilateral, even all body receptive fields. No neuron was found to be responsive to innocuous stimulation; (2) systemic morphine increased the firing rate of neurons inhibited by noxious stimulation, but decreased that of neurons excited by the same stimulation. Furthermore, the effects of morphine could be reversed by systemic naloxone; (3) 45 of Sm neurons examined could be divided into three different classes: off-cells that decreased the firing rate from tail heating just prior to occurrence of the tail-flick (TF) reflex (3140 +/- 167 ms, n = 27), on-cells that increased the firing rate just before the TF reflex (1720 +/- 240 ms, n = 8), and neutral-cells that did not respond to any stimuli and neuronal activities were not related to the TF reflex (n = 10). Findings of this study provided electrophysiological evidence for involvement of Sm neurons, as those in the rostral ventromedial medulla, in the opioid-receptor-mediated descending nociceptive modulation.

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