Response properties of nociceptive neurons in the caudal ventrolateral medulla (CVLM) in monoarthritic and healthy control rats: modulation of responses by the paraventricular nucleus of the hypothalamus (PVN).
نویسندگان
چکیده
We characterized response properties of neurons in the caudal ventrolateral medulla (CVLM), a structure involved in pain modulation. Electrophysiological recordings were performed in pentobarbitone-anesthetized control and monoarthritic rats. Noxious pinch, heat, cold and colorectal distension were used for peripheral test stimulation. To study central modulation of CVLM neurons and role in mediating descending pain regulation from the hypothalamus, glutamate was administered into the paraventricular nucleus of the hypothalamus (PVN). CVLM neurons gave excitatory, inhibitory or no response to noxious test stimulation. Response patterns for part of the neurons varied with submodality of test stimulation; e.g., a cell with an excitatory response to heat could give no or an inhibitory response to cold. Arthritis induced cell type-dependent changes in the spontaneous activity, most prominent of which was increased discharge rate of CVLM cells with an excitatory response to noxious stimulation. Significant arthritis-induced changes were also observed in the magnitudes of the nociceptive responses, among which was an increase in the pinch-induced excitatory response. Glutamate in the PVN of arthritic but not control animals suppressed the excitatory responses of CVLM cells, independent of the submodality of test stimulation and without influence on their spontaneous discharge rates. The results indicate that CVLM neurons give differential responses to noxious stimulation. Arthritis induces changes in response properties of CVLM neurons and in their central regulation by the PVN. These findings are in line with the evidence indicating that the CVLM plays a role in processing of nociceptive signals under inflammatory as well as control conditions.
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عنوان ژورنال:
- Brain research bulletin
دوره 86 1-2 شماره
صفحات -
تاریخ انتشار 2011