Dados do Trabalho

Título

Neuroplasticity involved in the reversal of neuropathic pain induced by motor cortex stimulation

Resumo

The motor cortex stimulation (MCS) have been widely used in clinical medicine as a tool for pain control, used in patients with different pain syndromes, mainly of a chronic nature, which do not respond satisfactorily to any type of conventional analgesia. Preliminary studies, obtained by our group, have demonstrated that MCS reverts the neuropathic pain in rats, inhibiting neurons of the ventral posterior lateral and medial thalamus nuclei and dorsal horn spinal cord, and activating neurons of the anterior cingulate cortex and central and basolateral nuclei of the amygdala. Despite this evidence, the mechanisms involved in that nociceptive modulation are not yet understood. The objective of this research project was to evaluate the neuroplasticity induced by MCS in a persistent peripheral neuropathic pain model in rats, investigating the participation of glial cells and of cannabinoids involved with the activation and inhibition of the nociceptive response, respectively. The methodology involved induction of neuropathic pain by chronic constriction injury of the sciatic nerve, implantation of transdural electrodes over the primary motor cortex and evaluation of the nociceptive response in tests of mechanical hyperalgesia and allodynia. Immunoblotting and immunohistochemical assays were performed to detected glial fibrillary acidic protein (GFAP, an astrocyte marker), OX-42 (a microglial marker) and cannabinoid receptor type 1 (CB1) in spinal cord obtained from sham rats or animals with neuropathic pain, stimulated or not. In animals with MCS reversed neuropathic pain, a decrease of microglial activation was seen, as well as increased CB1 immunolabel in the spinal cord, compared to unstimulated animals with neuropathic pain. The data obtained suggest that MCS inhibits spinal microglia, which contribute to the induction of nociceptive processes. Also, the cortical stimulation induces the activation of CB1, which is important for the modulation of pain sensitivity. These results will contribute to a better understanding of the role of the motor cortex in the modulation of neuropathic pain and to an improvement of therapeutic strategies to treat persistent pain.

Palavras Chave

Neuropathic pain; motor cortex stimulation; glial cells; cannabinoids