Implication of the neuropeptides methionine enkephalin, neurotensin and somatostatin of the caudal trigeminal nucleus in the experimental migraine

Primary peptidergic sensory neurons of the trigeminal ganglion that innervate the cerebral dura have been involved in the pathogenesis of headache, including the migraine. In addition, it is known that nociceptive central processes of the trigeminal neurons terminate in the caudal trigeminal nucleus. Moreover, the electrical stimulation of the trigeminal ganglion has been used as an experimental model in order to study the vascular headache, including the migraine. To study whether there is or not a decrease of the immunoreactivity for methionine enkephalin, somatostatin and neurotensin in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion. The trigeminal ganglia of Wistar albino rats of both sexes were electrically stimulated (frequency, 5 Hz; duration, 5 ms; intensity, 0,8 1.4 mA) and unilaterally for five minutes. Sections of the medulla oblongata containing the caudal trigeminal nucleus were obtained and processed for immunocytochemistry, in which specific antibodies were used against methionine enkephalin, neurotensin and somatostatin 28. In stimulated animals, we observed a decrease in the immunoreactivity for the three neuropeptides studied in the stimulated (ipsilateral) side, in comparison with the not stimulated side (contralateral). In control animals (not stimulated) the degree of the immunoreactivity was the same on both sides. 1. The decrease of the immunoreactivity in the ipsilateral side (stimulated) suggests that methionine enkephalin, neurotensin and somatostatin 28 are released in the caudal trigeminal nucleus after electrical stimulation of the trigeminal ganglion; 2. Methionine enkephalin and somatostatin 28 could act in the caudal trigeminal nucleus as inhibitors (with antinociceptive action) of another released exciters neuropeptides (with nociceptive action); and 3. These data will allow in the future to try new therapeutic strategies (e.g., the inhibition of the receptors implicated.), in order to alleviate certain headaches.