Viminol stereoisomers and lamina V interneurons activity: preliminary results.
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Biomedical subjects
Publications and source records attributed to J M Besson.
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(1) A similar proportion of cells in the VPM (24.7%), MGmc (24%), CM (26.8%) and CL (28.6%) is activated by electrical stimulation of the cat's dental pulp. However the thresholds are very different, cells belonging to the first group of the VPM being often activated by stimulation below 0.1 V. (2) Pain seems to be the unique sensation evoked by pulpal stimulation. A first group of cells somatotopically localized in the VPM displays a primary type of response. These cells can also be activated from an oral or perioral field. This fact is reminiscent of referred pain phenomenon often encountered in the clinic. (3) A second group of cells scattered in the VPM and activated by pulpal stimulation displays a non-primary type of response. (4) Strong pinching of the skin activates some MGmc cells tonically. Response characteristics of the MGmc cells after pulpal stimulation are heterogeneojs. (5) CM cells activated by pulpal stimulation display long latency responses whose properties are similar to those obtained after somatic stimulation. However, the latency of responses are shorter after limb stimulation than after pulpal stimulation.
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The changes in firing rate of mesencephalic reticular units after intra-arterial injection into the limbs of a potent nociceptive agent, bradykinin, were studied in cats (unanesthetized, immobilized with flaxedil and hyperventilated). 30 per cent of the d35 studied cells were affected, 56 per cent were excited, 23 per cent inhibited and 5 per cent had mixed effects. Among the 75 excited cells, the activation of 16 of them seemed to related to the arousa- processes (group A); for 56 cells the increase seemed dire-tly dependent on the nociceptive stimulation itself (group B). The changes of firing rate were repruducible; their latencies and durations were of the same order as the latencies and duration of the nociceptive reactions and painful sensation s, which have been obtained in animals and men after bradykinin injections. The modifications induced by bradykinin administration were suppressed by Ketamin and Thiopental.
In the cat, electrical stimulation of the inferior central nucleus of the raphe induces a powerful analgesia. This stimulation totally suppresses the behavioural reactions elicited by strong pinches applied to the tail or to the four limbs; it strongly modifies the threshold of the jaw opening reflex obtained by tooth pulp stimulation and considerably affects the behavioural reactions elicited by continuing such stimulation. The results can be considered as evidence that the mechanism of analgesia from the inferior raphe nucleus is similar to that already described in the dorsal raphe nucleus. The analgesia obtained by stimulation of raphe nuclei seems to be sustained by serotoninergic mechanisms and relationships between these are discussed. In preliminary experiments, analgesia induced by CI stimulation has been suppressed by administration of naloxone, a specific opiate antagonist.
1. In order to study descending influences of the brain stem upon the transmission of nociceptive messages at the spinal level, the activities of lumbar lamina V dorsal horn cells, induced by intra-arterial injection of brandykinin into the limbs, were recorded in unanaesthetized cats in both decerebrate and temporary spinal states (reversible cold block applied at the thoracic level). 2. In the decerebrate state, the intra-arterial injection of bradykinin had little or no effect. 3. During the reversible spinalization, the effects of bradykinin were revealed or considerably enhanced. As described in a previous study, in the C1-transected cat, three types of effects were encountered: excitatory, inhibiitory and mixed (inhibitory-excitatory). 4. These modifications observed after spinalization were generally associated with a large increase of the spontaneous firing rate. 5. These results emphasize, in the decerebrate cat, the importance of descending inhibitory controls exerted by the brain stem upon the transmission of nonciceptive messages at the spinal cord level.
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