Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The postictal immobility syndrome was examined in five experimental grand mal epilepsy models in an attempt to analyze separately the behavioral and underlying neurochemical aspects of the rigid-catatonic and flaccid-cataleptic states. Catalepsy and analgesia were found in varying degrees after maximal electroshock (MES), metrazol, picrotoxin, and Ro 5-3663 activated seizures. Signs of rigidity were noticed after the MES and picrotoxin seizures. Kindled seizures were followed by explosive behavior without signs of rigidity, catalepsy, and analgesia. Naloxone reduced the duration but not the score (intensity) of catalepsy and failed to selectively antagonize analgesia. The relative representation of the tonic stage of convulsions seemed to be the major determinant of the development of catatonic-cataleptic symptomatology. It is suggested that more than a single neurotransmitter system is involved in the postictal immobility syndrome and each epilepsy model has its unique neurochemical profile.
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PMID:Convulsant-specific architecture of the postictal behavior syndrome in the rat. 679 53

The post-ictal immobility syndrome is followed by a significant increase in the nociceptive thresholds in animals and men. In this interesting post-ictal behavioral response, endogenous opioid peptides-mediated mechanisms, as well as cholinergic-mediated antinociceptive processes, have been suggested. However, considering that many serotonergic descending pathways have been implicated in antinociceptive reactions, the aim of the present work is to investigate the involvement of 5-HT(2)-serotonergic receptor subfamily in the post-ictal antinociception. The analgesia was measured by the tail-flick test in seven or eight Wistar rats per group. Convulsions were followed by statistically significant increase in the tail-flick latencies (TFL), at least for 120 min of the post-ictal period. Male Wistar rats were submitted to stereotaxic surgery for introduction of a guide-cannula in the rhombencephalon, aiming either the nucleus raphe magnus (NRM) or the gigantocellularis complex. In independent groups of animals, these nuclei were neurochemically lesioned with a unilateral microinjection of ibotenic acid (1.0 microg/0.2 microL). The neuronal damage of either the NRM or nucleus reticularis gigantocellularis/paragigantocellularis complex decreased the post-ictal analgesia. Also, in other independent groups, central administration of ritanserin (5.0 microg/0.2 microL) or physiological saline into each of the reticular formation nuclei studied caused a statistically significant decrease in the TFL of seizing animals, as compared to controls, in all post-ictal periods studied. These results indicate that serotonin input-connected neurons of the pontine and medullarly reticular nuclei may be involved in the post-ictal analgesia.
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PMID:Involvement of 5-HT(2) serotonergic receptors of the nucleus raphe magnus and nucleus reticularis gigantocellularis/paragigantocellularis complex neural networks in the antinociceptive phenomenon that follows the post-ictal immobility syndrome. 1684 81