Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of the ventral hippocampal dentate granule neurons in the mu opioid receptor agonist-induced motor seizures and wet dog shakes was examined in this study. [NMe-Phe3-D-Pro4]morphiceptin (9.4 nmol) was injected into the left ventral hippocampus of rats 14 days after unilateral or bilateral colchicine (5 nmol/site) lesions of ventral hippocampal dentate granule cells and the subsequent behavioral and neuropathological responses were observed. [NMe-Phe3-D-Pro4]morphiceptin injected into control animals produced convulsions and numerous wet dog shakes that lasted for less than 1 h. [NMe-Phe-D-Pro4]morphiceptin-induced wet dog shakes were significantly reduced in unilateral colchicine-pretreated rats, and completely inhibited in bilateral colchicine-pretreated animals. In contrast, generalized motor seizures evoked by [NMe-Phe3-D-Pro4]morphiceptin were potentiated and prolonged in colchicine-pretreated animals as status epilepticus (sustained clonus of forepaws and head for more than 1 h) was observed in both unilateral and bilateral colchicine-pretreated animals but not in control rats. No morphological damage of granule or pyramidal cells was found in the ventral hippocampus of control animals following [NMe-Phe3-D-Pro4]morphiceptin injection. Colchicine treatment by itself produced a selective lesion of dentate granule cells. In colchicine-pretreated animals, [NMe-Phe3-D-Pro4]morphiceptin induced widespread seizure-related damage of CA3/CA1 pyramidal cells. These results suggest that dentate granule cells in the ventral hippocampus are essential for the elaboration of wet dog shakes. However, these neurons may play an inhibitory role in the spread of seizure activity within the hippocampus or limbic structures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventral hippocampal dentate granule cell lesions enhance motor seizures but reduce wet dog shakes induced by mu opioid receptor agonist. 216 33

Neurochemical studies document involvement of benzodiazepine (BDZ) and mu opioid receptors in seizure development and their possible age-related role during epileptogenesis. To study developmental changes of this role LiCl/pilocarpine status epilepticus (SE) was induced in P12, P25 and/or adult rats. This SE leads to epilepsy in all adult and subpopulation of immature rats. Using in vitro autoradiography, benzodiazepine (BDZ) and mu opioid receptor binding was evaluated 1 week (early phase of epileptogenesis) and 3 months (chronic phase) after SE in 27 brain structures involved in seizure generation and spread (amygdala, hippocampus, basal ganglia and thalamic nuclei). The pattern of receptor binding changes was related to the age at SE, interval after SE and to brain structures. Enhanced BDZ binding was found 1 week after SE in many cortical areas in P12 and also in the amygdala complex and dentate gyrus in both P12 and P25. No changes of BDZ binding occurred in adults at that time, but 3 months after SE a decrease of binding appeared in all evaluated areas in both adult and P25 but not P12 rats. This decrease did not reflect neuronal loss. mu opioid receptors were less significantly affected but clear tendency to decrease binding occurred in adult rats in various cortical, amygdala and thalamic regions early after SE. Changes were less expressed in immature rats. Our data support the hypothesis that age-related changes of receptor properties may participate in different functional consequences of SE including epileptogenesis (more common in older age groups) and behavioral changes.
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PMID:Effects of LiCl/pilocarpine-induced status epilepticus on rat brain mu and benzodiazepine receptor binding: regional and ontogenetic studies. 1791 68