Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Identification of the compounds preventing the biochemical changes underlying the epileptogenesis process is of great importance. We have previously shown that myo-inositol (MI) administration reduces kainic acid (KA) induced seizure scores. MI treatment effects on biochemical changes triggered by KA induced status epilepticus (SE) were investigated in the present study. After SE one group of rats was treated with saline, whereas the second group with MI. Control groups received either saline or MI administration. Changes in the amounts of following proteins were studied in the hippocampus and neocortex of rats: GLUR1 subunit of glutamate receptors, calcium/calmodulin-dependent protein kinase II (CaMKII), and heat shock protein 90. No changes were found 28-30h after experiments. However on 28th day of experiment the amounts of GLUR1 and CaMKII were strongly reduced in the hippocampus of KA treated animals but MI significantly halted this reduction. Obtained results indicate anti-epileptogenic features of MI on biochemical level.
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PMID:Myo-inositol treatment prevents biochemical changes triggered by kainate-induced status epilepticus. 1991 43

miR-124, a brain-specific microRNA, was originally considered as a key regulator in neuronal differentiation and the development of the nervous system. Here we showed that miR-124 expression was suppressed in patients with epilepsy and rats after drug induced-seizures. Intrahippocampal administration of a miR-124 duplex led to alleviated seizure severity and prolonged onset latency in two rat models (pentylenetetrazole- and pilocarpine-induced seizures), while miR-124 inhibitor led to shortened onset latency in pilocarpine-induced seizure rat models. Moreover, the result of local field potentials (LFPs) records further demonstrated miR-124 may have anti-epilepsy function. Inhibition of neuronal firing by miR-124 was associated with the suppression of mEPSC, AMPAR- and NMDAR-mediated currents, which were accompanied by decreased surface expression of NMDAR. In addition, miR-124 injection resulted in decreased activity and expression of cAMP-response element-binding protein1 (CREB1). a key regulator in epileptogenesis. A dual-luciferase reporter assay was used to confirm that miR-124 targeted directly the 3'UTR of CREB1 gene and repressed the CREB1 expression in HEK293T cells. Immunoprecipitation studies confirmed that the CREB1 antibody effectively precipitated CREB1 and NMDAR1 but not GLUR1 from rat brain hippocampus. These results revealed a previously unknown function of miR-124 in neuronal excitability and provided a new insight into molecular mechanisms underlying epilepsy.
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PMID:The microRNA miR-124 suppresses seizure activity and regulates CREB1 activity. 2699 91