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

Transient receptor potential canonical channel (TRPC) is a nonselective cation channel permeable to Ca(2+), which is expressed in many cell types, including neurons. However, the alterations in TRPC receptor expressions in response to status epilepticus (SE) have not been explored. Therefore, the present study was designated to elucidate the roles of TRPC3 and TRPC6 in neuronal death following SE. In non-SE animals, TRPC3 and TRPC6 immunoreactivity was abundantly detected in the dendrites of pyramidal cells and the cell bodies of dentate granule cells. Following SE, TRPC3 expression was significantly elevated in CA1-, CA3 pyramidal cells, and dentate granule cells, while TRPC6 expression was reduced in these regions. Pyrazole-3 (a TRPC3 inhibitor) effectively prevented up-regulation of neuronal TRPC3 expression induced by SE. Hyperforin (a TRPC6 activator) effectively prevented down-regulation of neuronal TRPC6 expression induced by SE. In addition, both Pyr3 and hyperforin effectively protected neuronal damages from SE. Therefore, the present study yields novel information regarding the role of TRPC3 and 6 in epileptogenic insults and suggests that TRPC 3 and 6 may be involved in neurodegeneration following SE.
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PMID:The reverse roles of transient receptor potential canonical channel-3 and -6 in neuronal death following pilocarpine-induced status epilepticus. 2292 17

Temporal lobe epilepsy (TLE) is the most common form of intractable epilepsy and is always accompanied with hippocampal sclerosis. The molecular mechanism of this pathological phenomenon has been extensively explored, yet remains unclear. Previous studies suggest that ion channels, especially calcium channels, might play important roles. Transient receptor potential canonical channel (TRPC) is a novel cation channel dominantly permeable to Ca(2+) and widely expressed in the human brain. We measured the expression of two subtypes of TRPC channels, TRPC3 and TRPC6, in temporal lobe epileptic foci excised from patients with intractable epilepsy and in hippocampus of mice with pilocarpine-induced status epilepticus (SE), an animal model of TLE. Cortical TRPC3 and TRPC6 protein expressions were significantly higher in TLE patients compared with those in controls. Expression of TRPC3 and TRPC6 protein also increased significantly in the CA3 region of the hippocampus of SE mice. Inhibition of TRPC3 by intracerebroventricular injection of anti-TRPC3 antibody prevented aberrant-sprouted mossy fiber collaterals in the CA3 region, while inhibition of TRPC6 by anti-TRPC6 antibody reduced dendritic arborization and spine density of CA3 pyramidal neurons. Our results indicate that TRPC3 and TRPC6 participate diversely in synaptic reorganization in the mossy fiber pathway in TLE.
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PMID:Upregulation and Diverse Roles of TRPC3 and TRPC6 in Synaptic Reorganization of the Mossy Fiber Pathway in Temporal Lobe Epilepsy. 2521 92