Journal
NEUROREPORT
Volume 15, Issue 2, Pages 259-262Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200402090-00009
Keywords
aquaporin-4; brain edema; epilepsy; glial cells; water transport
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Funding
- NEI NIH HHS [EY13574] Funding Source: Medline
- NHLBI NIH HHS [HL59198, HL73856] Funding Source: Medline
- NIDDK NIH HHS [DK43840, DK35124] Funding Source: Medline
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Mice deficient in the glial water channel aquaporin-4 (AQP4) show decreased cerebral edema and improved neurological outcome following water intoxication or ischemic challenge. In this report, we tested seizure susceptibility in AQP4(-/-) mice. AQP4(-/-) mice and wild-type controls were given the chemoconvulsant pentylenetetrazol (PTZ) and monitored for seizure activity. At 40 mg/kg PTZ, all wild-type mice exhibited seizure activity, whereas six of seven AQP4(-/-) mice did not exhibit seizure activity. At 50 mg/kg PTZ, both groups exhibited seizure activity; however, the latency to generalized (tonic-clonic) seizures was significantly lower in wildtype than AQP4(-/-) mice. These results suggest that glial water channels may modulate brain excitability and the initiation and generalization of seizure activity.
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