NBQX or Topiramate Treatment after Perinatal Hypoxia‐induced Seizures Prevents Later Increases in Seizure‐induced Neuronal Injury

Epilepsia - Tập 45 Số 6 - Trang 569-575 - 2004
Sookyong Koh1, Felicia D. Tibayan1, Joelle N. Simpson1, Frances E. Jensen1,2
1Department of Neurology
2Program in Neuroscience, Children's Hospital, Harvard Medical School, Boston, Massachusetts, U.S.A.

Tóm tắt

Summary:  Purpose: To evaluate the efficacy of NBQX (2,3‐dihydroxy‐6‐nitro‐7‐sulfamoylbenzo(f) quinoxaline‐2,3‐dione) and topiramate (TPM) given after hypoxia‐induced seizures in preventing the delayed effect of hypoxia on subsequent susceptibility to seizures and neuronal injury. Methods: We used “two‐hit” rodent seizure model to study the long‐term effect of perinatal hypoxia on later kainate (KA) seizure‐induced neuronal damage and investigated the therapeutic efficacy of a postseizure treatment protocol in reversing the conditioning effect of early‐life seizures. Results: Hypoxia at P10 induces seizures without cell death but causes an increase in susceptibility to second seizures induced by KA as early as 96 h after hypoxia, and this lowered seizure threshold persists to adulthood. Furthermore, perinatal hypoxia increases KA‐induced neuronal injury at postnatal day (P)21 and 28/30. Repeated doses of NBQX (20 mg/kg) or TPM (30 mg/kg) given for 48 h after hypoxia‐induced seizures prevent the increase in susceptibility to KA seizure‐induced hippocampal neuronal injury at P28/30. Conclusions: Our results suggest that α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionate (AMPA) receptor blockade after hypoxia prevents the priming effect of perinatal hypoxia‐induced seizures and that this protection occurs independent of its anticonvulsant action.

Từ khóa


Tài liệu tham khảo

Volpe JJ, 2000, Neurology of the newborn

10.1111/j.1528-1157.1984.tb04168.x

Legido A, 1991, Neurologic outcome after electroencephalographically proven neonatal seizures, Pediatrics, 88, 583

10.1111/j.1528-1157.1991.tb05614.x

10.1056/NEJM197611042951901

10.1056/NEJM198702263160901

10.1097/00004691-199703000-00003

10.1001/archneur.1964.00460150003001

10.1016/0887-8994(95)00022-8

10.1212/WNL.43.6.1083

10.1212/WNL.26.10.975

10.1002/ana.410130514

10.1111/j.1528-1157.1992.tb01746.x

10.1002/ana.410440602

10.1002/1531-8249(200003)47:3<336::AID-ANA9>3.0.CO;2-W

10.1152/jn.1998.79.1.73

10.1038/11330

10.1002/1531-8249(200006)47:6<729::AID-ANA5>3.0.CO;2-C

10.1016/0165-3806(84)90085-3

10.1523/JNEUROSCI.18-11-04285.1998

10.1523/JNEUROSCI.18-20-08382.1998

10.1212/WNL.53.5.915

10.1212/WNL.53.8.1754

10.1002/ana.1122

10.1002/ana.410290610

10.1002/hipo.450040307

10.1073/pnas.88.10.4157

10.1016/0306-4522(90)90117-M

10.1073/pnas.85.23.9346

10.1038/338500a0

10.1146/annurev.ne.14.030191.002115

10.1523/JNEUROSCI.21-20-08154.2001

10.1523/JNEUROSCI.22-08-03005.2002

10.1111/j.1528-1157.1995.tb00954.x

10.1126/science.283.5400.401

10.1177/41.1.7678025

10.1111/j.1471-4159.1991.tb02119.x

10.1038/jcbfm.1993.116

Buchan A, 1991, The N‐methyl‐d‐aspartate antagonist, MK‐801, fails to protect against neuronal damage caused by transient, severe forebrain ischemia in adult rats, J Neurosci, 11, 1049, 10.1523/JNEUROSCI.11-04-01049.1991

10.1007/BF00227969

Ying HS, 1997, Sublethal oxygen‐glucose deprivation alters hippocampal neuronal AMPA receptor expression and vulnerability to kainate‐induced death, J Neurosci, 17, 9536, 10.1523/JNEUROSCI.17-24-09536.1997

10.1523/JNEUROSCI.23-06-02112.2003

10.1523/JNEUROSCI.18-20-08356.1998

10.1016/0306-4522(84)90289-6

10.1016/S0306-4522(98)00609-5

10.1016/S0165-3806(96)00149-6

10.1016/S0006-8993(97)00819-6

10.1016/S0165-3806(00)00135-8

10.1016/0165-3806(92)90184-X

10.1002/ana.410340604

Wieser HG, Surgically remediable temporal lobe syndromes, 49

10.1056/NEJM199806113382402