on January 15, 2004
Published online before print January 15, 2004, doi: 10.1161/01.STR.0000113691.32026.06
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Submitted on September 23, 2003
From Clinica Neurologica, Dipartimento di Neuroscienze, Università di Tor Vergata, Rome (C.C., G.L., E.S., G.B., P.C.); Dipartimento di Neuroscienze, Psichiatria e Anestesiologia Università di Messina, Messina (F.P.); and IRCCS, Fondazione Santa Lucia, Rome (C.C., G.L., E.S., G.B., P.C.), Italy. * To whom correspondence should be addressed. E-mail: calabre{at}uniroma2.it.
Background and Purpose--The possible neuroprotective effect of endogenous Methods--Extracellular field potential recordings were obtained from rat corticostriatal slice preparations. In vitro ischemia was delivered by switching to an artificial cerebrospinal fluid solution in which glucose was omitted and oxygen was replaced with N2. Results--An irreversible loss of the field potentials recorded from striatal neurons was observed after 10 minutes of ischemia in control solution. Conversely, tiagabine and vigabatrin partially prevented the ischemia-induced field potential loss. Surprisingly, both GABAA and GABAB receptor antagonists blocked these effects. Accordingly, neuroprotection could be obtained only when GABAA and GABAB receptor agonists were coapplied, but not when a single agonist was given in isolation. Conclusions--Antiepileptic drugs targeting GABAergic transmission can exert neuroprotective effects against ischemia by increasing endogenous GABA levels and via the activation of both GABAA and GABAB receptors.
Accepted on October 29, 2003
Coactivation of GABAA and GABAB Receptor Results in Neuroprotection During In Vitro Ischemia
Cinzia Costa MD;
-aminobutyric acid (GABA) on the irreversible electrophysiological changes induced by in vitro ischemia on striatal neurons was investigated. In particular, the aim of the study was the characterization of the neuroprotective action of 2 antiepileptic drugs increasing GABAergic transmission such as tiagabine, a GABA transporter inhibitor, and vigabatrin, an irreversible inhibitor of GABA transaminase.
Key words: anticonvulsants • corpus striatum • electrophysiology • ischemia • receptors, GABA
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