| 19176980 |
Inaba Y, D'Antuono M, Bertazzoni G, Biagini G, Avoli M: Diminished presynaptic GABA (B) receptor function in the neocortex of a genetic model of absence epilepsy. Neurosignals. 2009;17(2):121-31. Epub 2009 Jan 29.
Changes in GABA (B) receptor subunit expression have been recently reported in the neocortex of epileptic WAG/Rij rats that are genetically prone to experience absence seizures. These alterations may lead to hyperexcitability by downregulating the function of presynaptic GABA (B) receptors in neocortical networks as suggested by a reduction in paired-pulse depression. Here, we tested further this hypothesis by analyzing the effects induced by the GABA (B) receptor agonist baclofen (0.1-10 microM) on the inhibitory events recorded in vitro from neocortical slices obtained from epileptic (> 180 day-old) WAG/Rij and age-matched, non-epileptic control (NEC) rats. We found that higher doses of baclofen were required to depress pharmacologically isolated, stimulus-induced IPSPs generated by WAG/Rij neurons as compared to NEC. We also obtained similar evidence by comparing the effects of baclofen on the rate of occurrence of synchronous GABAergic events recorded by WAG/Rij and NEC neocortical slices treated with 4-aminopyridine + glutamatergic receptor antagonists. In conclusion, these data highlight a decreased function of presynaptic GABA (B) receptors in the WAG/Rij rat neocortex. We propose that this alteration may contribute to neocortical hyperexcitability and thus to absence seizures. |
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