Changes in GABA(B) receptor subunit expression have been recently reported in the neocortexof epileptic WAG/Rij rats that are genetically prone to experience absence seizures.These alterations may lead to hyperexcitability by downregulating the function of presynapticGABA(B) receptors in neocortical networks as suggested by a reduction in paired-pulsedepression. Here, we tested further this hypothesis by analyzing the effects induced by theGABA(B) receptor agonist baclofen (0.1-10 μM) on the inhibitory events recorded in vitro fromneocortical slices obtained from epileptic (>180 day-old) WAG/Rij and age-matched, nonepilepticcontrol (NEC) rats. We found that higher doses of baclofen were required todepress pharmacologically isolated, stimulus-induced IPSPs generated by WAG/Rij neuronsas compared to NEC. We also obtained similar evidence by comparing the effects ofbaclofen on the rate of occurrence of synchronous GABAergic events recorded by WAG/Rijand NEC neocortical slices treated with 4-aminopyridine+glutamatergic receptor antagonists.In conclusion, these data highlight a decreased function of presynaptic GABA(B) receptorsin the WAG/Rij rat neocortex. We propose that this alteration may contribute toneocortical hyperexcitability and thus to absence seizures.

Diminished presynaptic GABA(B) receptor function in the neocortex of a genetic model of absence epilepsy / Y., Inaba; M., D'Antuono; G., Bertazzoni; Biagini, Giuseppe; M., Avoli. - In: NEUROSIGNALS. - ISSN 1424-862X. - STAMPA. - 17:2(2009), pp. 121-131. [10.1159/000197864]

Diminished presynaptic GABA(B) receptor function in the neocortex of a genetic model of absence epilepsy

BIAGINI, Giuseppe;
2009

Abstract

Changes in GABA(B) receptor subunit expression have been recently reported in the neocortexof epileptic WAG/Rij rats that are genetically prone to experience absence seizures.These alterations may lead to hyperexcitability by downregulating the function of presynapticGABA(B) receptors in neocortical networks as suggested by a reduction in paired-pulsedepression. Here, we tested further this hypothesis by analyzing the effects induced by theGABA(B) receptor agonist baclofen (0.1-10 μM) on the inhibitory events recorded in vitro fromneocortical slices obtained from epileptic (>180 day-old) WAG/Rij and age-matched, nonepilepticcontrol (NEC) rats. We found that higher doses of baclofen were required todepress pharmacologically isolated, stimulus-induced IPSPs generated by WAG/Rij neuronsas compared to NEC. We also obtained similar evidence by comparing the effects ofbaclofen on the rate of occurrence of synchronous GABAergic events recorded by WAG/Rijand NEC neocortical slices treated with 4-aminopyridine+glutamatergic receptor antagonists.In conclusion, these data highlight a decreased function of presynaptic GABA(B) receptorsin the WAG/Rij rat neocortex. We propose that this alteration may contribute toneocortical hyperexcitability and thus to absence seizures.
2009
17
2
121
131
Diminished presynaptic GABA(B) receptor function in the neocortex of a genetic model of absence epilepsy / Y., Inaba; M., D'Antuono; G., Bertazzoni; Biagini, Giuseppe; M., Avoli. - In: NEUROSIGNALS. - ISSN 1424-862X. - STAMPA. - 17:2(2009), pp. 121-131. [10.1159/000197864]
Y., Inaba; M., D'Antuono; G., Bertazzoni; Biagini, Giuseppe; M., Avoli
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11380/421112
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