Acta Physiologica 2010; Volume 200, Supplement 681
Abstracts of the 61st National Congress of the Italian Physiological Society
MODULATION OF GABAA-MEDIATED CURRENTS BY GABAB RECEPTORS IN TEMPORAL PYRAMIDAL NEURONS IN CONTROL OR EPILEPTIC TISSUE
Abstract number: O11
FUCILE1,2 S, MARTINELLO2,3 K, MORACE2,3 R, ESPOSITO2,4 V, DI GENNARO2 G, LIMATOLA1,2 C
1Dipartimento di Fisiologia e Farmacologia, Sapienza Universit di Roma
2IRCCS NEUROMED, Pozzilli (IS)
3Dottorato di Ricerca in Neurofisiologia, Sapienza Universit di Roma
4Dipartimento di Neurochirurgia, Sapienza Universit di Roma
The neurotransmitter GABA acts on both ionotropic GABAA and metabotropic GABAB receptors. The repetitive GABA application on pyramidal neurons in temporal cortex slices makes evident an activity-dependent decrease of the GABAA-mediated current amplitudes (IGABA rundown), significantly higher in mesial temporal lobe epilepsy than in control conditions. Repetitive applications of muscimol, a selective agonist of GABAA receptors, induce a larger rundown than GABA, suggesting that GABAB activation exerts a modulatory action on IGABA. Thus, our objective was the description of the role of GABAB receptors in the GABAA receptor modulation, in different epileptic or control tissues.
In control rat temporal neurons, the co-application of muscimol and baclofen (selective GABAB agonist) produced a smaller IGABA rundown than using only muscimol, while co-application of GABA and CGP55845 (selective GABAB antagonist) significantly increased GABAA receptor instability. By contrast, in epileptic tissue this modulation was absent. The activation of GABAB receptors was also able to modify the miniature inhibitory GABAergic synaptic currents recorded from human and rat neurons, reducing in the epileptic tissue the amount of electrical charge flowing through GABAA receptors in a single synaptic event. We conclude that the activation of GABAB receptors affects the GABAA receptors expressed on the same neuron, and this modulation determines in epileptic tissue a lower level of inhibition.
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Acta Physiologica 2010; Volume 200, Supplement 681 :O11