IFIBYNE   05513
INSTITUTO DE FISIOLOGIA, BIOLOGIA MOLECULAR Y NEUROCIENCIAS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Role of 5-HT1A and 5HT2A in the modulation of GABA release from the thalamic reticular nucleus
Autor/es:
GOITIA B; GARCIA-RILL E; BISAGNO V; URBANO FJ
Lugar:
HUERTA GRANDE, CORDOBA ARGENTINA
Reunión:
Congreso; XXVIII CONGRESO ANUAL DE LA SOCIEDAD ARGENTINA DE INVESTIGACIÓN EN NEUROCIENCIAS. REUNIÓN SATELITE/NEUROBIOLOGÍA DEL COMPORTAMIENTO: NEUROETOLOGÍA y NEUROBIOLOGÍA DE LA MEMORIA EN EL CONO SUR; 2013
Institución organizadora:
SOCIEDAD ARGENTINA DE INVESTIGACIÓN EN NEUROCIENCIAS.
Resumen:
ORAL PRESENTATION----PhD. STUDENTS------------------------------------------------- Methylphenidate (MPH), a drug widely used to treat children diagnosed with ADHD, and cocaine (Coc) inhibit the re-uptake of dopamine and norepinephrine. Cocaine, unlike MPH, also inhibits the re-uptake of serotonin (5-HT). Previously, we observed that the frequency of spontaneous GABA release from thalamic reticular nucleus (Ret) neurons is increased in slices from mice treated with a Coc binge, but not in those from animals treated with MPH, suggesting that the effect of Coc is mediated by changes in serotonergic transmission. We recorded miniature inhibitory post-synaptic potentials (mIPSPs) from ventrobasal nucleus neurons in the presence of 5-HT and 5-HT1A or 5HT2A/2C agonists ((±)-8-OH-DPAT, (±)-DOI hydrochloride; both 10 microM) and antagonists (ketanserin, NAN-190 hydrobromide; both 25 microM). Our results show that the effect of bath-applied 5-HT (100 microM) on mIPSP frequency resembles that of Coc, and that even though both types of agonists lead to an increase in frequency, the effect of the 5-HT1A agonist was stronger. Surprisingly, the 5HT2A antagonist also had the same effect, which could be explained by a biphasic behavior of the 5HT2A receptors in Ret neurons GABAergic terminals.Our findings suggest that Coc-induced effects on thalamic serotonergic transmission might be mediated by presynaptic 5-HT receptors (on the terminals of Ret neurons) and that these effects could be responsible for the thalamocortical dysrhythmia observed in humans and animal models of Coc use.