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Real-time measurements of synaptic autoinhibition produced by serotonin release in cultured leech neurons

dc.creatorCercós, Montserrat G.
dc.creatorDe-Miguel, Francisco F.
dc.creatorTrueta, Citlali
dc.date.accessioned2017-06-30T04:02:03Z
dc.date.available2017-06-30T04:02:03Z
dc.date.issued2009es_ES
dc.identifier2463es_ES
dc.identifier.issn0022-3077es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/7104
dc.identifier.urihttps://doi.org/10.1152/jn.00107.2009es_ES
dc.language.isoenges_ES
dc.publisherBethesda Md : American Physiological Societyes_ES
dc.relation102 (2) 1075-1085 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleReal-time measurements of synaptic autoinhibition produced by serotonin release in cultured leech neuronses_ES
dc.typearticlees_ES
dc.contributor.affiliationDepartamento de Neurofisiología, Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz, Calz. México-Xochimilco 101, Col. San Lorenzo Huipulco, Deleg. Tlalpan, C.P. 14370 México, D.F. Méxicoes_ES
dc.contributor.emailctrueta@imp.edu.mxes_ES
dc.relation.jnabreviadoJ NEUROPHYSIOLes_ES
dc.relation.journalJournal of Neurophysiologyes_ES
dc.identifier.placeEstados Unidoses_ES
dc.date.published2009es_ES
dc.identifier.organizacionInstituto Nacional de Psiquiatría Ramón de la Fuente Muñizes_ES
dc.identifier.eissn1522-1598es_ES
dc.identifier.doi10.1152/jn.00107.2009es_ES
dc.description.monthAgoes_ES
dc.description.abstractotrodiomaWe studied autoinhibition produced immediately after synaptic serotonin (5-HT) release in identified leech Retzius neurons, cultured singly or forming synapses onto pressure-sensitive neurons. Cultured Retzius neurons are isopotential, thus allowing accurate recordings of synaptic events using intracellular microelectrodes. The effects of autoinhibition on distant neuropilar presynaptic endings were predicted from model simulations. Following action potentials (APs), cultured neurons produced a slow hyperpolarization with a rise time of 85.4 ± 5.2 ms and a half-decay time of 252 ± 17.4 ms. These inhibitory postpotentials were reproduced by the iontophoretic application of 5-HT and became depolarizing after inverting the transmembranal chloride gradient by using microelectrodes filled with potassium chloride. The inhibitory postpotentials were reversibly abolished in the absence of extracellular calcium and absent in reserpine-treated neurons, suggesting an autoinhibition due to 5-HT acting on autoreceptors coupled to chloride channels. The autoinhibitory responses increased the membrane conductance and decreased subsequent excitability. Increasing 5-HT release by stimulating with trains of ten pulses at 10 or 30 Hz produced 23 ± 6 and 47 ± 2% of AP failures, respectively. These failures were reversibly abolished by the serotonergic antagonist methysergide (140 _M). Moreover, reserpine-treated neurons had only 5 ± 4% of failures during trains at 10 Hz. This percentage was increased to 35 ± 4% by iontophoretic application of 5-HT. Increases in AP failures correlated with smaller postsynaptic currents. Model simulations predicted that the autoinhibitory chloride conductance reduces the amplitude of APs arriving at neuropilar presynaptic endings. Altogether, our results suggest that 5-HT autoinhibits its subsequent release by decreasing the excitability of presynaptic endings within the same neuron.es_ES
dc.subject.meshmAction potentials-Drug effectses_ES
dc.subject.meshmAdrenergic uptake inhibitors-Pharmacologyes_ES
dc.subject.meshmAnimalses_ES
dc.subject.meshmCalcium-Metabolismoes_ES
dc.subject.meshmCells, culturedes_ES
dc.subject.meshmElectric stimulationes_ES
dc.subject.meshmExtracellular space-Metabolismoes_ES
dc.subject.meshmLeecheses_ES
dc.subject.meshmMembrane potentials-Drug effectses_ES
dc.subject.meshmMethysergide-Pharmacologyes_ES
dc.subject.meshmModels, neurologicales_ES
dc.subject.meshmNeural inhibition-Drug effectses_ES
dc.subject.meshmNeural inhibition-Physiologyes_ES
dc.subject.meshmNeurons-Drug effectses_ES
dc.subject.meshmNeurons-Physiologyes_ES
dc.subject.meshmPotassium chloride-Metabolismes_ES
dc.subject.meshmReserpine-Pharmacologyes_ES
dc.subject.meshmSerotonin-Metabolismes_ES
dc.subject.meshmSerotonin antagonists-Pharmacologyes_ES
dc.subject.meshmSynapses-Drug effectses_ES
dc.subject.meshmSynapses-Physiologyes_ES
dc.subject.meshmSynaptic transmission-Drug effectses_ES
dc.subject.meshmSynaptic transmission-Physiologyes_ES
dc.subject.meshmTime factorses_ES
dc.subject.meshmAdrenergic uptake inhibitorses_ES
dc.subject.meshmSerotonin antagonistses_ES
dc.subject.meshmSerotonines_ES
dc.subject.meshmPotassium chloridees_ES
dc.subject.meshmReserpinees_ES
dc.subject.meshmCalciumes_ES
dc.subject.meshmMethysergidees_ES
dc.subject.kwAutoinhibiciónes_ES
dc.subject.kwSerotonina sinápticaes_ES
dc.subject.kwSinapsises_ES
dc.subject.kwSerotoninaes_ES
dc.subject.koAutoinhibitiones_ES
dc.subject.koSynaptic serotonines_ES
dc.subject.koSynapsees_ES
dc.subject.koSerotonines_ES


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