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dc.contributor.authorDargaei, Zahraen
dc.date2014-07-22 15:04:28.154
dc.date.accessioned2014-07-23T14:57:55Z
dc.date.available2014-07-23T14:57:55Z
dc.date.issued2014-07-23
dc.identifier.urihttp://hdl.handle.net/1974/12314
dc.descriptionThesis (Master, Physiology) -- Queen's University, 2014-07-22 15:04:28.154en
dc.description.abstractThe bag cell neurons of Aplysia initiate reproductive behaviour by secreting egg-laying hormone during a prolonged period of synchronous and repetitive firing known as the afterdischarge. Electrical coupling facilitate the functional syncytium between bag cell neurons. We used dual tight-seal whole-cell recording to examine the biophysical properties and modulation of electrical synapses between pairs of cultured bag cell neurons. Transjunctional voltage did not influence junctional conductance. Presynaptically evoked action potentials transferred through gap junctions to elicit postsynaptic electrotonic potentials (ETPs). Bag cell neurons did not show dye coupling; hence, the permeability of electrical synapses was tested using block of K+ current. Presynaptic neurons were whole-cell loaded with Cs+ or TEA and transfer measured by suppression of postsynaptic K+ current. Cs+, but not TEA, reduced the K+ current in electrically-coupled neighbours. In addition, the gap junction blockers meclofenamic acid, niflumic acid, and nitrobenzoic acid, but not glycyrrhetinic acid and quinine, considerably attenuated junctional current. The afterdischarge is accompanied by an increase in intracellular Ca2+ and upregulation of PKC. Elevating Ca2+ with a train of voltage steps, which mimics the onset of the afterdischarge, decreased junctional conductance. The inhibition was most effective when Ca2+ entry occurred in both electrically-coupled neurons. Depletion of Ca2+ from the mitochondria, but not the endoplasmic reticulum, also attenuated junctional communication. Buffering Ca2+ with high intracellular EGTA prevented uncoupling, as did inhibition of CaM kinase. Application of a PKC activator modestly decreased junctional current, while elevating Ca2+ along with PKC inhibited electrical synapses to an even greater extent than Ca2+ alone. Our results suggest that PKC and Ca2+-dependent activation of CaM kinase inhibit electrical signalling. This may contribute to an enhancement of neuronal excitability leading to the secretion of reproductive hormone. Ca2+ influx also decreased the amplitude and time course of the ETP, which may improve synchrony by preventing lengthy ETPs and out-of-phase postsynaptic action potentials. Thus, modulation of electrical coupling may act as a means to enhance and sustain the release of reproductive hormone.en
dc.language.isoengen
dc.relation.ispartofseriesCanadian thesesen
dc.rightsThis publication is made available by the authority of the copyright owner solely for the purpose of private study and research and may not be copied or reproduced except as permitted by the copyright laws without written authority from the copyright owner.en
dc.subjectJunctional Currenten
dc.subjectAfterdischargeen
dc.subjectNeuroendocrine Cellen
dc.subjectGap Junctionen
dc.titleCharacterization and Modulation of Electrical Coupling Between Molluscan Neuroendocrine Cellsen
dc.typethesisen
dc.description.degreeM.Sc.en
dc.contributor.supervisorMagoski, Neil S.en
dc.contributor.departmentPhysiologyen
dc.degree.grantorQueen's University at Kingstonen


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