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dc.contributor.authorFan, Ping.en_US
dc.date.accessioned2014-10-21T12:38:44Z
dc.date.available1992
dc.date.issued1992en_US
dc.identifier.otherAAINN80114en_US
dc.identifier.urihttp://hdl.handle.net/10222/55316
dc.descriptionHyperammonemia and hypoglycemia are metabolic disorders which interfere with the function of the central nervous system. Cellular mechanisms of disturbed neuronal function in these two conditions were investigated in rat hippocampal slices with the use of extracellular and intracellular recording.en_US
dc.descriptionSynaptic transmission from Schaffer-collaterals to CA1 pyramidal neurons was diminished by as little as 0.5 mM NH$\sb4$Cl. During the presence of 1-4 mM NH$\sb4\sp+,$ brain concentrations seen in hepatic encephalopathy, the membrane potential of CA1 neurons depolarized with no significant change in input resistance. Quisqualate-induced inward currents, which were sensitive to CNQX, were blocked, glutamate-induced currents were slightly reduced, while NMDA-induced currents were greatly facilitated.en_US
dc.descriptionLow glucose concentrations (0.2-1 mM) seen in hypoglycemia caused mostly biphasic membrane potential changes: a small initial hyperpolarization followed by a large depolarization. Occasionally only one of these potential changes was observed. Input resistance of the neurons always decreased. Low glucose also interfered with synaptic transmission: first the generation of action potentials by EPSPs was inhibited, while later the size of EPSPs decreased. Quisqualate and NMDA currents were first potentiated, then inhibited.en_US
dc.descriptionResults suggest that NH$\sb4\sp+$ depresses transmission by eliminating quisqualate-induced responses that are mainly responsible for EPSPs, while low glucose probably shunts EPSPs so that they can no longer generate action potentials at the axon hillock. This impairment in synaptic transmission is likely to contribute to neurological abnormalities seen in hyperammonemia and hypoglycemia.en_US
dc.descriptionThesis (Ph.D.)--Dalhousie University (Canada), 1992.en_US
dc.languageengen_US
dc.publisherDalhousie Universityen_US
dc.publisheren_US
dc.subjectBiology, Neuroscience.en_US
dc.subjectBiology, Animal Physiology.en_US
dc.subjectBiophysics, General.en_US
dc.titleCellular mechanisms of the neurotoxicity caused by hyperammonemia and hypoglycemia.en_US
dc.typetexten_US
dc.contributor.degreePh.D.en_US
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