Synaptic and non-synaptic mechanisms underlying low calcium bursts in the in vitro hippocampal slice |
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Authors: | N Agopyan M Avoli |
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Institution: | (1) Montreal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, 3801 University Street, H3A 2B4 Montréal, Québec, Canada;(2) Present address: Department of Physiology, McGill University, McIntyre Medical Building, H3G 1Y6 Montréal, Québec, Canada |
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Abstract: | Summary 1. The epileptiform activity generated by lowering extracellular Ca++] was studied in the CA1 subfield of rat hippocampal slices maintained in vitro at 32° C. Extracellular and intracellular recordings were performed with NaCl and KCl filled microelectrodes. 2. Synaptic potentials evoked by stimulation of the stratum radiatum and alveus were blocked upon perfusion with artificial cerebrospinal fluid (ACSF) containing 0.2 mM Ca++, 4 mM Mg++. Blockade of synaptic potentials was accompanied by the appearance of synchronous field bursts which either occurred spontaneously or could be induced by stimulation of the alveus. 3. Both spontaneous and stimulus-induced low Ca++ bursts recorded extracellularly in stratum pyramidale consisted of a negative potential shift with superimposed population spikes. This extracellular event was closely associated with intracellularly recorded action potentials rising from a prolonged depolarization shift. Steady hyperpolarization of the cell membrane potential decreased the amplitude of the depolarizing shift suggesting that synaptic conductance were not involved in the genesis of the low Ca++ burst. 4. Spontaneous depolarizing inhibitory potentials recorded in normal ACSF with KCl filled microelectrodes were reduced in size in low Ca++ ACSF. However, small amplitude potentials could still be observed at a time when low Ca++ bursts were generated by hippocampal CA1 pyramidal neurons. 5. Bicuculline methiodide, an antagonist of -aminobutyric acid (GABA), was capable of modifying the frequency of occurrence and the shape of synchronous field bursts. The effects evoked by bicuculline methiodide were, however, not observed when 81–100% of NaCl was replaced with Na-Methylsulphate. Hence, it was concluded that in low Ca++ ACSF even though large release of transmitter such as those following electrical activation of stratum radiatum or alveus cannot be observed, small spontaneous release of the inhibitory transmitter GABA seems to persist. 6. Substitution of NaCl with Na-Methylsulphate also caused changes in the synchronous field bursts which were different from those observed following application of bicuculline methiodide. These findings suggest that in low Ca++ ACSF, in addition to residual GABAergic Cl- mechanisms, non-synaptic Cl- conductances might play a role in controlling the excitability of hippocampal neurons.Supported by grants from the MRC of Canada (MA-8109) and Sick Children Foundation to MA |
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Keywords: | Epilepsy Hippocampus Inhibition Low Ca++ Cl- conductances |
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