The Journal of Neurophysiology Vol. 77 No. 5 May 1997, pp. 2349-2359
Copyright ©1997 The American Physiological Society

Enhancement of Whole Cell Synaptic Currents by Low Osmolarity and by Low [NaCl] in Rat Hippocampal Slices

Rong Huang, Daniel F. Bossut, and George G. Somjen

Departments of Cell Biology and Neurobiology, Duke University Medical Center, Durham, North Caroline 27710

Huang, Rong, Daniel F. Bossut, and George G. Somjen. Enhancement of whole cell synaptic currents by low osmolarity and by low [NaCl] in rat hippocampal slices. J. Neurophysiol. 77: 2349-2359, 1997. We recorded whole cell currents of patch-clamped neurons in stratum pyramidale of CA1 region of rat hippocampal tissue slices. Synaptic currents were evoked by orthodromic stimulation while holding potential of the neuron was varied from hyperpolarized to depolarized levels. Extracellular osmolarity (_o) was lowered by superfusion with artificial cerebrospinal fluid in which NaCl concentration ([NaCl]) was reduced. The effect of low extracellular NaCl was tested in additional trials in which NaCl was substituted by isosmolar fructose. Both lowering of _o and isosmotic lowering of extracellular [NaCl] ([NaCl]_o) caused reversible increase of excitatory postsynaptic currents. The effect of lowering _o was concentration dependent, and it was significantly stronger than the effect of equivalent isosmotic lowering of [NaCl]_o. Inhibitory postsynaptic currents also increased in many but not in all cases. Lowering of _o caused a prolongation of the time constant of relaxation of the capacitive charging current induced by small hyperpolarizing voltage steps. A virtual input capacitance, calculated by dividing this time constant by the input resistance, increased during hypotonic exposure. Isosmotic lowering of [NaCl]_o had no effect on time constant or input capacitance. Depolarizing voltage commands evoked spikelike inward currents presumably representing Na⁺-dependent action potentials generated outside the voltage-clamped region of the cell. These current spikes became smaller in low _o and in low [NaCl]_o. Broader, voltage-dependent, presumably Ca²⁺-mediated inward currents became more prominent during hypotonic exposure. We conclude that lowering of [NaCl]_o causes enhancement of excitatory synaptic transmission. Transmission may be facilitated by the uptake of Ca²⁺ into presynaptic terminals as well as into postsynaptic target neurons, induced by the low [NaCl]_o. Lowering of _o enhances synaptic transmission more than does a corresponding isosmotic lowering of [NaCl]. The excess increase recorded from the cell soma in low _o may in part be due to changing electrotonic length caused by the swelling of dendrites.

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