Abstracts

RATIONALE: Brain functions are based on the dynamic interaction of excitatory and inhibitory synapses. A balance between the excitatory and inhibitory inputs is critical for neuronal circuits to be functional. Unbalance between the two systems may cause epileptic seizures. We investigated the roles of kainate type (KAR) of glutamate receptors in modulation of inhibitory GABAergic transmission. METHODS: Interneuronal action potential-evoked unitary IPSCs (uIPSCs) were recorded using dual patch-clamp techniques in synaptically coupled pairs of interneurons and CA1 pyramidal neurons in hippocampal slices. RESULTS: Perfusion of AMPA/KA receptor antagonist, CNQX, caused an increase in the failure rate of uIPSCs in low-failure pairs, whereas AMPA receptor antagonists, GYKI53655 or SYM2206 had no effects. Low concentrations of KA (200 nM) increased the success rate of uIPSCs in high-failure pairs. The effect was abolished when extracellular calcium was changed to 0.5 mM. High concentrations of KA (10 M) depressed uIPSCs in low-failure pairs, but induced a biphasic response in high-failure pairs: an early increase in the success rate and a delayed decrease in the amplitude of uIPSCs. CONCLUSIONS: Basal or low concentrations of glutamate potentiate individual GABAergic synapses by increasing the release probability. This potentiation may play a role in maitaining the balance between the excitatory and inhibitory inputs. However, high levels of glutamate depress low-failure GABAergic synapses.