Aims: The aim of this study is to describe the current state of knowledge about the physiology of kainate type glutamate receptors as modulators of GABAergic synaptic transmission in the hippocampus.
Development: The activation of kainate receptors (KR) located in the presynaptic terminal of the interneurons reduces GABAergic synaptic transmission at the interneuron principal cell synapse in the CA1 layer of the hippocampus. This diminished release of GABA involves a metabotropic effect, and an that activation of both a pertussis toxin sensitive G protein and protein kinase C is required. In these same interneurons there is also a population of KR with an ionotropic effect in the somatodendritic compartment, which depolarise them and give rise to a massive release of neurotransmitter when activated. It has very recently been shown that activating KR by submicromolar concentrations of agonist can bring about an increase in the release of GABA, an effect described principally in the interneuron interneuron synapses, although the mechanism by which the KR produce this effect is yet to be described.
Conclusions: KR act in the hippocampus as modulators of GABA release; they increase or decrease it and hence play a part in maintaining the exquisite balance of neuronal excitability. In abnormal conditions they can also notably upset the balance of this excitability and give rise to firing patterns of an epileptic kind, among other disorders.