Potassium - Chloride Ion Transporter 2 (kcc2) And Synaptic Plasticity

Bursting and rhythmic activity is a characteristic feature of neuronal processing, which is critically regulated by gamma-aminobutyric acid type A (GABA_A) receptors-mediated inhibition in brain. GABA_A receptors-mediated inhibition plays a pivotal role in regulating glutamatergic synaptic plasticity and circuit output. Enhancing inhibition via GABA_A receptors contributes to anesthetic-induced impairment of long-term potentiation (LTP) of excitatory synaptic transmission, which may account for general anesthesia-associated memory impairment (amnesia). The K~+-Cl~- cotransporter 2 (KCC2) is an important factor in determining inhibitory GABAergic synaptic strength via controlling intracellular chloride gradient besides the contribution of GABA_A receptor. Although much knowledge has been gained regarding activity-dependent downregulation of KCC2 in many pathological conditions, the potential change and contribution of KCC2 in regulating circuit activity and synaptic plasticity in physiological process is still unknown.Interestingly, GlyR only shows tonic effects as no glycinergic synaptic transmission was recorded in hippocampal neuron. However, there is little knowledge about the function and significance of GlyR in central nervous system. We wonder that whether it involves in the regulation of spontaneous circuit activity via KCC2-dependent intracellular chloride concentration.Using acute prepared hippocampal slices, cultured hippocampal neurons, Immunoblotting, electrophysiological recording and immunocytological methods, we investigated the following 3 questions: 1. Whether KCC2 contributes to LTP...