Plasticity of Hippocampal Excitatory-Inhibitory Balance: Missing the Synaptic Control in the Epileptic Brain

Figure 1

Glutamatergic and GABAergic long-term plasticity and tripartite neuronal-astroglial network in normal and epileptic brain. (a) During physiological neuronal activity, coincidence between postsynaptic depolarization and glutamatergic (orange) and GABAergic interneuron (green) simultaneously activated induces increase of synaptic efficacy (i.e., mean amplitude of postsynaptic response) in both glutamatergic [CB1] synapses (LTP) at the same time of a decrease of efficacy of GABAergic transmission (LTD; A). (B) By GABAergic and glutamatergic input integration, the net increase in membrane potential falls below the seizure threshold (ST). (b) During epileptiform neuronal activity, astroglial hyperexcitation through Rs, GluRs, and/or eCBsRs activation, which increases the intracellular Ca²⁺ release of astroglial glutamate, increasing the excitatory neurotransmission while inhibitory transmission remains unchanged (A). (B) In this condition, glutamatergic/GABAergic rate results in an excitatory imbalance, exceeding the seizure threshold.

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