Abstract
Epilepsy is characterized by recurrent seizures due to abnormal hyperexcitation of neurons. Recent studies have suggested that the imbalance of excitation and inhibition (E/I) in the central nervous system is closely implicated in the etiology of epilepsy. In the brain, GABA is a major inhibitory neurotransmitter and plays a pivotal role in maintaining E/I balance. As such, altered GABAergic inhibition can lead to severe E/I imbalance, consequently resulting in excessive and hypersynchronous neuronal activity as in epilepsy. Phospholipase C (PLC) is a key enzyme in the intracellular signaling pathway and regulates various neuronal functions including neuronal development, synaptic transmission, and plasticity in the brain. Accumulating evidence suggests that neuronal PLC is critically involved in multiple aspects of GABAergic functions. Therefore, a better understanding of mechanisms by which neuronal PLC regulates GABAergic inhibition is necessary for revealing an unrecognized linkage between PLC and epilepsy and developing more effective treatments for epilepsy. Here we review the function of PLC in GABAergic inhibition in the brain and discuss a pathophysiological relationship between PLC and epilepsy.
Highlights
Released brain-derived neurotrophic factor (BDNF) increased the expression of GABAA receptor β2, β3 subunits in the postsynaptic neuronal surface, and enhanced GABAergic response [159]
Much needs to be further investigated, a recent hypothesis of excitation and inhibition (E/I) imbalance in the etiology of epilepsy advanced our understanding of the molecular, cellular, and synaptic mechanisms underlying epilepsy
It has been demonstrated that despite their small population, GABAergic neurons and GABAergic inhibition have a powerful effect in maintaining optimal E/I balance
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Γ-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the brain and using GABA, GABAergic inhibitory neurons primarily regulate the excitability of neurons. PLC isodifferentially expressed among tissues and regulates the complex cellular functions in a zyme is differentially expressed among tissues and regulates the complex cellular functissue-dependent manner. Among these isozymes, PLCβ and PLCγ are major tions in a tissue-dependent manner. PLC signaling signaling cascades cascades and and functions functions in in the the brain External ligands ligands such such as as neurotransmitters neurotransmitters and and Figure neurotrophic factors bind to and activate the upstream transmembrane receptors of PLC. Activation of PLC hydrolyzes phospholipid PIP2 into IP3 and DAG and these second of receptor tyrosine.
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