Abstract
Although glutamate is the most important excitatory neurotransmitter of the central nervous system (CNS), its excessive extracellular concentration leads to unrestrained continuous depolarization of neurons, a toxic process known as excitotoxicity. γ-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the CNS, and GABAergic inhibitory neurons primarily normalize the glutamate-induced excitability of neurons. Interest in glutamate excitotoxicity as etiological mechanisms of many neurological disorders (ND) has been recently expanded following its implication in the pathogenesis of Huntington's disease, Alzheimer's disease (AD), Parkinson's disease (PD), and autism spectrum disorders (ASD) as the most prevalent brain diseases. Phospholipase C (PLC) is a key enzyme in the intracellular signaling pathway that controls numerous neuronal functions comprising neuronal growth, synaptic transmission, and plasticity in the CNS. Accumulating evidence suggests that neuronal PLC greatly contributes to multiple aspects related to brain functions. This review outlines the different molecular mechanisms relating PLC to glutamate excitotoxicity and GABAergic functions, and discusses the pathophysiological relationship between PLC and ND.
Published Version
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