Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 6, Pages -Publisher
MDPI
DOI: 10.3390/ijms22063149
Keywords
Phospholipase C (PLC); γ -aminobutyric acid (GABA); excitatory; inhibitory balance (E; I balance); GABAergic inhibition; epilepsy
Funding
- Basic Science Research Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [2020R1A2C1005492]
- National Research Foundation of Korea [2020R1A2C1005492] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Epilepsy is characterized by abnormal hyperexcitation of neurons. Recent studies suggest that the imbalance of excitation and inhibition in the central nervous system is closely implicated in the etiology of epilepsy. GABA in the brain plays a pivotal role in maintaining the balance between excitation and inhibition.
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.
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