关键词: GABAergic inhibition Phospholipase C (PLC) epilepsy excitatory/inhibitory balance (E/I balance) γ-aminobutyric acid (GABA)

Mesh : Animals Anticonvulsants / pharmacology therapeutic use Biomarkers Disease Susceptibility Epilepsy / diagnosis drug therapy etiology metabolism GABA Antagonists / pharmacology therapeutic use Humans Isoenzymes Receptors, GABA / metabolism Signal Transduction / drug effects Synapses / metabolism Synaptic Transmission Type C Phospholipases / metabolism gamma-Aminobutyric Acid / metabolism

来  源:   DOI:10.3390/ijms22063149   PDF(Sci-hub)   PDF(Pubmed)

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.
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