Abstract
Epilepsy is a common brain disorder characterized by recurrent epileptic seizures with neuronal hyperexcitability. Apart from the classical imbalance between excitatory glutamatergic transmission and inhibitory γ-aminobutyric acidergic transmission, cumulative evidence suggest that cholinergic signaling is crucially involved in the modulation of neural excitability and epilepsy. In this review, we briefly describe the distribution of cholinergic neurons, muscarinic, and nicotinic receptors in the central nervous system and their relationship with neural excitability. Then, we summarize the findings from experimental and clinical research on the role of cholinergic signaling in epilepsy. Furthermore, we provide some perspectives on future investigation to reveal the precise role of the cholinergic system in epilepsy.
Highlights
More than 70 million people have epilepsy worldwide, accounting for about 1% of the population, which makes it one of the most common neurological conditions [1]
In the central nervous system (CNS), ACh acts as a neuromodulator released from key groups of cholinergic neurons, which mainly consist of two primary cell types including long-projecting cholinergic neurons and local cholinergic interneurons
The long-term potentiation (LTP) is expressed postsynaptically by a raise of amino-3-hydroxy5-methyl-4-isoxazole propionic acid receptors (AMPARs) and N-methylD -aspartate glutamate receptors (NMDARs) or GABAA R response, and presynaptically via an increased Glu or GABA release probability, which are all induced by mAChRs signaling transduction
Summary
More than 70 million people have epilepsy worldwide, accounting for about 1% of the population, which makes it one of the most common neurological conditions [1]. Numerous studies have shown that the systemic administration of cholinergic agonists carbachol or pilocarpine have long been known to induce seizure activity [6]. Findings from both experimental and clinical research indicated dysfunctional cholinergic signaling in epilepsy. We recently found that the selective activation of cholinergic neurons in the medial septum (MS) by using optogenetics could produce obvious anti-seizure effects [7]. These data collectively support the notion that cholinergic signaling may play a critical but heterogeneous role in epilepsy. We revisit the considerable recent progress in cholinergic modulation of epilepsy and propose an integrative perspective of its contribution to epilepsy
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