Dear Colleagues,

Epilepsy is a chronic neurological disorder affecting approximately 65 million people worldwide, and it is characterized by the occurrence of recurrent and unprovoked seizures. This hallmark is the result of the uncontrolled and excessive synchronized electrical activity of central neurons. Although the mechanisms underlying the onset of seizures are far from being elucidated, the disruption of the balance between excitation and inhibition has a central role in epileptogenesis.

Numerous cellular and molecular abnormalities have been described during the latent period that precedes the appearance of spontaneous seizures which may contribute to epileptogenesis, namely, changes in gene expression, alterations in neurotransmitter receptor and ion channel function and distribution, axonal sprouting, and synaptic reorganization. In the vertebrate central nervous system (CNS), neuronal excitation is mainly mediated by the excitatory neurotransmitters glutamate and acetylcholine, while neuronal inhibition is primarily mediated by γ-aminobutyric acid (GABA). In physiological conditions, neuronal excitation and inhibition in the CNS maintain a delicate balance, which can be broken in pathological conditions, resulting in neurological disorders such as epilepsy. The direct cause of convulsive seizures is thought to result from increased excitability or decreased inhibition in the brain, though the detailed mechanisms are still unclear.

The treatments currently used in epilepsy reduce seizures’ frequency and intensity, but there is still no available cure. The development of novel therapeutics requires a better understanding of the basic molecular mechanisms that initially trigger the numerous downstream mechanisms mediating epileptogenesis, which ultimately result in the hyperexcitability characteristic of epilepsy—namely, alterations in synaptic function and synaptic plasticity. Moreover, the study of the molecular and cellular mechanisms regulating the cross talk between synaptic excitation and inhibition is crucial for the understanding the causes leading to the disruption of neuronal circuits’ stability in epilepsy.

This provides an incentive to further explore the molecular mechanisms of synaptic (dys)function that characterize epilepsy. This Special Issue welcomes submissions of original research articles, reviews, and short communications focusing on the mechanisms underlying neurotransmission and synaptic function dysregulation found in epilepsy, therefore certainly increasing our knowledge in the field.

Dr. Filipe V. Duarte
Dr. Miranda Mele
Guest Editors

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• epilepsy
• excitation
• inhibition
• neurotransmission
• synaptic function
• synaptic plasticity