Abstract
Background Neuronal L-type voltage-gated calcium channels (LTCCs) were shown to be involved in the control of neuronal excitability, synaptic plasticity and gene expression. These mechanisms are altered in epileptic tissue and are thought to contribute to epileptogenesis. Hence, LTCCs are interesting targets for epileptic and anti-epileptic therapy. However, their role in epilepsy, whether LTCCs enhance or reduce epileptiform/epileptogenic activity, remained unclear. The aim of this study was to identify in which manner LTCCs contribute and/or modulate electrical excitation.
Highlights
Neuronal L-type voltage-gated calcium channels (LTCCs) were shown to be involved in the control of neuronal excitability, synaptic plasticity and gene expression
Using ion channel blockers and ion-exchange experiments we provide evidence that LTCCs couple to both
Varying pulse length and current strength we obtained evidence that ADPs are activated at a lower LTCC activity than AHPs
Summary
Neuronal L-type voltage-gated calcium channels (LTCCs) were shown to be involved in the control of neuronal excitability, synaptic plasticity and gene expression. These mechanisms are altered in epileptic tissue and are thought to contribute to epileptogenesis. LTCCs are interesting targets for epileptic and anti-epileptic therapy. Their role in epilepsy, whether LTCCs enhance or reduce epileptiform/epileptogenic activity, remained unclear. The aim of this study was to identify in which manner LTCCs contribute and/or modulate electrical excitation
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