Action of carbamazepine on epileptiform activity of the verartidine model in CA1 neurons

• Published in: Brain research Vol. 885; no. 2; pp. 289 - 294
• Main Authors: Otoom, Sameer A., Alkadhi, Karim A.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 08-12-2000; Amsterdam Elsevier; New York, NY
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Anticonvulsants - pharmacology; Anticonvulsants. Antiepileptics. Antiparkinson agents; Biological and medical sciences; Brain slice; Carbamazepine; Carbamazepine - pharmacology; Evoked bursting; Hippocampus; Hippocampus - drug effects; Hippocampus - physiology; Male; Medical sciences; Membrane Potentials - drug effects; Membrane Potentials - physiology; Neuropharmacology; Pharmacology. Drug treatments; Rats; Rats, Sprague-Dawley; Sodium Channels - drug effects; Sodium Channels - physiology; Spontaneous bursting; Therapeutic; Veratridine; Veratridine - pharmacology; Evoked bursting; Veratridine; Spontaneous bursting; Therapeutic; Brain slice; Carbamazepine; Hippocampus; Animal model; Rat; Epilepsy; Rodentia; Central nervous system; Discharge pattern; Electrophysiology; Anticonvulsant; Vertebrata; Mammalia; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)02977-2

The veratridine epileptiform model was utilized to assess the antiepileptic effect of Carbamazepine (CBZ) in rat hippocampal CA1 pyramidal neurons using conventional intracellular recording techniques. In the veratridine model, where brain slices are treated with veratridine (0.3 μM), a single intracellular stimulus evokes epileptiform bursting. Additionally, spontaneous epileptiform activity commonly appears on prolonged exposure to veratridine in this model. In this model, therapeutic (7–15 μM) and high (50 μM) concentrations of CBZ inhibited the evoked and spontaneous epileptiform bursting in a concentration- and voltage-dependent manner. At all concentrations tested, CBZ produced inhibition of epileptiform activity without affecting the membrane resting potential or input resistance. However, at 50 μM, the drug increased the firing threshold of neurons. These results confirm the suitability of this model for testing sodium channel-dependent antiepileptic agents.