Kindling induces an asymmetric enhancement of N-type Ca2+ channel density in the dendritic fields of the rat hippocampus

Nuclear localization of Cav2.2 and its distribution in the mouse central nervous system, and changes in the hippocampus during and after pilocarpine-induced status epilepticus

“…Our result was consistent with the reports by Bernstein et al. [33,34]. Based on previous study showing intracellular redistribution of Ca v 2.2 channels after ω‐conotoxin and Cd 2+ stimulation [52], it is speculated that during SE, Ca v 2.2 channels may be redistributed to different subcellular compartments (that is, soma, axon and dendrites) of the same neurone in CA3 pyramidal neurones and in granule cells in the dentate gyrus leading to the increase of Ca v 2.2 channels in mossy fibres or dendrites of CA3 pyramidal neurones and decease of Ca v 2.2 channels in somas of granule cells and CA3 pyramidal neurones.…”

“…However, the enhancement in the surface density of N‐type VDCCs in CA1 neurones was reported by Bernstein et al. [33,34]. The difference may be caused by the animal models used in different research groups.…”

“…As one of the important subtypes of calcium channels, N‐type calcium channel changes at different stages of epileptogenesis in animal models of epilepsy. An enhancement of N‐type VDCCs in the dendritic fields of CA1 and CA3 areas of hippocampus has been reported in amygdala‐kindled rat brain [33,34]. In the kainic acid model, a decrement of Ca v 2.2 in the stratum lucidum of CA3 area was observed in both young and aged rats [35].…”

Voltage‐dependent Calcium Channel Abnormalities in Hippocampal CA3 Neurons of Spontaneously Epileptic Rats

“…Such abnormal hippocampal excitation due to a Ca 2+ channel abnormality is considered to be involved in induction of epileptic seizures, because the L‐type Ca 2+ channel antagonist S‐312‐d inhibited tonic convulsions in SERs (Amano et al, 2004), although the neuronal circuit, including the hippocampus, involved in the seizures remains to be determined. In other epileptic model animals, kindling is known to induce an increase in density of N‐type Ca 2+ channels and an alternation in low‐ and high‐voltage–activated Ca 2+ channels in the hippocampus (Mody et al, 1990; Vreugdenhil and Wadman, 1992; Faas et al, 1996; Bernstein et al, 1999). Interestingly, an increase in conductance in the T‐type Ca 2+ channel has been found in reticular thalamic neurons of genetic absence epilepsy rats from Strasbourg (GAERS) that show absence seizures (Tsakiridou et al, 1995).…”

“…Neuronal hyperexcitability of hippocampal pyramidal neurons has also been reported in tottering mice (Kostopoulos and Psarropoulou, 1990) and kindled rats (King et al, 1985; Bragdon et al, 1988; Stringer and Lothman, 1988). Furthermore, enhancement of the Ca 2+ current (Vreugdenhil and Wadman, 1992, 1994; Faas et al, 1996) and N‐type Ca 2+ channel density (Bernstein et al, 1999) in hippocampal neurons have been observed in kindling rats. Thus abnormalities in Ca 2+ channel functions are considered to contribute to the epileptogenesity of SERs.…”