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Cav1.2, Cav1.3, and Cav2.1 in the mouse hippocampus during and after pilocarpine‐induced status epilepticus

Cav1.2, Cav1.3, and Cav2.1 in the mouse hippocampus during and after pilocarpine‐induced status... Calcium binding proteins are well known to be expressed by different groups of hippocampal interneurons; however, whether voltage‐dependent calcium channels (Cav) are also localized in these neurons, changed during and after status epilepticus (SE), and involved in epileptic activity have not been reported. In the present study, we showed the colocalization of three subtypes of voltage‐gated calcium channels (Cav1.2, Cav1.3, or Cav2.1) with different calcium binding proteins such as calbindin (CB), calretinin (CR), and parvalbumin (PV). At early stages during and after pilocarpine‐induced status epilepticus (PISE), significant changes of expression of Cav1.2, Cav1.3 (L‐type), and Cav2.1 (P/Q‐type) were found in different groups of hippocampal neurons. Induced expression of Cav1.3 or Cav2.1 in reactive astrocytes was shown at 1 week and 2 months after PISE. At the latter time point, higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunoposivie neurons were observed in gliotic CA1 area. We therefore conclude that voltage‐gated calcium channels are expressed by different groups of hippocampal interneurons in the mouse. At acute stages during and after PISE, up‐ or down‐regulation of Cav1.2, Cav1.3, or Cav2.1 in functionally different groups of interneurons in CA1 area may be related to the changes of their plasticity. Up‐regulation of Cav1.2, Cav1.3, or Cav2.1 in granule cells may be directly related to the occurrence of SE. The induced expression of Cav1.3 or Cav2.1 in reactive astrocytes at 1 week and 2 months after PISE suggests that Cav1.3 or Cav2.1‐related calcium signaling in reactive astrocytes may be involved in initiation, maintenance or spread of seizure activity. In gliotic CA1 area at chronic stage (i.e., 2 months after PISE), the occurrence of higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunopositive neurons may suggest that such colocalizations may be linked to the survival or loss of particular group of hippocampal neurons. © 2007 Wiley‐Liss, Inc. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Hippocampus Wiley

Cav1.2, Cav1.3, and Cav2.1 in the mouse hippocampus during and after pilocarpine‐induced status epilepticus

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References (32)

Publisher
Wiley
Copyright
Copyright © 2007 Wiley Subscription Services
ISSN
1050-9631
eISSN
1098-1063
DOI
10.1002/hipo.20263
pmid
17265461
Publisher site
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Abstract

Calcium binding proteins are well known to be expressed by different groups of hippocampal interneurons; however, whether voltage‐dependent calcium channels (Cav) are also localized in these neurons, changed during and after status epilepticus (SE), and involved in epileptic activity have not been reported. In the present study, we showed the colocalization of three subtypes of voltage‐gated calcium channels (Cav1.2, Cav1.3, or Cav2.1) with different calcium binding proteins such as calbindin (CB), calretinin (CR), and parvalbumin (PV). At early stages during and after pilocarpine‐induced status epilepticus (PISE), significant changes of expression of Cav1.2, Cav1.3 (L‐type), and Cav2.1 (P/Q‐type) were found in different groups of hippocampal neurons. Induced expression of Cav1.3 or Cav2.1 in reactive astrocytes was shown at 1 week and 2 months after PISE. At the latter time point, higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunoposivie neurons were observed in gliotic CA1 area. We therefore conclude that voltage‐gated calcium channels are expressed by different groups of hippocampal interneurons in the mouse. At acute stages during and after PISE, up‐ or down‐regulation of Cav1.2, Cav1.3, or Cav2.1 in functionally different groups of interneurons in CA1 area may be related to the changes of their plasticity. Up‐regulation of Cav1.2, Cav1.3, or Cav2.1 in granule cells may be directly related to the occurrence of SE. The induced expression of Cav1.3 or Cav2.1 in reactive astrocytes at 1 week and 2 months after PISE suggests that Cav1.3 or Cav2.1‐related calcium signaling in reactive astrocytes may be involved in initiation, maintenance or spread of seizure activity. In gliotic CA1 area at chronic stage (i.e., 2 months after PISE), the occurrence of higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunopositive neurons may suggest that such colocalizations may be linked to the survival or loss of particular group of hippocampal neurons. © 2007 Wiley‐Liss, Inc.

Journal

Hippocampus – Wiley

Published: Jan 1, 2007

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