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Effects of GABAergic transmissions on the immunoreactivities of calcium binding proteins in the gerbil hippocampus
Author(s) -
Kwak SungEun,
Kim JiEun,
Kim DukSoo,
Jung JuYoung,
Ho Won Moo,
Kwon OhShin,
Choi SooYoung,
Kang TaeCheon
Publication year - 2005
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20482
Subject(s) - gerbil , muscimol , medicine , endocrinology , gabaa receptor , hippocampus , hippocampal formation , bicuculline , gabaergic , gabab receptor , agonist , biology , baclofen , neuroscience , inhibitory postsynaptic potential , receptor , ischemia
Although reduced calcium binding protein (CBP) immunoreactivities in the epileptic hippocampus have been well established, it has been controversial that these changes may directly indicate neuronal degeneration. In the present study, therefore, we investigated CBP expressions in the gerbil hippocampus following treatment with γ‐aminobutyric acid (GABA) receptor antagonists in order to assess whether altered CBP expressions are the result of either abnormal excitation or indicative of neuronal damage/degeneration. Seizure‐sensitive (SS) gerbils showed a loss/decline of CBP immunoreactivities in some hippocampal neurons as compared with seizure‐resistant (SR) gerbils. In muscimol (GABA A receptor agonist) treated SS gerbils, expression levels of CBP were enhanced as compared with saline‐treated SS gerbils. Bicuculline (a GABA A receptor antagonist) treatment markedly reduced CBP immunoreactivities in hippocampal neurons of the SR gerbil. Baclofen (a GABA B receptor agonist) treatment increased CBP immunoreactivities in the hippocampus of SS gerbils, although its effect was lower than that of muscimol treatment. Moreover, phaclofen (GABA B receptor antagonist) treated SR gerbil showed reduction in calbindin D‐28K immunoreactivity, not parvalbumin immunoreactivity, in the hippocampus. These findings therefore suggest that reduced CBP immunoreactivities may be the consequence of abnormal discharge caused by loss of GABAergic inhibition rather than an indication of the neuronal damage/degeneration. J. Comp. Neurol. 485:153–164, 2005. © 2005 Wiley‐Liss, Inc.