Effects of GABAergic transmissions on the immunoreactivities of calcium binding proteins in the gerbil hippocampus.
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 gamma-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.
Kwak
Sung-Eun
SE
Department of Anatomy, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.
Kim
Ji-Eun
JE
Kim
Duk-Soo
DS
Jung
Ju-Young
JY
Won
Moo Ho
MH
Kwon
Oh-Shin
OS
Choi
Soo-Young
SY
Kang
Tae-Cheon
TC
D000818:Animals; D001418:Baclofen / Q000031:analogs & derivatives* / Q000494:pharmacology; D001640:Bicuculline / Q000494:pharmacology; D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002452:Cell Count / Q000379:methods; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology*; D005849:Gerbillinae; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D007150:Immunohistochemistry / Q000379:methods; D009118:Muscimol / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010320:Parvalbumins / Q000378:metabolism; D064030:S100 Calcium Binding Protein G / Q000378:metabolism; D012640:Seizures / Q000139:chemically induced / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D064032:Calbindin 2; D064026:Calbindins; D002135:Calcium-Binding Proteins; D018755:GABA Agonists; D018756:GABA Antagonists; D010320:Parvalbumins; D064030:S100 Calcium Binding Protein G; C052329:phaclofen; D009118:Muscimol; D005680:gamma-Aminobutyric Acid; D001418:Baclofen; D001640:Bicuculline