The selective effects of somatostatin- and GABA-mediated transmissions on voltage gated Ca2+ channel immunoreactivity in the gerbil hippocampus.
To identify whether altered expressions of voltage gated Ca(2+) channel (VGCC) are linked to inhibitory transmission abnormalities in the gerbil hippocampus, we investigated the effects of GABA receptor or somatostatin receptor (SST) antagonists/agonists on VGCC immunoreactivity in vivo. VGCC immunoreactivities in the hippocampus were significantly higher in seizure sensitive (SS) gerbils than in seizure resistant (SR) gerbils. P/Q-type VGCC immunoreactivity in the gerbil hippocampus was reduced by enhancement in GABA(A) and GABA(B) receptor-mediated transmission, but not by SST-mediated transmission. N-type VGCC immunoreactivity was reduced only by a SST agonist, whereas L-type (alpha1C) VGCC immunoreactivity was reduced only by a GABA(A) receptor agonist, and L-type (alpha1D) VGCC immunoreactivity was modulated by the GABA(B) receptor acting drugs. These findings provide a comprehensive description of the differential responses of VGCC subunits to alteration in GABAergic or somatostatinergic transmission. These findings also suggest that up-regulated VGCC immunoreactivity may be consequence of the neuronal excitability caused by a reduction in inhibitory neurotransmission in the gerbil hippocampus.
Kim
Duk-Soo
DS
Department of Anatomy, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.
Kwak
Sung-Eun
SE
Kim
Ji-Eun
JE
Kim
Jin-Sang
JS
Won
Moo Ho
MH
Kang
Tae-Cheon
TC
D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism; D020864:Calcium Channels, N-Type / Q000187:drug effects / Q000378:metabolism; D020865:Calcium Channels, P-Type / Q000187:drug effects / Q000378:metabolism; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004827:Epilepsy / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D004833:Epilepsy, Temporal Lobe / Q000378:metabolism / Q000503:physiopathology; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D005849:Gerbillinae; D006624:Hippocampus / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D007150:Immunohistochemistry; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D011963:Receptors, GABA-A / Q000378:metabolism; D017481:Receptors, Somatostatin / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D013004:Somatostatin / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D020864:Calcium Channels, N-Type; D020865:Calcium Channels, P-Type; D018755:GABA Agonists; D018756:GABA Antagonists; D058785:GABA-A Receptor Agonists; D058787:GABA-A Receptor Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D011963:Receptors, GABA-A; D017481:Receptors, Somatostatin; D013004:Somatostatin; D005680:gamma-Aminobutyric Acid