Early induction of secretoneurin expression following kainic acid administration at convulsant doses in the rat and gerbil hippocampus.
The expression of secretogranin-II and its major proteolytic product secretoneurin (SN) is under the control of neuronal excitation, as demonstrated by treating rats with the excitotoxic kainic acid (KA). Differences in the structure and function of the hippocampus in rats and gerbils have been described; these suggest possible differential reactive responses to KA. In the present study, the SN immunostaining pattern in relation with cell damage is analyzed from 6 h to 4 days following KA administration in rats and gerbils. Dramatic differences in the expression of SN were found in the hippocampal complex following KA administration in gerbils and rats. A robust increase in SN immunoreactivity was detected in the pyramidal cell layer of the rat hippocampus, especially in the CA1 area. In the gerbil, however, a strong increase in SN immunostaining was detected in interneurons of the hippocampal formation, as shown by double-labeling immunohistochemistry to SN and the calcium-binding proteins parvalbumin, calbindin, and calretinin. In addition, no damage (in the hippocampal formation) or moderate damage (in the entorhinal cortex) was observed in the gerbil, in contrast to the rat. The administration of KA and the GABA-B receptor inhibitors (CGP56999A or CGP36742) to the gerbil resulted in a strong rise in SN immunoreactitivty in the CA1 pyramidal cell layer of the hippocampus, as in the rat. However, no increased cell damage was observed under these conditions. The present data provide evidence of a species-differential reactive response to KA that might be based, in part, on distinct inhibitory intrahippocampal circuitry.
Marti
E
E
Laboratori de Neurobiologia Cellular i Molecular, Biologia Cellular i Anatomia Patològica Department, Facultat de Medicina, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain. emarti@iname.com
Blasi
J
J
Ferrer
I
I
D000818:Animals; D064032:Calbindin 2; D064026:Calbindins; D002864:Chromogranins; D003292:Convulsants; D004827:Epilepsy / Q000139:chemically induced / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists; D018756:GABA Antagonists / Q000494:pharmacology; D058788:GABA-B Receptor Antagonists; D005849:Gerbillinae; D006624:Hippocampus / Q000737:chemistry / Q000378:metabolism* / Q000503:physiopathology*; D007150:Immunohistochemistry; D007608:Kainic Acid; D009479:Neuropeptides / Q000032:analysis / Q000096:biosynthesis*; D009943:Organophosphorus Compounds / Q000494:pharmacology; D010320:Parvalbumins / Q000032:analysis; D010721:Phosphinic Acids / Q000494:pharmacology; D011506:Proteins / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D064030:S100 Calcium Binding Protein G / Q000032:analysis; D053381:Secretogranin II
C102659:CGP 56999A; C576512:Calb2 protein, rat; D064032:Calbindin 2; D064026:Calbindins; D002864:Chromogranins; D003292:Convulsants; D018690:Excitatory Amino Acid Agonists; D018756:GABA Antagonists; D058788:GABA-B Receptor Antagonists; D009479:Neuropeptides; D009943:Organophosphorus Compounds; D010320:Parvalbumins; D010721:Phosphinic Acids; D011506:Proteins; D064030:S100 Calcium Binding Protein G; D053381:Secretogranin II; C079148:(3-aminopropyl)(n-butyl)phosphinic acid; C081159:secretoneurin; D007608:Kainic Acid