Early induction of secretoneurin expression following kainic acid administration at convulsant doses in the rat and gerbil hippocampus

Abstract

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.

Species-Difference of Cyclooxygenase-2 in the Hippocampus of Rodents

“…It has been reported that neuronal COX-2 transgenic mice are more susceptible to kainic acid excitotoxicity [7]. This result is supported by previous studies that the extent of neuronal damage in gerbils induced by kainic acid was minor when compared with that of the rat [3,12]. In addition, differential expression patterns for caspases and transcription factor c-fos were recently described in the rat and gerbil, following systemic administration of kainic acid [3]: similar distribution pattern of caspase and c-fos was observed in kainic acid treated gerbils and rats although minimized in gerbils.…”

Secretoneurin: A New Player in Angiogenesis and Chemotaxis Linking Nerves, Blood Vessels and the Immune System

“…In contrast to immediate-early gene expression, ProSN mRNA levels may better reflect specific changes in neuronal secretory activity associated with transmitter release and detect also those coupled to a decreased activity. amphetamine rat striatum +50% [81] phencyclidine rat prefrontal cortex increase [82] lithium differentiated PC12 +60% [83] haloperidol, clozapine rat striatum, raphe +290% [66] clozapine rat prefrontal cortex increase [84] citalopram rat zona inserta +50% [66] kainate rat hippocampus increase [85] kainate rat, gerbil hippocampus increase [86] kainate rat hippocampus +600% [87] kainate rat hippocampus +600% [88] reserpine rat adrenal medulla +150% [89] reserpine rat hypothalamus, brain stem +250% [90] histamine bovine chromaffin cells +400% [91] nicotine, prostaglandin E bovine chromaffin cells +330% [33,69] PACAP bovine chromaffin cells +60% [69,92] amphoterin (RAGE receptor agonist) mouse neuroblastoma cells +350% [93] hormones/trophic factors: estrogen male rat pituitary +155% [94] estrogen female rat hypothalamus +350% [95] adrenalectomy rat hypothalamus +380% [96] lactation rat hypothalamus +240% [96] ovariectomy female rat pituitary +300% [95,97] NGF rat PC12 cells +460% [98] bFGF human neuroblastoma cells +420% [99] EGF GH4 pituitary tumor cells +600% [100] interleukin 1 bovine chromaffin cells +230% [101] TNF-α bovine chromaffin cells +300% [101] hypoxia:…”

Secretoneurin promotes neuroprotection and neuronal plasticity via the Jak2/Stat3 pathway in murine models of stroke

“…Although several articles have reported a correlation between SN and neurological diseases including Alzheimer disease (3)(4)(5), Parkinson disease (8), and epilepsy (9,10), little literature has examined the role of SN in stroke (7). Human stroke is a leading cause of death and disability worldwide (11), and as yet there is no effective treatment that enhances stroke recovery.…”