Abstract
We have demonstrated previously in primary cultures of mouse cerebellar granule cells (CGCs) that endogenously synthesized pituitary adenylate cyclase-activating polypeptide (PACAP) contributes at least in part to the activity-dependent survival of CGCs (Tabuchi et al. [2001] Neurosci. Res. 39:85-93). In this study, we have demonstrated that expression of vasoactive intestinal polypeptide (VIP), a member of the same VIP/secretin/glucagon family as PACAP, was activated markedly by Ca2+ influx through L-type voltage-dependent Ca2+ channels (L-VDCCs), which could be induced under the depolarizing condition induced by high concentration of potassium (K+) in the medium. The activation of VIP mRNA expression, different from that of PACAP, was dependent partly on de novo protein synthesis. On the other hand, mRNA expression of secretin and PACAP/VIP receptors (PAC 1, VPAC1, and VPAC2) was not activated by the Ca2+ influx; rather, PAC1 mRNA expression was reduced. Exogenously added VIP prevented apoptosis of CGCs under nondepolarizing conditions, the effect of which was mediated specifically through the VPAC 1 receptor. Furthermore, the survival of CGCs under depolarizing conditions could be mediated partly through VPAC1, the contribution of which was much less than that of PAC1. These findings indicate that PACAP and VIP genes are coordinately activated by the Ca2+ signals in CGCs, but the contribution of VIP to the activity-dependent survival of CGCs is quite small.
Original language | English |
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Pages (from-to) | 26-34 |
Number of pages | 9 |
Journal | Journal of Neuroscience Research |
Volume | 77 |
Issue number | 1 |
DOIs | |
State | Published - 2004/07/01 |
Keywords
- Calcium
- Cell survival
- Gene expression
- PACAP
- VIP
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience