Abstract
Previous reports have demonstrated that glutamate stimulates c-fos mRNA expression in primary cultures of mouse cerebral cortical neurons. We show here that vasoactive intestinal peptide (VIP) induces c-fos mRNA expression; however, this effect of VIP is completely inhibited by the noncompetitive NMDA receptor antagonist MK-801, therefore indicating that VIP stimulates c- fos expression in a glutamate-dependent manner. A similar effect was observed with pituitary adenylate cyclase-activating polypeptide27 (PACAP27). At the intracellular level, coactivation of protein kinases A and C mediates the glutamate-dependent stimulation of c-fos expression evoked by VIP, because either H-89 or staurosporin inhibits the effect of VIP as well as that of glutamate. These results point to a 'biochemical AND gate' mechanism, which implies the obligatory activation of both protein kinases A and C in the transduction of c-fos expression. In summary, this article provides evidence that VIP and PACAP27 potentiate the effect of glutamate, the principal effector on c-fos expression, suggesting that both peptides can increase the 'throughput' or 'strength' of glutamate-containing circuits in the cerebral cortex.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1-9 |
| Number of pages | 9 |
| Journal | Journal of Neurochemistry |
| Volume | 65 |
| Issue number | 1 |
| State | Published - Jul 1995 |
| Externally published | Yes |
Keywords
- Cerebral cortex
- Glutamate
- Modulation
- Pituitary adenylate cyclase
- Vasoactive intestinal peptide
- activating polypeptide27
- c-fos
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Biochemistry