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Lack of light-induced elevation of renal sympathetic nerve activity and plasma corticosterone levels in PACAP-deficient mice. |
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Notes for this articleAuthors report that PACAP KO mice fail to show the expected increase in renal sympathetic nerve activity, circulating corticosterone (plasma), and cFOS expression in SCN.
This finding is similar to the VIP KO model, which also shows deficits in the light-responsive pathways. Unfortunately, it does not bring us any closer to determining whether the presence of these neuropeptides is crucial in the brain or in the peripheral nervous system.
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AbstractPACAP is a neurotransmitter involved in the signal transduction of light stimulation in the suprachiasmatic nucleus (SCN). Light stimulation affects autonomic nerve activity via the SCN, and here we tested whether PACAP participates in light-induced regulation of sympatho-adrenal activity by using PACAP-deficient (Adcyap1(-/-)) mice. Light stimulation (100 lux, 30min) significantly elevated both renal sympathetic nerve activity (RSNA), which was monitored on a digital oscilloscope, and plasma corticosterone levels in wild-type mice, but both responses were almost abolished in Adcyap1(-/-) mice. Although light-induced c-Fos expression in the SCN was observed in both genotypes, the numbers of c-Fos positive cells were significantly decreased in Adcyap1(-/-) mice. These data suggest that PACAP signaling pathway is involved in light-induced stimulation of RSNA and plasma corticosterone release through SCN of brain.
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