Phase delays to light and gastrin-releasing peptide require the protein kinase A pathway

Roxanne Sterniczuk, Glenn R. Yamakawa, Tara Pomeroy, Michael C. Antle

Research output: Contribution to journalArticleResearchpeer-review

5 Citations (Scopus)


Daily photic resetting of the circadian system relies on the transmission of light information from the retina to retinorecipient cells within the ventrolateral suprachiasmatic nucleus (SCN) core, and subsequent activation of rhythmic clock cells in the dorsolateral region. Some neurochemicals such as gastrin-releasing peptide (GRP) mimic the phase shifting effects of light and induce Ca2+-dependent gene expression in the SCN. Activation of the cAMP-response element binding protein (CREB) is necessary for Ca2+-dependent transcription to occur and accompanies behavioral phase shifting; however, several biochemical cascades are involved in this phenomenon. One pathway that has been implicated in photic responses involves protein kinase A (PKA). It is not known if this pathway participates in mediating phase shifts to GRP. Here we show that preventing PKA activation attenuates both light- and GRP-induced phase shifts in locomotor behavior, but only during the early-subjective night. This finding demonstrates that activation of PKA is an important component in the photic signaling pathway and may mediate GRP output signaling from the SCN core to the shell; however, this effect appears to be temporally dependent.

Original languageEnglish
Pages (from-to)24-29
Number of pages6
JournalNeuroscience Letters
Publication statusPublished - 24 Jan 2014
Externally publishedYes


  • Gastrin-releasing peptide
  • KT5720
  • Light
  • Neuropeptide
  • Photic phase shifting
  • Suprachiasmatic nucleus

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