GABAergic signaling induces divergent neuronal Ca2+ responses in the suprachiasmatic nucleus network

Robert P. Irwin, Charles N. Allen

Research output: Contribution to journalArticlepeer-review

67 Scopus citations


Intercellular communication between γ-aminobutyric acid (GABA)ergic suprachiasmatic nucleus (SCN) neurons facilitates light-induced phase changes and synchronization of individual neural oscillators within the SCN network. We used ratiometric Ca2+ imaging techniques to record changes in the intracellular calcium concentration ([Ca2+]i) to study the role of GABA in interneuronal communication and the response of the SCN neuronal network to optic nerve stimulations that mimic entraining light signals. Stimulation of the retinohypothalamic tract (RHT) evoked divergent Ca2+ responses in neurons that varied regionally within the SCN with a pattern that correlated with those evoked by pharmacological GABA applications. GABAA and GABAB receptor agonists and antagonists were used to evaluate components of the GABA-induced changes in [Ca2+]i. Application of the GABAA receptor antagonist gabazine induced changes in baseline [Ca2+]i in a direction opposite to that evoked by GABA, and similarly altered the RHT stimulation-induced Ca2+ response. GABA application induced Ca 2+ responses varied in time and region within the SCN network. The NKCC1 cotransporter blocker, bumetanide, and L-type calcium channel blocker, nimodipine, attenuated the GABA-induced rise of [Ca2+]i. These results suggest that physiological GABA induces opposing effects on [Ca2+]i based on the chloride equilibrium potential, and may play an important role in neuronal Ca2+ balance, synchronization and modulation of light input signaling in the SCN network.

Original languageEnglish (US)
Pages (from-to)1462-1475
Number of pages14
JournalEuropean Journal of Neuroscience
Issue number8
StatePublished - Oct 2009


  • Chloride cotransporter
  • Circadian rhythm
  • Retinohypothalamic tract
  • Synaptic transmission

ASJC Scopus subject areas

  • General Neuroscience


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