QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, October 24, 2007, 27(43):11748-11757; doi:10.1523/JNEUROSCI.1840-07.2007

This Article Full Text Full Text (PDF) Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Irwin, R. P. Articles by Allen, C. N. Search for Related Content PubMed PubMed Citation Articles by Irwin, R. P. Articles by Allen, C. N.

 Previous Article  |  Next Article 

Behavioral/Systems/Cognitive
Calcium Response to Retinohypothalamic Tract Synaptic Transmission in Suprachiasmatic Nucleus Neurons

Robert P. Irwin and Charles N. Allen

Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, Portland, Oregon 97239

Correspondence should be addressed to Dr. Robert P. Irwin, Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, L-606, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239. Email: irwinr{at}ohsu.edu

Glutamate released from retinohypothalamic tract (RHT) synapses with suprachiasmatic nucleus (SCN) neurons induces phase changes in the circadian clock presumably by using Ca²⁺ as a second messenger. We used electrophysiological and Ca²⁺ imaging techniques to simultaneously record changes in the membrane potential and intracellular calcium concentration ([Ca²⁺]_i) in SCN neurons after stimulation of the RHT at physiologically relevant frequencies. Stimulation of the RHT sufficient to generate an EPSP did not produce detectable changes in [Ca²⁺]_i, whereas EPSP-induced action potentials evoked an increase in [Ca²⁺]_i, suggesting that the change in postsynaptic somatic [Ca²⁺]_i produced by synaptically activated glutamate receptors was the result of membrane depolarization activating voltage-dependent Ca²⁺ channels. The magnitude of the Ca²⁺ response was dependent on the RHT stimulation frequency and duration, and on the SCN neuron action potential frequency. Membrane depolarization-induced changes in [Ca²⁺]_i were larger and decayed more quickly in the dendrites than in the soma and were attenuated by nimodipine, suggesting a compartmentalization of Ca²⁺ signaling and a contribution of L-type Ca²⁺ channels.

RHT stimulation at frequencies that mimicked the output of light-sensitive retinal ganglion cells (RGCs) evoked [Ca²⁺]_i transients in SCN neurons via membrane depolarization and activation of voltage-dependent Ca²⁺ channels. These data suggest that for Ca²⁺ to induce phase advances or delays, light-induced signaling from RGCs must augment the underlying oscillatory somatic [Ca²⁺]_i by evoking postsynaptic action potentials in SCN neurons during a period of slow spontaneous firing such as occurs during nighttime.

Key words: circadian rhythm; suprachiasmatic nucleus; action potential; retinal ganglion cells; synaptic transmission; calcium

---

Received April 23, 2007; revised Aug. 16, 2007; accepted Sept. 12, 2007.

Correspondence should be addressed to Dr. Robert P. Irwin, Center for Research on Occupational and Environmental Toxicology, Oregon Health & Science University, L-606, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239. Email: irwinr{at}ohsu.edu

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help