Abstract

Acetylcholine (ACh) was the first neurotransmitter identified as a regulator of mammalian circadian rhythms. When injected in vivo, cholinergics induced biphasic clock resetting at night, similar to nocturnal light exposure. However, the retinohypothalamic tract connecting the eye to the suprachiasmatic nucleus (SCN) uses glutamate (GLU) to transmit light signals. We here resolve this long-standing paradox. Whereas injection of the cholinergic agonist, carbachol, into the mouse ventricular system in vivo induced light-like effects, direct application to the SCN in vitro or in vivo induced a distinct response pattern: phase advance of circadian rhythms throughout the nighttime. These results indicate that a new regulatory pathway, involving an extra-SCN cholinergic synapse accessible via ventricular injection, mediates the light-like cholinergic clock resetting reported previously.

Original languageEnglish (US)
Pages (from-to)489-496
Number of pages8
JournalExperimental Neurology
Volume193
Issue number2
DOIs
StatePublished - Jun 2005

Fingerprint

Carbachol
Circadian Rhythm
Suprachiasmatic Nucleus
Cholinergic Agents
Light
Cholinergic Agonists
Injections
Synapses
Acetylcholine
Neurotransmitter Agents
Glutamic Acid

Keywords

  • Acetylcholine
  • Carbachol
  • Circadian clock
  • Glutamate
  • Mouse
  • Suprachiasmatic nucleus

ASJC Scopus subject areas

  • Neurology
  • Neuroscience(all)

Cite this

New light on an old paradox : Site-dependent effects of carbachol on circadian rhythms. / Buchanan, Gordon F.; Gillette, Martha U.

In: Experimental Neurology, Vol. 193, No. 2, 06.2005, p. 489-496.

Research output: Contribution to journalArticle

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