Abstract
Previous studies have suggested a role for histamine in mediating effects of light on rodent circadian systems. We combined behavioural and neuroanatomical studies to analyze the potential role of histamine in circadian rhythm regulation of Syrian hamsters. The effects of histamine and the selective H2 receptor agonist dimaprit on free-running locomotor activity rhythms were monitored. In addition, histamine projections were mapped immunohistochemically. Histamine (0.5 μ1 of 1 mM) microinjected into the region of the suprachiasmatic nucleus induced very small delay phase-shifts, which were significantly greater than those elicited by vehicle at Circadian time (CT) 18. No other significant differences were observed. Dimaprit (0.5 μ1 of 1 mM) microinjected into the region of the suprachiasmatic nucleus at CT 6 and CT 18, induced very small phase-shifts which were significantly different from the effects of vehicle, but did not resemble those of light. Numerous cell bodies immunopositive for histamine were found in the tuberomammillary nucleus of the posterior hypothalamus, while histamine immunoreactive fibres were seen in the periventricular nucleus and paraventricular nucleus of the anterior hypothalamus. The suprachiasmatic nuclei were largely devoid of immunostaining. Finally, preliminary electrophysiological studies demonstrated that ionophoretic application of histamine and the H2 receptor agonist dimaprit elicit inconsistent and weak responses in the hamster suprachiasmatic nucleus in vitro. The results presented here show that microinjections of HA or dimaprit into the SCN region do not mimic the effects of light on hamster circadian rhythms, and the SCN of the Syrian hamster is almost devoid of histaminergic fibres. These studies suggest that histamine does not play a prominent role in circadian rhythm regulation in this species.
Original language | English |
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Pages (from-to) | 1-9 |
Number of pages | 9 |
Journal | Brain Research |
Volume | 783 |
Issue number | 1 |
DOIs | |
Publication status | Published - Feb 2 1998 |
Bibliographical note
Funding Information:This research was supported by grants from the US Air Force Office of Scientific Research (F49620-96-1-0038) and the Natural Sciences and Engineering Research Council of Canada (A0305) to BR and by a grant from the Medical Research Council (MRC) of Canada (MT11312) to KS. HDP was supported by an MRC Postdoctoral Fellowship. We are grateful to Donna Goguen, Victoria Muise, and Joan Burns for their excellent technical assistance.
ASJC Scopus Subject Areas
- General Neuroscience
- Molecular Biology
- Clinical Neurology
- Developmental Biology
PubMed: MeSH publication types
- Journal Article
- Research Support, Non-U.S. Gov't
- Research Support, U.S. Gov't, Non-P.H.S.