Autoradiographic localization of 2-[125I]iodomelatonin binding sites in the brains of C3H/HeN and C57BL/6J strains of mice

Siuciak, Judith A.; Fang, Junming; Dubocovich, Margarita L.

doi:10.1016/0014-2999(90)90328-4

Cited by 69 publications

(44 citation statements)

References 8 publications

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“…These observations suggest the presence of functional melatonin receptors in the SCN of both mice strains. Indeed, we and others (Siuciak et al 1990) found similar time-dependent patterns of 125 I-melatonin (Mel) binding in the SCN of both mice strains (C. von Gall, H.-W. Korf, J.H. Stehle, unpublished).…”

Section: Melatonin and Signalling Events In The Endogenous Oscillatorsupporting

confidence: 62%

Organisation of the circadian system in melatonin-proficient C3H and melatonin-deficient C57BL mice: a comparative investigation

2002

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In all vertebrates melatonin is rhythmically synthesised in the pineal gland and functions as a hormonal message encoding for the duration of darkness. This review focuses on the role of melatonin in the circadian organisation of mammals by comparing signal transduction mechanisms in the pineal organ, the suprachiasmatic nucleus and the hypophyseal pars tuberalis in melatonin-proficient (C3H) and melatonin-deficient (C57BL) mice strains. Surprisingly, the major signal transduction cascades in the pineal organ did not differ between the two mouse strains. With regard to the suprachiasmatic nucleus, the site of the endogenous clock, it was found that melatonin at most sets the gain for clock error signals mediated via the retinohypothalamic tract, but has no effect on the rhythm generation itself or on the maintenance of the oscillation. In contrast, melatonin plays an essential role in the control of the hypophyseal pars tuberalis. Here it acts in concert with adenosine to elicit rhythms in clock gene expression. Melatonin opens a temporally restricted gate for adenosine to induce cyclic AMP (cAMP)-sensitive genes by sensitising the adenylyl cyclase. This interaction, which grants a temporally precise regulation of gene expression, may reflect the central role of melatonin, i.e. in synchronising peripheral clock cells that require unique phasing of output signals with the master clock in the brain.

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Section: Melatonin and Signalling Events In The Endogenous Oscillatorsupporting

confidence: 62%

Organisation of the circadian system in melatonin-proficient C3H and melatonin-deficient C57BL mice: a comparative investigation

2002

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“…Because C57BL/6J mice are known to express melatonin receptors in the PT (29,30), we next examined the effect of melatonin injections on gene expression in C57BL/6J mice to test whether C57BL/6J mice are capable of responding to the melatonin signal. As a result, expression of TSHB, CGA, and DIO2 was suppressed, whereas DIO3 expression was induced by melatonin administration (Mann-Whitney U test, P Ͻ 0.05, n ϭ 4-5; Fig.…”

Section: Resultsmentioning

confidence: 99%

Involvement of thyrotropin in photoperiodic signal transduction in mice

Ono¹,

Hoshino²,

Yasuo

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

250

241

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Local thyroid hormone catabolism within the mediobasal hypothalamus (MBH) by thyroid hormone-activating (DIO2) and -inactivating (DIO3) enzymes regulates seasonal reproduction in birds and mammals. Recent functional genomics analysis in birds has shown that long days induce thyroid-stimulating hormone production in the pars tuberalis (PT) of the pituitary gland, which triggers DIO2 expression in the ependymal cells (EC) of the MBH. In mammals, nocturnal melatonin secretion provides an endocrine signal of the photoperiod to the PT that contains melatonin receptors in high density, but the interface between the melatonin signal perceived in the PT and the thyroid hormone levels in the MBH remains unclear. Here we provide evidence in mice that TSH participates in this photoperiodic signal transduction. Although most mouse strains are considered to be nonseasonal, a robust photoperiodic response comprising induced expression of TSHB (TSH ␤ subunit), CGA (TSH ␣ subunit), and DIO2, and reduced expression of DIO3, was observed in melatonin-proficient CBA/N mice. These responses could not be elicited in melatonin-deficient C57BL/6J, but treatment of C57BL/6J mice with exogenous melatonin elicited similar effects on the expression of the abovementioned genes as observed in CBA/N after transfer to short-day conditions. The EC was found to express TSH receptor (TSHR), and ICV injection of TSH induced DIO2 expression. Finally, we show that melatonin administration did not affect the expression of TSHB, DIO2, and DIO3 in TSHR-null mice. Taken together, our findings suggest that melatonin-dependent regulation of thyroid hormone levels in the MBH appears to involve TSH in mammals.circadian rhythm ͉ melatonin ͉ pars tuberalis ͉ photoperiodism ͉ type 2 and 3 iodothyronine deiodinases O rganisms living outside the tropics detect and predict seasonal changes in day length (photoperiod) to adapt various metabolic and behavioral functions to the environment. This mechanism, called photoperiodism, allows animals to control the timing of reproduction so that they can raise their offspring in spring and summer when food is most abundant. Among vertebrates, birds possess a highly sophisticated photoperiodic mechanism and show robust responses to photoperiodic changes. Taking advantage of the elaborate avian photoperiodic system, we have recently revealed the gene cascade regulating the photoperiodic response of reproduction in Japanese quail (Coturnix japonica) by using a functional genomics approach (1, 2). Exposure to long days induced thyroid-stimulating hormone (TSH), a heterodimer of the TSH ␤ subunit (TSHB), and the common glycoprotein ␣ subunit (CGA, also called TSH ␣ subunit), in the pars tuberalis (PT) of the pituitary gland. TSH triggers the expression of type 2 iodothyronine deiodinase (DIO2) in the ependymal cells (EC) lining the ventrolateral walls of the third ventricle (i.e., the infundibular recess) within the mediobasal hypothalamus (MBH). DIO2 is a thyroid hormoneactivating enzyme that converts the prohormone thyroxine...

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“…Luzindol, however, was ineffective at any of the times investigated in the C57BL/6J and ND/4 ). Melatonin binding sites show some differences between the C3H/HeN and C57BL/ 6J (Siuciak et al 1990). This may be secondary in importance to a naturally occurring mutation in Nacetyltransferase which is present in a number of inbred strains, including the C57BL/6J, but not in the C3H/HeJ.…”

Section: Gaba B Receptorsmentioning

confidence: 97%

Feeling Strained? Influence of Genetic Background on Depression-Related Behavior in Mice: A Review

2006

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Depression is a growing pandemic in developed societies. The use of inbred mouse strains in pre-clinical psychiatric research has proven to be a valuable resource. Firstly, they provide the background for genetic manipulations that aid in the discovery of molecular pathways that may be involved in major depression. Further, inbred mouse strains are also being used in the determination of genetic and environmental influences that may pre-dispose or trigger depression-related behavior. This review aims to highlight the utility of inbred mouse strains in depression research, while providing an overview of the current state of research into behavioral differences between strains in paradigms commonly used in the field. Neurochemical differences that may underlie strain differences are examined, and some caveats and cautions associated with the use of inbred strains are highlighted.

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Autoradiographic localization of 2-[125I]iodomelatonin binding sites in the brains of C3H/HeN and C57BL/6J strains of mice

Cited by 69 publications

References 8 publications

Organisation of the circadian system in melatonin-proficient C3H and melatonin-deficient C57BL mice: a comparative investigation

Organisation of the circadian system in melatonin-proficient C3H and melatonin-deficient C57BL mice: a comparative investigation

Involvement of thyrotropin in photoperiodic signal transduction in mice

Feeling Strained? Influence of Genetic Background on Depression-Related Behavior in Mice: A Review

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