Investigation of circadian rhythms in a genetically anophthalmic mouse strain: Correlation of activity patterns with suprachiasmatic nuclei hypogenesis

Scheuch, George C.; Johnson, Wayne; Conner, Robert L.; Silver, Jerry

doi:10.1007/bf00619149

Cited by 24 publications

(6 citation statements)

References 17 publications

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“…The techniques of induced mutagenesis and modem molecular genetics have yielded remarkable results identifying genetic loci that affect pacemaker behavior in Drosophila and Neurospora (for review, see Hall and Rosbash, 1987). "Clock mutations" in rodents are also known: there are congenitally anophthalmic rats (Richter, 197 1;Ibuka, 1987) and mice (Scheuch et al, 1982;Gattermann et al, 1987) that do not entrain to light-dark (LD) cycles, mice with hypogenesis of the SCN that show disorganized circadian locomotor rhythmicity (Scheuch et al, 1982;Noguchi et al, 1986), mice that do not synthesize pineal melatonin (Ebihara et al, 1987) and golden hamsters with a mutation that shortens their pacemaker's free-running circadian period (Ralph and Menaker, 1988). Natural genetic differences (polymorphisms) manifested by inbred strains of rodents also suggest that genetic background affects circadian rhythmicity (e.g., Ebihara et al, 1978;Oliverio and Malomi, 1979;Possidente and Hegmann, 1980;Connolly and Lynch, 198 1;Peleg et al, 1982;Btittner and Wollnik, 1984;Beau, 1988) but more work is needed in this area.…”

Section: Circadianmentioning

confidence: 99%

Circadian timekeeping in BALB/c and C57BL/6 inbred mouse strains

1990

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Circadian rhythms of locomotion (wheel-running activity) in 12 inbred mouse strains were recorded for interstrain differences in tau DD, the endogenous (free-running) period of the circadian pacemaker measured in constant environmental darkness. The results indicate that 1 or more genetic loci influence the value of tau DD, and a large (50 min) difference in mean tau DD between 2 of the strains, BALB/cByJ and C57BL/6J, allowed further characterization of the origins and inheritance of the polymorphic expression of this circadian pacemaker property. The interstrain difference in mean tau DD was associated with an interstrain difference in light-induced shifts of the phase of the free-running locomotor rhythm; the BALB/c strain (with the shorter mean tau DD) displayed relatively fewer advance phase shifts. Neither the history of previous light exposure, albinism, nor elevated circulating testosterone levels could account for the interstrain difference in mean tau DD. The value of tau DD based on the circadian rhythm of drinking activity (with the running wheel removed) was longer than that based on locomotion; this discrepancy was significantly greater and more variable in BALB/c than in C57BL/6 mice, though the interstrain difference in mean tau DD could not be attributed entirely to this effect. Reciprocal F1 hybrids of BALB/c x C57BL/6 matings revealed dominance of the C57BL/6 genotype, no sex linkage, and a significant (but small) maternal effect. Examination of CXB recombinant inbred strains provided no support for the hypothesis of monogenic inheritance. Further study of inherited differences in the BALB/c and C57BL/6 strains may be a useful noninvasive experimental approach for investigation of the neurobiological substrates of circadian rhythmicity.

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Section: Circadianmentioning

confidence: 99%

Circadian timekeeping in BALB/c and C57BL/6 inbred mouse strains

1990

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“…mutant mice. Subsequent experiments by Scheuch and coworkers did show, however, that anophthalmic mice often exhibit varying degrees of hypogenesis of the SCN (21). Animals with substantial SCN hypogenesis showed abnormal circadian rhythmicity.…”

Section: Eocp In Vertebrates 149mentioning

confidence: 90%

“…For example, a genetically anophthalmic mouse strain (ZRDCT-An) is characterized by abnormalities in several brain areas, including the suprachiasmatic nucleus (SCN) (21). Moreover, heterozygous mice of this anophthalmic strain, with normal visual perception, are nevertheless unable to entrain to a light-dark cycle (22).…”

Section: Mutant Strainsmentioning

confidence: 99%

“…Thus, as with organ excision, genetic mutation may potentially have an impact on noncircadian physiology and behavior that may feed back directly or indirectly on the circadian timing system. For example, Scheuch and coworkers found wide interindividual variation in the circadian activity cycles of their anophthalmic mice that could not always be traced to neuroanatomical abnormalities (21).…”

Section: Mutant Strainsmentioning

confidence: 99%

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Extraocular Phototransduction and Circadian Timing Systems in Vertebrates

Campbell

Murphy

Suhner

2001

Chronobiology International

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It is widely accepted that, for organisms with eyes, the daily regulation of circadian rhythms is made possible by light transduction through those organs. Yet, it has been demonstrated repeatedly in recent years that ocular light receptors that mediate vision, at least in mammals, are not the same photoreceptors involved in circadian regulation. Moreover, it has been recognized for many years that circadian regulation can occur in organisms without eyes. In fact, extraocular circadian phototransduction (EOCP) appears to be a phylogenetic rule for the vast majority of species. EOCP has been reported in every nonmammalian species studied to date. In mammals, however, the story is very different. This paper presents findings from studies that have examined specifically the capacity for EOCP in vertebrate species. In addition, the literature addressing noncircadian aspects of extraocular phototransduction is briefly discussed. Finally, possible mechanisms underlying EOCP are discussed, as are some of the implications of the presence, or absence, of EOCP across phylogeny.

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“…Instead, per 01 could have been brain damaged such that the neural substrates of the rhythmic attributes formed abnormally or not at all. In this regard, it is well known that physical destruction of a pacemaker structure in the mammalian brain leads to arrhythmic locomotion (see, e.g., Weaver 1998), which also can result from neuroanatomical injury caused by a mutation (see, e.g., Scheuch et al 1982).…”

Section: The Power and Problems Associated With Multiple Alleles At Rmentioning

confidence: 99%

Principles and Problems Revolving Round Rhythm-related Genetic Variants

Hall¹,

Chang²,

Doleželová³

2007

Cold Spring Harbor Symposia on Quantitative Biology

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Much of what is known about the regulation of circadian rhythms has stemmed from the induction, recognition, or manufacture of genetic variants. Such investigations have been especially salient in chronobiological analyses of Drosophila. Many starting points for elucidation of rhythmic processes operating in this insect entailed the isolation of mutants or the design of engineered gene modifications. Various features of the principles and practices associated with the genetic approach toward understanding clock functions, and chronobiologically related ones, are discussed from perspectives that are largely genetic as such, although intertwined with certain neurogenetic and molecular-genetic concerns when appropriate. Key themes in this treatment connect with the power and problems associated with multiply mutant forms of rhythm-related genes, with the opportunistic or problematical aspects of multigenic variants that are in play (sometimes surprisingly), and with a question as to how forceful chronogenetic inferences have been in terms of elucidating the mechanisms of circadian pacemaking.What'dya say we bust up this joint?Rodney Dangerfield (1980) Cold Spring Harbor Symposia on Quantitative Biology, Volume LXXII.

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Investigation of circadian rhythms in a genetically anophthalmic mouse strain: Correlation of activity patterns with suprachiasmatic nuclei hypogenesis

Cited by 24 publications

References 17 publications

Circadian timekeeping in BALB/c and C57BL/6 inbred mouse strains

Circadian timekeeping in BALB/c and C57BL/6 inbred mouse strains

Extraocular Phototransduction and Circadian Timing Systems in Vertebrates

Principles and Problems Revolving Round Rhythm-related Genetic Variants

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