Calbindin expression in the hamster SCN is influenced by circadian genotype and by photic conditions

LeSauter, Joseph; Stevens, Paula; Jansen, Heiko T.; Lehman, Michael N.; Silver, Rae

doi:10.1097/00001756-199910190-00007

Cited by 26 publications

(14 citation statements)

References 12 publications

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“…These findings reinforce previous observations that indicated a tendency for slightly larger phase delays in Calb1 −/− mice (Kriegsfeld et al, 2008), although in that study, CT16 was investigated for phase delays in contrast to CT14 in our study. Comparable to the results in mice, a role for CB in phase shifting was observed in hamsters (LeSauter et al, 1999). This correlation between our observation in mice and the one in hamsters would suggest similar functions of CB in both species.…”

Section: Discussionsupporting

confidence: 79%

Lack of Calbindin-D28k Alters Response of the Murine Circadian Clock to Light

Stadler

Schmutz

Schwaller

et al. 2010

Chronobiology International

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A strong stimulus adjusting the circadian clock to the prevailing light-dark cycle is light. However, the circadian clock is reset by light only at specific times of the day. The mechanisms mediating such gating of light input to the CNS are not well understood. There is evidence that Ca 2+ ions play an important role in intracellular signaling mechanisms, including signaling cascades stimulated by light. Therefore, Ca 2+ is hypothesized to play a role in the light-mediated resetting of the circadian clock. Calbindin-D28k (CB; gene symbol: Calb1) is a Ca 2+ binding protein implicated in Ca 2+ homeostasis and sensing. The absence of this protein influences Ca 2+ buffering capacity of a cell, alters spatio-temporal aspects of intracellular Ca 2+ signaling, and hence might alter transmission of light information to the circadian clock in neurons of the suprachiasmatic nuclei (SCN). We tested mice lacking a functional Calb1 gene (Calb1 −/−) and found an increased phase-delay response to light applied at circadian time (CT) 14 in these animals. This is accompanied by elevated induction of Per2 gene expression in the SCN. Period length and circadian rhythmicity were comparable between Calb1 −/− and wild-type animals. Our findings indicate an involvement of CB in the signaling pathway that modulates the behavioral and molecular response to light.

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Section: Discussionsupporting

confidence: 79%

Lack of Calbindin-D28k Alters Response of the Murine Circadian Clock to Light

Stadler

Schmutz

Schwaller

et al. 2010

Chronobiology International

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“…There is some evidence that photic input reaches the CaBP perikarya: (1) Light exposure at circadian time (CT) 18 induces Fos protein expression in 79% of the CaBP-ir cells within the subnucleus; (2) Hamsters housed in constant darkness for 7 weeks show a significant increase in the number of CaBP-ir perikarya. This effect of housing in DD is more pronounced in Tau mutant hamsters (LeSauter et al, 1996b) and correlates with the greater phase-shifting effects of light in the mutant (Grosse et al, 1995). In summary, evidence from light-induced Fos, lesion, and transplantation studies is consistent with the suggestion that cells of the CaBP subregion are the locus of circadian pacemakers regulating entrained and free-running locomotor rhythms.…”

supporting

confidence: 68%

Retinal Innervation of Calbindin-D28K Cells in the Hamster Suprachiasmatic Nucleus: Ultrastructural Characterization

et al. 2000

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The authors have described a subregion of the hamster hypothalamic suprachiasmatic nucleus (SCN) containing cells that are immunopositive for the cytosolic calcium-binding protein, Calbindin-D 28K (CaBP). Several lines of evidence indicate that this region may constitute the site of the pacemaker cells that are responsible for the regulation of circadian locomotor rhythms. First, 79% of the CaBP-immunoreactive (ir) neurons express Fos in response to photic stimulation, indicating that they are close to or part of the input pathway to pacemakers. Second, at the light microscopy level, retinal terminals innervate the CaBP subnucleus. Finally, destruction of this subnucleus renders animals arrhythmic in locomotor activity. In this study, the authors examined the ultrastructural relationship between cholera toxin (CTβ) labeled retinal fibers and the CaBP-ir subregion within the hamster SCN. CTβ-ir retinal terminals make primarily axo-somatic, symmetric, synaptic contacts with CaBP-ir perikarya. In addition, retinal terminals form synapses with CaBP processes as well as with unidentified profiles. There are also complex interactions between retinal terminals, CaBP perikarya, and unidentified profiles. Given that axo-somatic synaptic input has a more potent influence on a cell's electrical activity than does axo-dendritic synaptic input, cells of the CaBP subregion of the SCN are ideally suited to respond rapidly to photic stimulation to reset circadian pacemakers.Keywords calcium-binding proteins; calbindin-D 28K ; CaBP; pacemaker; suprachiasmatic nucleus; retinal terminals; electron microscopy; circadian rhythmsThe suprachiasmatic nucleus (SCN) of the hypothalamus is the site of the putative circadian clock in mammals (see Klein et al., 1991). The circadian system regulates the periodicity of many rhythmic responses in mammals including rest-wake cycles (see Moore-Ede et al., 1982), electrical activity, and neuropeptide levels (Inouye, 1996), to name a few. In the absence of exogenous stimuli, the circadian clock oscillates with a periodicity that is close to 24 h. The circadian timing system also has the capacity to entrain or synchronize the organism to the exogenous geo-solar cycle. The primary neural substrate responsible for the © 2000 Sage Publications, Inc.Correspondence to: Maria-Teresa Romero. transduction of exogenous photic stimuli is the retinohypothalamic tract (RHT), a monosynaptic pathway projecting from the retina to the SCN (Card and Moore, 1991;Moore, 1996). A secondary pathway, the geniculo-hypothalamic tract, also provides photic input to the circadian pacemaker. Photic information is integrated in the SCN to produce a stable phase relationship between physiological and behavioral activity and the environmental light-dark cycle (Meijer, 1991). While it is clear that the SCN is the site of the circadian pacemaker, the precise identity of retinorecipient cells that mediate entrainment remains to be elucidated. NIH Public AccessWe recently described cells immunopositive for Calbindin-D 28K (...

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“…However, the distribution of many neuropeptides and other chemical markers allows recognition of a similar suprachiasmatic 'nucleus' in gymnophionans that topologically corresponds to its counterparts in other vertebrates. The content of CBPs, particularly CB, in the suprachiasmatic nucleus has been related to the control of circadian rhythms [LeSauter et al, 1999;Arvanitogiannis et al, 2000;Bryant et al, 2000;LeSauter et al, 2009;Stadler et al, 2010]. This nucleus is the primary circadian pacemaker that reinforces their oscillations and synchronizes its components in response to light input [Welsh et al, 2010].…”

Section: Nontelencephalic Secondary Prosencephalon and Hypothalamusmentioning

confidence: 99%

Localization of Calbindin-D28k and Calretinin in the Brain of Dermophis Mexicanus (Amphibia: Gymnophiona) and Its Bearing on the Interpretation of Newly Recognized Neuroanatomical Regions

Morona¹,

López²,

González³

2011

Brain Behav Evol

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The analysis of the distribution of the calbindin-D28k and calretinin immunoreactive (CBir and CRir) systems recently described in the brain of anuran and urodele amphibians was very useful for the interpretation of many otherwise indistinct brain regions and cell masses. In the present study we have followed a similar approach to investigate the distribution of CBir and CRir cell bodies and fibers in the brain of Dermophis mexicanus, a member of the much neglected third amphibian order of gymnophionans. The pattern of distribution obtained showed particular characteristics in Dermophis, such as the existence of abundant CRir elements in the olfactory bulbs and CBir and CRir cell populations in pallial areas. The distinct distribution of the two proteins allowed the tentative identification of currently described subregions, mainly in the amygdaloid complex and hypothalamic areas. The analysis of the diencephalon and brainstem distribution framed in the neuromeric model highlighted common traits with other amphibians but also specific features. Therefore, the immunohistochemical detection of calcium-binding proteins has served to discern cell populations and has helped to demonstrate neuronal heterogeneity. However, it should be pointed out that a straightforward comparison based only on the presence of these proteins should not be made due to the great variability observed in well-established homologous regions in the brain of different vertebrates, as evidenced within the class Amphibia.

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Calbindin expression in the hamster SCN is influenced by circadian genotype and by photic conditions

Cited by 26 publications

References 12 publications

Lack of Calbindin-D28k Alters Response of the Murine Circadian Clock to Light

Lack of Calbindin-D28k Alters Response of the Murine Circadian Clock to Light

Retinal Innervation of Calbindin-D28K Cells in the Hamster Suprachiasmatic Nucleus: Ultrastructural Characterization

Localization of Calbindin-D28k and Calretinin in the Brain of Dermophis Mexicanus (Amphibia: Gymnophiona) and Its Bearing on the Interpretation of Newly Recognized Neuroanatomical Regions

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