Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Calbindins”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,225 records · Page 68Linked to original sources
PubMed2006

Separate neurochemical classes of sympathetic postganglionic neurons project to the left ventricle of the rat heart.

The sympathetic innervation of the rat heart was investigated by retrograde neuronal tracing and multiple label immunohistochemistry. Injections of Fast Blue made into the left ventricular wall labelled sympathetic neurons that were located along the medial border of both the left and right stellate ganglia. Cardiac projecting sympathetic postganglionic neurons could be grouped into one of four neurochemical populations, characterised by their content of calbindin and/or neuropeptide Y (NPY). The subpopulations of neurons contained immunoreactivity to both calbindin and NPY, immunoreactivity to calbindin only, immunoreactivity to NPY only and no immunoreactivity to calbindin or NPY. Sympathetic postganglionic neurons were also labelled in vitro with rhodamine dextran applied to the cut end of a cardiac nerve. The same neurochemical subpopulations of sympathetic neurons were identified by using this technique but in different proportions to those labelled from the left ventricle. Preganglionic terminals that were immunoreactive for another calcium-binding protein, calretinin, preferentially surrounded retrogradely labelled neurons that were immunoreactive for both calbindin and NPY. The separate sympathetic pathways projecting to the rat heart may control different cardiac functions.

Amidines↗
PubMed1992

Convergence and segregation of septal and median raphe inputs onto different subsets of hippocampal inhibitory interneurons.

The convergence and segregation of medial septal and median raphe afferents in the innervation of different subpopulations of GABAergic interneurons was investigated in the rat hippocampal formation. Following local injections of 5,7-dihydroxytryptamine into the median raphe nucleus destroying all serotonergic neurons, iontophoretic injections of Phaseolus vulgaris leucoagglutinin (PHAL) into the medial septum resulted in anterograde labelling of axons in the hippocampus. The labelled varicose fibres made multiple contacts with calbindin D28K-, parvalbumin-, and cholecystokinin-immunoreactive interneurons. These results disproved the possibility that PHAL-labelled afferents innervating hippocampal interneurons following septal PHAL injections would have been raphe axons passing through the injection site. In the second set of experiments a double anterograde tracing technique (PHAL from the septum and biotinylated-PHAL from the median raphe) and a triple or double immunostaining procedure was used to determine the types of interneurons (calbindin D28K-, parvalbumin-, or cholecystokinin-immunoreactive) innervated by one, or the other, or both pathways. The results showed that parvalbumin-containing neurons were innervated by septal afferents but avoided by raphe axons, whereas calbindin D28K-containing cells, and to a smaller extent cholecystokinin-containing cells served as targets for both pathways. In some cases the same individual calbindin D28K- or cholecystokinin-containing neurons received multiple contacts from afferents of both septal and raphe origin. Thus, our results indicate that different subcortical nuclei modulate largely different inhibitory circuits in the hippocampal formation. However, considering the occasional convergence of the two subcortical nuclei not only onto the same type, but even onto the same individual calbindin D28K-containing interneurons, we propose that a particular inhibitory function, most probably feed-forward inhibition in the distal dendritic region, is under the control of both pathways.

Afferent Pathways↗
PubMed2005

Expression of calcium-binding proteins in the proliferative zones around the corticostriatal junction of rabbits during pre- and postnatal development.

Herein we asked whether cells expressing calcium-binding proteins around the corticostriatal junction are of pallial or subpallial origin. Brains of rabbit embryos between embryonic day E18 and E28 and postnatal day 0-P22 were immunoreacted with monoclonal antibodies raised against calretinin, calbindin and parvalbumin. At E18-E21, calbindin- and calretinin-immunoreactive cells were seen in distinct proliferative zones in the vicinity of the corticostriatal junction. Whereas calbindin-immunoreactive neurons were in the ventricular zone of the ventral pallium (the medial wall of the lateral ventricular angle), calretinin-immunoreactive cells were, nearby, in the subventricular zone of the subpallium at the lateral edge of the lateral ganglionic eminence. From E25 to P22, both calbindin- and calretinin-immunoreactive cells appeared in the pallial ventricular and subventricular zones around the lateral ventricular angle. Some of these cells resembled migratory neuroblasts. Parvalbumin-immunoreactive cells appeared at P5-P10, albeit they were almost negligible in the proliferative zones around the corticostriatal junction and the lateral ventricular angle. The results suggest that a number of the calbindin-expressing neurons that are generated in mid-gestation and postnatally are of pallial origin. They also indicate that only a few of the late-generated calretinin-immunoreactive cells may have a pallial source. The origin of the parvalbumin-immunoreactive cells was not ascertained in the present study.

Animals↗
PubMed2005

Calcium-binding protein distribution in the retina of strepsirhine and haplorhine primates.

Calcium-binding proteins are involved in numerous functional roles in the retina and are widely distributed in almost all retinal neurons. The present study aimed to characterize the distribution of the calcium-binding proteins calbindin, calretinin, parvalbumin and recoverin in relation to retinal cell types in a strepsirhine primate (mouse lemur, Microcebus) in comparison with primate species of the three main haplorhine lineages (marmoset, macaque and human), as well as a rodent (gerbil, Taterillus). The main findings show that whereas the recoverin antibody labels both rod and cone photoreceptors in all species, calbindin consistently labels cones, but not rods, in the haplorhine primates marmoset, macaque and human, but none of the photoreceptors in the mouse lemur. Marmoset and macaque also show a distinct label of cone outer segments with calretinin. Depending on the species, bipolar cells express calbindin and/or recoverin, while amacrine, horizontal and ganglion cells are labeled to varying degrees with calbindin, calretinin and parvalbumin. Haplorhine and strepsirhine primates clearly differ in the expression of calcium-binding protein expression in horizontal cells. In all haplorhine species, horizontal cells are densely labeled with parvalbumin whereas in mouse lemur horizontal cells express calbindin but not parvalbumin. Several characteristics of the calcium-binding immunostaining in the retina of the mouse lemur are similar to those observed in the rodent, and distinguish this species from the diurnal haphorhine primates. These differences may be related to adaptations of retinal structure and function to the nocturnal niche, since nocturnal strepsirhine and haphorhine (Tarsius and Aotus) primates share some features of calcium-binding expression.

Aged↗
PubMed2004

Age-related increases in calcium-binding protein immunoreactivity in the cochlear nucleus of hearing impaired C57BL/6J mice.

Aging C57BL/6J (C57) mice (1-30 months old), were used to study calcium-binding protein immunoreactivity (parvalbumin, calbindin and calretinin) in the cochlear nucleus. A quantitative stereological method, the optical fractionator was used to determine the total number of neurons, and the total number of immunostained neurons in the posteroventral- and dorsal cochlear nuclei (PVCN and DCN). A statistically significant age-related decrease of the total number of neurons was found in the PVCN and DCN using Nissl staining. In the DCN, an age-related increase in the total number of parvalbumin-positive neurons was found, while no changes in the total number of calbindin or calretinin positive neurons were demonstrated. In the PVCN, the total number of parvalbumin, calbindin, or calretinin positive neurons remained stable with increasing age. The percentage of parvalbumin, calbindin, and calretinin positive neurons significantly increased in the DCN, and the percentage of parvalbumin and calbindin-positive neurons increased in the PVCN. These findings imply that there is a relative up-regulation of calcium-binding proteins in neurons that had not previously expressed these proteins. This plastic response in the profoundly hearing impaired C57 mouse may be a survival strategy for cochlear nucleus neurons.

Adaptation, Physiological↗
PubMed2006

Decreased susceptibility to oxidative stress underlies the resistance of specific dopaminergic cell populations to paraquat-induced degeneration.

The vulnerability of different dopaminergic cell populations to damage caused by the herbicide paraquat was assessed by stereological counts of tyrosine hydroxylase-positive and calbindin-D28k-immunoreactive neurons in A9 (substantia nigra pars compacta) and A10 (ventral tegmental area and other cell groups). In saline-treated control mice, tyrosine hydroxylase-immunoreactive neurons represented 80% and 45% of the total neuronal population in A9 and A10, respectively, and the number of calbindin-D28k-positive neurons was five times greater in A10 than A9. Sequential injections with paraquat resulted in a significant loss of dopaminergic neurons in A9. In contrast, tyrosine hydroxylase-positive cells in A10 were spared from paraquat-induced degeneration. Furthermore, expression of calbindin-D28k was consistently associated with neuronal resistance to the herbicide in both A9 and A10. Paraquat exposure also induced oxidative stress as indicated by an increase in the number of midbrain cells positive for 4-hydroxy-2-nonenal, a marker of lipid peroxidation. Co-localization studies revealed that calbindin-D28k immunoreactivity overlapped with tyrosine hydroxylase labeling and that, after paraquat administration, (i) the vast majority of midbrain 4-hydroxy-2-nonenal-immunoreactive cells were dopaminergic (tyrosine hydroxylase-immunoreactive), (ii) tyrosine hydroxylase/4-hydroxy-2-nonenal-positive neurons were much more prevalent in A9 than A10, and (iii) all calbindin-D28k-containing neurons were characterized by lack of lipid peroxidation (4-hydroxy-2-nonenal immunoreactivity). Results in this paraquat model emphasize that, despite sharing a similar dopaminergic phenotype, different groups of midbrain neurons vary dramatically in their vulnerability to injury. Data also indicate that these differences are attributable, at least in part, to a varying susceptibility of dopaminergic cell populations to oxidative stress.

Aldehydes↗
PubMed1999

Horizontal cells of the rat retina are resistant to degenerative processes induced by ischemia-reperfusion.

The fate of calbindin D28k (calbindin)-labeled horizontal cells in the ischemic rat retina induced by increasing intraocular pressure was investigated by immunocytochemistry using an antiserum against calbindin. In the normal retina, strong calbindin-like immunoreactivity was seen in the horizontal cells, and the density of the labelled horizontal cells was 815.3+/-15.2 per mm2. The thickness of the treated retina became progressively thinner with increasing reperfusion time after the ischemic insult due to a loss of retinal cells in the inner and outer nuclear layers. However, the densities of the horizontal cells per mm2 were 814.0+/-26.4 at 1 week, 813.3+/-20.8 at 2 weeks, and 812.6+/-11.5 at 4 weeks, indicating that horizontal cells did not degenerate during experimental periods. Thus, calbindin may have a protective role for horizontal cells to ischemic insult by its ability to buffer calcium influx in the rat retina.

Albinism↗
PubMed1997

Chemically defined neuron groups and their subpopulations in the glomerular layer of the rat main olfactory bulb--II. Prominent differences in the intraglomerular dendritic arborization and their relationship to olfactory nerve terminals.

In the glomerular layer of the rat main olfactory bulb, we previously reported three chemically defined interneuron groups: GABA-like immunoreactive, calretinin-immunoreactive and Calbindin-D28k-immunoreactive groups [Kosaka K. et al. (1995) Neurosci. Res. 23, 73-88]. In the present study, we analysed the structural features of these three neuron groups using confocal laser scanning light microscopy, focusing on their dendritic arborization pattern, especially on their close apposition to olfactory receptor terminals labeled by olfactory marker protein. Each glomerulus consisted of two zones, the olfactory nerve zone and the non-olfactory nerve zone. The former was mainly occupied by olfactory nerve preterminals and terminals as well as their targets, postsynaptic fine dendritic portions of intrinsic neurons. The latter non-olfactory nerve zone was occupied mainly by olfactory marker protein-negative profiles. Processes of GABAergic neurons and those of one of their subpopulations, tyrosine hydroxylase-immunoreactive neurons, were numerous both in the olfactory nerve and non-olfactory nerve zones, resulting in their frequent close apposition to olfactory marker protein-immunoreactive elements. Combined confocal laser scanning light microscopic electron microscopic examination revealed synaptic contacts from olfactory nerve terminals on tyrosine hydroxylase-immunoreactive processes at these sites of close apposition. In contrast, calretinin-immunoreactive and Calbindin-D28k-immunoreactive processes, particularly Calbindin-D28k-immunoreactive ones, were distributed almost exclusively in the non-olfactory nerve zone, as if they avoided the olfactory nerve zone, showing a net or honeycomb pattern. Thus, calretinin-immunoreactive and Calbindin-D28k-immunoreactive processes were not or very rarely closely apposed to olfactory nerve terminals. These findings suggested that there might be some differences among chemically defined interneuronal groups in their synaptic contacts from olfactory nerves. Further quantitative image analysis clearly exhibited the prominent differences among these neuron groups in their intraglomerular dendritic arborization in relation with the olfactory nerve zone, i.e. the percentages of the area in the olfactory nerve zone occupied by GABAergic and tyrosine hydroxylase-immunoreactive processes were about 10%, respectively, whereas those of calretinin-immunoreactive and Calbindin-D28k-immunoreactive processes were only about 1% and 0.3%, respectively. These findings suggested that so-called periglomerular cells in glomeruli might be heterogeneous not only in their chemical nature, but also in their dendritic arborization pattern and synaptic contacts from olfactory nerve terminals.

Animals↗
PubMed1995

Ameloblasts and odontoblasts, target-cells for 1,25-dihydroxyvitamin D3: a review.

The basic features on the vitamin D endocrine system, synthesis of the main metabolite 1,25-dihydroxyvitamin D3 (1,25) and its genomic action mediated via the vitamin D receptor (VDR), are reviewed. Calbindin-D9k, calbindin-D28k and osteocalcin are presented as the most-extensively investigated vitamin D-dependent calcium-binding proteins. The action of 1,25 on the basic process of proliferation and differentiation is introduced. Then, the basis of the systemic theory of vitamin D action on teeth (clinical and experimental data and the dissimilar distribution of VDR and of potential vitamin D-dependent proteins in dental cells) are exposed. Finally, the data obtained with calbindin-D9k, calbindin-D28k, osteocalcin and VDR, which supports the theory that ameloblasts and odontoblasts are target-cells for 1,25 is presented. As a perspective, a cross-survey of the 1,25 and tooth-related literature is proposed which may indicate potential target-genes for 1,25 in teeth as done previously for calbindins-D.

Ameloblasts↗
PubMed1996

Fibroblast growth factor-2 protects entorhinal layer II glutamatergic neurons from axotomy-induced death.

The entorhinal cortex is a major relay between the hippocampus and other cortical and subcortical regions. Glutamatergic axons from layer II neurons form the entorhinal cortical projection to the hippocampus via the perforant pathway. We have demonstrated previously that lesion of the perforant pathway causes the death of approximately 30% of entorhinal layer II (ECL2) neurons. To elucidate mechanisms contributing to neuronal death and to investigate strategies preventing it, we identified the phenotype of the vulnerable neuronal population. Sections were immunolabeled with antibodies to the neuronal markers NeuN, glutamate, and calbindin-D28k, and to receptors for fibroblast growth factor-2 (FGFR1) and NMDA (NMDAR1) and were examined using confocal microscopy. Calbindin immunoreactivity was strikingly lamina-specific to ECL2, where one-third of all ECL2 neurons were calbindin-positive. Localization of glutamate revealed that half of the glutamatergic ECL2 neurons coexpressed calbindin. Quantification using unbiased stereology at 9 weeks after lesion of the perforant pathway revealed that the only ECL2 neuronal population that experienced a significant (70%) loss (20% of the total) was the population of glutamatergic ECL2 neurons that did not coexpress calbindin. All ECL2 neurons expressed FGFR1; therefore, we tested the role of FGF-2 in the survival of glutamatergic ECL2 neurons. We grafted fibroblasts genetically engineered to express nerve growth factor or FGF-2 and found that only FGF-2 grafts prevented loss of the vulnerable glutamatergic/calbindin-negative neurons. We present a hypothesis for the selective vulnerability of these glutamatergic/calbindin-negative ECL2 neurons and address the role of FGF-2 in neuronal rescue.

Afferent Pathways↗
PubMed1997

Activity-dependent regulation of calcium-binding proteins in the developing rat olfactory bulb.

Intracellular calcium, important in a variety of second messenger cascades, is regulated in part by calcium-binding proteins such as calretinin, parvalbumin, and calbindin. These proteins are highly concentrated in the rat main olfactory bulb and are localized in distinct neuronal populations. In the present study, postnatal expression was characterized immunohistochemically in normal rats and in rats with functional olfactory deprivation caused by unilateral naris closure, a manipulation that attenuates electrical activity in the bulb. Bulbs were examined from rats that had undergone naris closure or sham surgery on either postnatal day 1 (P1) or P30 and were allowed varying subsequent survival times. Each of the calcium-binding proteins showed both distinct patterns of early expression and differential susceptibility to olfactory restriction. For example, at P10, the densest immunoreactivity was observed for calretinin, a protein whose expression was the least affected by naris closure. After occlusion from P1-P30, there was a 30% reduction in the density of calbindin-immunoreactive profiles in the glomerular layer, and parvalbumin-immunoreactive profiles were reduced by 64% in the external plexiform layer. Unlike many other changes induced by deprivation, the effects of olfactory restriction on calbindin and parvalbumin expression were not age dependent: naris closure from P30-P60 caused similar substantial decreases in calbindin and parvalbumin immunoreactivities. These data demonstrate that the expression of calbindin and parvalbumin in rat bulb is regulated, in part, by afferent activity that is associated with full sensory experiences. The reductions of these calcium-binding proteins following olfactory deprivation are likely to be commensurate with altered control of intracellular calcium.

Animals↗
PubMed1998

New insights into cyclosporine A nephrotoxicity by proteome analysis.

Using two-dimensional gel electrophoresis (2-DE), we recently discovered an association between decreased calcium-binding protein, calbindin-D 28 kDa, urinary calcium wasting and intratubular corticomedullary calcifications in rat kidney. This observation prompted us to investigate kidney tissues of other species, including man. In this paper we show that in dogs and monkeys, which are generally devoid of cyclosporine A (CsA)-mediated nephrotoxicity, renal calbindin levels were not affected by the CsA treatment whereas in CsA-treated human kidney-transplant recipients with renal vascular or tubular toxicity, a marked decrease in renal calbindin-D 28 kDa protein level was found in most of the kidney biopsy sections. The present results strongly suggest that calbindin is a marker for CsA-nephrotoxicity. The discovery of calbindin-D 28 kDa being involved in CsA toxicity has evolved from the application of 2-DE and has not been reported previously, proving that proteomics can provide essential information in mechanistic toxicology. Considering the current improvements in proteome methods it is expected that high throughput proteomics will become an indispensable tool in preclinical safety testing.

Animals↗
PubMed1992

Postnatal X-ray irradiation effects on glomerular layer of rat olfactory bulb: quantitative and immunocytochemical analysis.

In the rat olfactory bulb, the majority of interneurons in the glomerular layer (GL) are supposed to be generated during first postnatal week. Low and repeated doses of X-rays (200 rad x 4 and 200 rad x 6) were used during this period to impair the development of interneurons. The resulting effects of olfactory bulb neurons were examined stereologically and immunocytochemically in animals of 4 and 12 weeks of age. Quantitative analysis showed that, 1) the volume of the GL decreased to 55% (1200 rad) - 70% (800 rad) of control, 2) numerical cell densities in GL decreased to 40% (1200 rad) - 60% (800 rad) of control, thus resulting in 3) a decrease of the total cell number in GL to 20% (1200 rad) - 40% (800 rad) of control in irradiated olfactory bulbs of animals 4 weeks old. In comparison, mitral cells, which are generated prenatally, were much less affected (total cell number: 70-80% of control), indicating a selective loss of cells generated during the first postnatal week in GL. Effects on somata and processes immunoreactive for GABA, tyrosine hydroxylase (TH), calbindin D-28K and parvalbumin (PV) were examined in irradiated bulbs of both 4 and 12 week-old rats. All of these immunoreactive elements showed a drastic decrease in all layers. Semiquantitative analysis showed that in the GL, calbindin D-28K immunoreactive (calbindin D-28K(+)) neurons decreased more extensively than TH immunoreactive (TH(+)) and GABA-like immunoreactive (GABA(+)) neurons; that is, TH(+) and GABA(+) neurons decreased to 20% (1200 rad) - 40% (800 rad) of control, whereas calbindin D-28K(+) neurons decreased to 10% (1200 rad) - 30% (800 rad) of control in the GL of irradiated bulbs. These findings indicated that larger proportions of calbindin D-28K(+) neurons might be generated during the first postnatal week than those of GABA(+) and TH(+) neurons. Furthermore, in irradiated bulbs the proportion of GABA(-)TH(+) cells in TH(+) cells increased to about twice of control, and the estimated total numbers of GABA(-)TH(+) cells in irradiated rats were 95% (800 rad) and 40% (1200 rad) of control. These observations suggest that the majority of GABA(-)TH(+) neurons were less affected by X-ray irradiation during the first postnatal week and thus that they might be generated in the prenatal period. Since during the first 2 postnatal weeks, neurons showing GABA(-)TH(+) were not seen in GL (Kosaka et al. 1987a), the majority of GABA(-)TH(+) neurons in adult olfactory bulb were assumed to change their phenotype at some postnatal developmental period.

Animals↗
PubMed2003

Development of the outer retina in the mouse.

Mice represent a valuable species for studies of development and disease. With the availability of transgenic models for retinal degeneration in this species, information regarding development and structure of mouse retina has become increasingly important. Of special interest is the differentiation and synaptogenesis of photoreceptors since these cells are predominantly involved in hereditary retinal degenerations. Thus, some of the keys to future clinical management of these retinal diseases may lie in understanding the molecular mechanisms of outer retinal development. In this study, we describe the expression of markers for photoreceptors (recoverin), horizontal cells (calbindin), bipolar cells (protein kinase C; PKC) and cytoskeletal elements pivotal to axonogenesis (beta-tubulin and actin) during perinatal development of mouse retina. Immunocytochemical localization of recoverin, calbindin, PKC and beta-tubulin was monitored in developing mouse retina (embryonic day (E) 18.5 to postnatal day (PN) 14), whereas f-actin was localized by Phalloidin binding. Recoverin immunoreactive cells, presumably the photoreceptors, were observed embryonically (E 18.5) and their number increased until PN 14. Neurite projections from the immunoreactive cells towards the outer plexiform layer (OPL) were noted at PN 0 and these processes reached the OPL at PN 7 coincident with histological evidence for the differentiation of the OPL. Outer segments, all the cell bodies in the ONL, as well as the OPL were immunoreactive to recoverin at PN 14. Calbindin immunoreactive horizontal cells were also present in E 18.5 retinas. These cells became progressively displaced proximally as the ONL developed. A calbindin immunoreactive plexus was seen in the OPL at PN 7. PKC immunoreactive bipolar cells developed postnatally, becoming distinguished at PN 7. Both beta-tubulin and actin immunoreactive cells were present in the IPL as early as E 18.5; however, appearance of processes labeled with these markers in the OPL was delayed until PN 7, concurrent with the first appearance of photoreceptor neurites, development of the horizontal cell plexus, and development of synaptophysin immunoreactivity at this location. These results provide a developmental timeframe for the expression of recoverin, calbindin, synaptophysin, beta-tubulin and actin. Our findings suggest that the time between PN 3 and PN 7 represents a critical period during which elements of the OPL are assembled.

Aging↗
PubMed1997

Development of the tecto-thalamic projection neurons and the differential expressions of calcium-binding proteins in the rat.

We studied expression of calbindin-D 28 K and parvalbumin in tecto-thalamic projection neurons and during the formation of their tecto thalamic projections using a double-labeling with Fluoro-Gold. To discern the completion of these projections, Fluoro Gold, an opalescent fluorescent dye, was injected into the dorsal lateral geniculate and/or the lateral posterior nucleus in rats of various ages from neonates to adults. After one day's survival, the brains were removed and sections of the brain were immunohistochemically processed using Cy3, a red fluorescent dye, as a marker for calbindin-D 28 K or parvalbumin. The three types of tecto thalamic neurons, which have been described previously in the adult rats, were identified in the present study. The results revealed that in developing rats: 1) A population of medium-sized neurons (the presumed pyriform cells) express calbindin-D 28 K as early as the day of birth prior to the formation of their tecto thalamic projection that occured on postnatal day 4. Most (over 90%) of them project to the dorsal lateral geniculate nucleus; 2) A population of large neurons (the presumed wide-field vertical cells) express calbindin-D 28 K on postnatal day 7, and most of them (over 90%) project to the lateral posterior nucleus; 3) Another population of medium-sized neurons (the presumed narrow-field cells) express parvalbumin on post-natal day 17, but only a half (45%) of them project to the dorsal lateral geniculate nucleus. In the developing nervous system, calcium ions play important roles in the biological and molecular events underlying neural development. Changes in the free intracellular calcium ion level, indicating neuronal activity has been reported to be correlated with onset of calbindin-D 28 K or parvalbumin-immunoreactivity that participate in the regulation of intracellular calcium homeostasis in neurons. Therefore, the present findings may reflect distinct developmental events in the different classes of tectal relay neurons that form parallel visual pathways, but which have such different functions as the detection of luminance, discrimination of direction, and the detection of fast movements.

Animals↗
PubMed1999

Relationships among age, eggshell thickness and vitamin D metabolism and its expression in the laying hen.

Hens forming uncalcified shells synthesized less 1,25-hydroxycholecalciferol (1,25(OH)2D3) and less duodenal and eggshell gland (ESG) calbindin than normal laying hens. Hens forming thin shells had lower intestinal and ESG calbindin and its mRNA. Reducing ESG calcium (Ca2+) transport by the carbonic anhydrase inhibitor acetazolamide, but not by dietary Ca2+ restriction, reduced ESG calbindin and its mRNA. Two sub-populations of hens characterized by shell thickness (ST) maintained this characteristic throughout the whole production period. The differences between the two sub-populations increased with age. In old laying hens, the two sub-populations responded differently to dietary Ca2+ restriction and to exogenous 1,25(OH)2D3. Those forming a thin shell responded to 1,25(OH)2D3 by a significant improvement in ST. The results suggest that: (a) the mechanism responsible for Ca2+ transport to the egg shell consists of a vitamin D-dependent absorption of Ca2+ and a multi-factor-dependent transfer of Ca2+ to the shell; (b) both steps are, most likely, calbindin-mediated; however, the induction of calbindin gene expression in the ESG is predominantly calcium-dependent; and (c) the apparent defect in vitamin D metabolism or its expression in old hens is typical of, or even exclusive, to thin-shell-forming hens.

Acetazolamide↗
PubMed2004

Downregulation of Ca(2+) and Mg(2+) transport proteins in the kidney explains tacrolimus (FK506)-induced hypercalciuria and hypomagnesemia.

FK506 (tacrolimus) and dexamethasone are potent immunosuppressants known to induce significant side effects on mineral homeostasis, including hypercalciuria and hypomagnesemia. However, the underlying molecular mechanisms remain unknown. The present study investigated the effects of FK506 and dexamethasone on the expression of proteins involved in active Ca(2+) reabsorption: the epithelial Ca(2+) channel TRPV5 and the cytosolic Ca(2+)-binding protein calbindin-D(28K). In addition, the renal expression of the putative Mg(2+) channel TRPM6, suggested to be involved in transcellular Mg(2+) reabsorption, was determined. Administration of FK506 to rats by daily oral gavage during 7 d significantly enhanced the urinary excretion of Ca(2+) and Mg(2+) and induced a significant hypomagnesemia. FK506 significantly decreased the renal mRNA expression of TRPV5 (62 +/- 7% relative to controls), calbindin-D(28K) (9 +/- 1%), and TRPM6 (52 +/- 8%), as determined by real-time quantitative PCR analysis. Furthermore, semiquantitative immunohistochemistry showed reduced renal protein abundance of TRPV5 (24 +/- 5%) and calbindin-D(28K) (29 +/- 4%), altogether suggesting that downregulation of these transport proteins is responsible for the FK506-induced Ca(2+) and Mg(2+) wasting. In contrast, dexamethasone significantly enhanced renal TRPV5 (150 +/- 15%), calbindin-D(28K) (177 +/- 23%), and TRPM6 (156 +/- 20%) mRNA levels along with TRPV5 (211 +/- 8%) and calbindin-D(28K) (176 +/- 5%) protein abundance in the presence of significantly increased Ca(2+) and Mg(2+) excretion. This indicated that these proteins are directly or indirectly regulated by dexamethasone. In conclusion, FK506 and dexamethasone induce renal Ca(2+) and Mg(2+) wasting, albeit by different mechanisms. Downregulation of specific Ca(2+) and Mg(2+) transport proteins provides a molecular mechanism for FK506-induced hypercalciuria and hypomagnesemia, whereas dexamethasone positively regulates these proteins.

Animals↗
PubMed1991

Structure of the human brain calcium-binding protein calretinin and its expression in bacteria.

Calbindin D28k and calretinin are two closely related intracellular calcium-binding proteins belonging to the troponin C superfamily. Calbindin is known to be involved in the vitamin-D-dependent calcium absorption through intestinal and renal epithelia, while the function of neuronal calbindin and calretinin is poorly understood. Using antibodies directed against chick intestinal calbindin D28k, human calretinin cDNA clones were isolated from brain cDNA libraries. The sequence of the calretinin cDNA revealed an open reading frame of 271 codons coding for a protein of 31,520 Da, and sharing 58% identical residues with human calbindin D28k. Calretinin contains five presumably active and one presumably inactive calcium-binding domains. Comparison with the partial sequences available for chick and guinea pig calretinins revealed that the protein is highly conserved in evolution (evolutionary rate: 0.27 x 10(-9) amino acid-1 year-1). The calretinin message was detected in the brain, while absent from heart muscle, kidney, liver, lung, spleen, stomach and thyroid gland. Recombinant calretinin was expressed in Escherichia coli, and the calcium-binding properties were confirmed on both the natural and the recombinant proteins. Part of the human gene coding for calretinin was isolated and the region corresponding to the promoter and the first exon was sequenced.

Amino Acid Sequence↗