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PubMed1999

Distribution of the catecholaminergic neurons in the central nervous system of human embryos and fetuses.

The catecholaminergic cell groups in the human brain, denominated from A1 to A17, display some striking anatomical differences with those described in the rodent. These differences are essentially observed in the extent of the dopaminergic neurons and especially their axonal fields in the telencephalon. Immunocytochemistry for tyrosine-hydroxylase and dopamine-ss-hydroxylase allowed the visualization of the precocious human catecholaminergic groups as early as 4.5 postovulatory weeks. Maps of tyrosine-hydroxylase positive neurons generated in the different rhombomeres, midbrain, and prosomeres are shown following the prosomeric model introduced by Puelles and Rubenstein [(1993) Trends Neurosci. 16:472-476]. Such a description is convenient to compare catecholaminergic systems in different mammalian species and provide clear anatomical landmarks of the embryonic substantia nigra (midbrain and prosomeres 1 and 2), that are necessary for transplantation of neural tissue in Parkinson's disease. The development and early specification of the dopaminergic neurons expressing calbindin D28K phenotype in the substantia nigra and in the ventral tegmental area are described. The catecholaminergic axons enter the anlage of the cerebral cortex just after the formation of the cortical plate, from 7 postovulatory weeks on. They invade the subplate layer where they wait for 4 weeks before penetrating the cortical plate. At midgestation, the different areas and layers of the frontal cerebral wall are invaded by the catecholaminergic axons, before the layering of the cortex is completed, in a pattern of fiber distribution similar to that described in the adult human brain. The early pattern of development of the catecholamine systems appeared to be phylogenetically well preserved in mammals, but specific features emerging during the differentiation period are unique to humans.

Animals↗
PubMed2004

Injury in the spinal cord may produce cell death in the brain.

Functional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute spinal cord injury (SCI), and conducted a series of experiments, the study examining the morphological changes in the brain following the spinal injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to SCI model. Rats were laminectomized and SCI was induced using NYU spinal impactor at T9 segment. The behavioral test was performed. Electrophysiologically, motor evoked potentials (MEPs) were recorded. The animals were subjected to morphological study at 12, 24, 48, 72 h, and 1 week, postoperatively. Locomotor deficits were observed after SCI, and changes in the amplitudes and latencies of the MEPs were observed. The morphological changes were evidenced by terminal TUNEL staining and Calbindin-D(28K) immunohistochemistry. The TUNEL-positive cells were located at the brain motor cortex after SCI. TUNEL-positive cells were seldom found 4 h after injury. In addition, Calbindin-D28K immunoreactive neurons were observed in the motor cortex after injury. These results suggest that apoptosis may play an important role in the pathophysiology of the brain motor cortex following acute spinal cord injury and functions that were deteriorated after SCI may be related to these electrophysiological and morphological changes.

Animals↗
PubMed1998

Nonobligate role of early or sustained expression of immediate-early gene proteins c-fos, c-jun, and Zif/268 in hippocampal mossy fiber sprouting.

Axon sprouting in dentate granule cells is an important model of structural plasticity in the hippocampus. Although the process can be triggered by deafferentation, intense activation of glutamate receptors, and other convulsant stimuli, the specific molecular steps required to initiate and sustain mossy fiber (MF) reorganization are unknown. The cellular immediate early genes (IEGs) c-fos, c-jun, and zif/268 are major candidates for the initial steps of this plasticity, because they encode transcription factors that may trigger cascades of activity-dependent neuronal gene expression and are strongly induced in all experimental models of MF sprouting. The mutant mouse stargazer offers an important opportunity to test the specific role of IEGs, because it displays generalized nonconvulsive epilepsy and intense MF sprouting in the absence of regional cell injury. Here we report that stargazer mice show no detectable elevations in c-Fos, c-Jun, or Zif/268 immediate early gene proteins (IEGPs) before or during MF growth. Experimental results in stargazer, including (1) a strong IEGP response to kainate-induced convulsive seizures, (2) no IEGP response after prolongation of spike-wave synchronization, (3) no IEGP increase at the developmental onset of seizures or after prolonged seizure suppression, and (4) unaltered levels of the intracellular Ca2+-buffering proteins calbindin-D28k or parvalbumin, exclude the possibility that absence of an IEGP response in stargazer is either gene-linked or suppressed by known refractory mechanisms. These data demonstrate that increased levels of these IEGPs are not an obligatory step in MF-reactive sprouting and differentiate the early downstream molecular cascades of two major seizure types.

Animals↗
PubMed1996

Transient neuronal population of the internal capsule in the developing human cerebrum.

The present study reveals the presence of a distinct group of cells, resembling reticular thalamic neurones, in the internal capsule during fetal development. This cell population rapidly decreases in size during early infancy and few cells are apparent in the 1-year-old infant. Internal capsule cells are well differentiated, multipolar or polymorphous, AChE (acetylcholinesterase)-reactive neurones. The following specific molecular markers were demonstrated in the neurones of the internal capsule: MAP2 (microtubule-associated protein 2), somatostatin, calbindin-D28K and p75 low-affinity NGF (nerve growth factor) receptor. A group of neurones described here corresponds to the perireticular thalamic nucleus found in certain mammalian species, hitherto unidentified in the primate brain, which may play an important role during development.

Acetylcholinesterase↗
PubMed2006

Typical and atypical antipsychotic drugs target dopamine and cyclic AMP-regulated phosphoprotein, 32 kDa and neurotensin-containing neurons, but not GABAergic interneurons in the shell of nucleus accumbens of ventral striatum.

Specific neurons in the brain are the primary targets of the action of antipsychotic drugs. Identification and characterization of the nature of these neurons are important for understanding how antipsychotic drugs produce their effects. In previous studies GABAergic/dynorphinergic neurons were identified as a principal cell target of antipsychotic drugs in the shell of nucleus accumbens. In the present study, we further characterized which subpopulations of GABAergic neurons in this area respond after acute administration of antipsychotic drugs. Rats were treated with the typical antipsychotic haloperidol, or the prototype atypical antipsychotic clozapine and killed two hours after treatment. In appropriate sections of brain, double immunofluorescence labeling was performed with antibodies directed against markers specific to candidate cell types and Fos-like proteins (a marker to identify drug-induced cell activation). We reported here that haloperidol- and clozapine-activated neurons showed the following features: 1) approximately 54-57% of them express dopamine and cyclic AMP-regulated phosphoprotein, 32 kDa (a marker for GABAergic medium spiny projection neurons), 2) they appear rarely to be GABAergic interneurons, marked by the calcium binding proteins, parvalbumin, calretinin or calbindin-D28K, 3) about 84-86% of them express the neuropeptide neurotensin (a neurotransmitter most often associated with projection neurons in the site tested). The results suggest that most of the antipsychotic drug-activated neurons in the shell of nucleus accumbens are likely to be neurotensin containing projection neurons.

Animals↗
PubMed1999

Enriched environment increases neurogenesis in the adult rat dentate gyrus and improves spatial memory.

The fetal and even the young brain possesses a considerable degree of plasticity. The plasticity and rate of neurogenesis in the adult brain is much less pronounced. The present study was conducted to investigate whether housing conditions affect neurogenesis, learning, and memory in adult rats. Three-month-old rats housed either in isolation or in an enriched environment were injected intraperitoneally with bromodeoxyuridine (BrdU) to detect proliferation among progenitor cells and to follow their fate in the dentate gyrus. The rats were sacrificed either 1 day or 4 weeks after BrdU injections. This experimental paradigm allows for discrimination between proliferative effects and survival effects on the newborn progenitors elicited by different housing conditions. The number of newborn cells in the dentate gyrus was not altered 1 day after BrdU injections. In contrast, the number of surviving progenitors 1 month after BrdU injections was markedly increased in animals housed in an enriched environment. The relative ratio of neurogenesis and gliogenesis was not affected by environmental conditions, as estimated by double-labeling immunofluorescence staining with antibodies against BrdU and either the neuronal marker calbindin D28k or the glial marker GFAp, resulting in a net increase in neurogenesis in animals housed in an enriched environment. Furthermore, we show that adult rats housed in an enriched environment show improved performance in a spatial learning test. The results suggest that environmental cues can enhance neurogenesis in the adult hippocampal region, which is associated with improved spatial memory.

Aging↗
PubMed2006

Potential value of changes in cell markers in organotypic hippocampal cultures associated with chronic EtOH exposure and withdrawal: comparison with NMDA-induced changes.

BACKGROUND: Previous studies have shown that withdrawal from ethanol (EtOH) exposure induces neuronal damage, as indicated by propidium iodide (PI) uptake, in organotypic hippocampal slice cultures. This is prevented by MK801, suggesting that damage is "excitotoxic," resulting from activation of N-methyl-d-aspartate (NMDA) receptors by endogenous glutamate. To avoid reliance on a single indicator, and to enable assessment of recovery from the EtOH withdrawal (EWD) insult, we assessed changes in cell markers for neurons and glia, as well as cell division, following either EWD or NMDA challenge (as a positive control). METHODS: Organotypic cultures from postnatal day (PND) 8 rats were cultured for 5 days before exposure to EtOH (mean concentration approximately 65 mM) for 10 days before EWD. Cultures of the same "days in vitro" age (DIV16) were exposed to NMDA (200 microM) for 1 hour. Neuronal injury was visualized using PI and indices of neurons, glia, or cell division were measured at intervals up to 10 days following the neurotoxic insults. Each time point and measurement used separate slice cultures, and these were treated as separate experiments with paired controls. Regional neuronal content was assessed by neuronal nuclear protein (NeuN) and calbindin D28k (Calb), glial content by glial fibrillary acidic protein (GFAP), and cell division by bromodeoxyuridine (BrdU) incorporation, all measured immunohistochemically. RESULTS: Chronic exposure to EtOH was associated with a dramatic reduction in BrdU incorporation in all regions of cultures. Propidium iodide fluorescence in the CA1 region was elevated significantly after EWD and more so after NMDA challenge. Reduced immunoreactivity (IR) of NeuN and Calb suggested that loss of neurons resulted from the EWD insult. Bromodeoxyuridine incorporation was initially depressed even further by EWD, but had returned to control levels after 3 days. In contrast, following NMDA insult, BrdU incorporation was significantly and persistently elevated above control levels after 3 days. Glial fibrillary acidic protein was reduced immediately after both EWD and NMDA challenge. Several days after EWD, expression of neuronal and glial markers, although variable, had generally returned to control levels. In contrast, NeuN IR remained significantly reduced after NMDA challenge. CONCLUSIONS: In general, the use of additional markers supports data obtained with PI uptake alone and suggests that neurons (and glia) are lost from the culture following EWD or NMDA challenge. These cell markers recover several days after EWD, but it is unclear whether functional recovery accompanies these changes. If the dramatic effect of EtOH exposure and EWD on BrdU incorporation reflects reduced neuro- and gliogenesis, it is likely that this adversely affects long-term recovery from EWD. Finally, some markers showed significant and consistent changes after EWD, whereas others did not. This information may facilitate the use of this model in evaluation of potential medications that protect against and/or promote recovery from neurotoxicity.

Animals↗
PubMed1999

Intranuclear inclusions in subtypes of striatal neurons in Huntington's disease transgenic mice.

R6/2 transgenic mice express exon 1 of an abnormal human Huntington's disease (HD) gene and develop a neurological phenotype similar to HD. These mice develop ubiquitinated neuronal intranuclear inclusions (NII) which might play a central role in the pathophysiology of HD. We studied the distribution of NII in subpopulations of striatal neurons in 12-week-old R6/2 transgenic mice using fluorescent double label immunohistochemistry. We observed that most of the Calbindin-D28K positive projection neurons (89%) and the Parvalbumin positive interneurons (86%) showed ubiquitinated NII. In interneurons, however, which contain either choline acetyltransferase, neuronal nitric oxide synthase, or Calretinin, the frequency of NII was much lower (22%, 8%, 9%, respectively). Our data suggest that subpopulations of striatal neurons differ remarkably in their capability of forming ubiquitinated NII. Interneurons which are known to resist neurodegeneration in HD show less NII.

Animals↗
PubMed1999

Expression of the cannabinoid receptor CB1 in distinct neuronal subpopulations in the adult mouse forebrain.

Cannabinoids can modulate motor behaviour, learning and memory, cognition and pain perception. These effects correlate with the expression of the cannabinoid receptor 1 (CB1) and with the presence of endogenous cannabinoids in the brain. In trying to obtain further insights into the mechanisms underlying the modulatory effects of cannabinoids, CB1-positive neurons were determined in the murine forebrain at a single cell resolution. We performed a double in situ hybridization study to detect mRNA of CB1 in combination with mRNA of glutamic acid decarboxylase 65k, neuropeptide cholecystokinin (CCK), parvalbumin, calretinin and calbindin D28k, respectively. Our results revealed that CB1-expressing cells can be divided into distinct neuronal subpopulations. There is a clear distinction between neurons containing CB1 mRNA either at high levels or low levels. The majority of high CB1-expressing cells are GABAergic (gamma-aminobutyric acid) neurons belonging mainly to the cholecystokinin-positive and parvalbumin-negative type of interneurons (basket cells) and, to a lower extent, to the calbindin D28k-positive mid-proximal dendritic inhibitory interneurons. Only a fraction of low CB1-expressing cells is GABAergic. In the hippocampus, amygdala and entorhinal cortex area, CB1 mRNA is present at low but significant levels in many non-GABAergic cells that can be considered as projecting principal neurons. Thus, a complex mechanism appears to underlie the modulatory effects of cannabinoids. They might act on principal glutamatergic circuits as well as modulate local GABAergic inhibitory circuits. CB1 is very highly coexpressed with CCK. It is known that cannabinoids and CCK often have opposite effects on behaviour and physiology. Therefore, we suggest that a putative cross-talk between cannabinoids and CCK might exist and will be relevant to better understanding of physiology and pharmacology of the cannabinoid system.

Amygdala↗
PubMed1988

Developmental and regional changes of mRNA for a cerebellar protein (spot 35) in the rat brain.

Spot 35 protein is a cerebellar Ca-binding protein. Because Southern blot analysis showed evidence for the nucleotide sequence of spot 35 protein cDNA in the rat genome, we applied cDNA to quantitate the mRNA of rat spot 35 protein. The size of this mRNA was about 1,900 nucleotides in length, and that of mRNA from bovine cerebellum was larger. We also examined the developmental changes and regional distribution of spot 35 protein mRNA in rat brains by dot-blot analysis using cDNA as a probe. During postnatal days 1-20, a rapid increase of mRNA levels was observed. Further, the level of mRNA for spot 35 protein was found in the cerebellum and was negligible in the cerebral cortex, striatum, and hippocampus.

Animals↗
PubMed1988

Modulation of rat calbindin-D28 gene expression by 1,25-dihydroxyvitamin D3 and dietary alteration.

We have used a specific cDNA to the mammalian 28,000 Mr vitamin D-dependent calcium binding protein (calbindin-D28k) to study the regulation of the expression of this mRNA in rat kidney and brain. The effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) and dietary alteration on genomic expression were characterized by both Northern and slot blot analysis. Administration of 1,25-(OH)2D3 for 7 days (25 ng/day) to vitamin D-deficient rats resulted in a marked increase in renal calbindin-DmRNA, renal calbindin, and serum calcium. When vitamin D-deficient rats were supplemented for 10 days with calcium (3% calcium gluconate in the water, 2% calcium in the diet) serum calcium levels were similar to the levels observed in the 1,25-(OH)2D3-treated rats. However, in the calcium-supplemented rats the levels of renal calbindin and renal calbindin mRNA were similar to the levels observed in the vitamin D-deficient rats, suggesting that calcium alone without vitamin D does not regulate renal calbindin gene expression in vivo. In dietary alteration studies in vitamin D-replete rats, renal calbindin protein and mRNA increased 2.5-fold in rats fed diets low in phosphate providing evidence that in the rat the nutritional induction of calbindin is accompanied by a corresponding alteration in the concentration of its specific mRNA. Under low dietary calcium conditions, the levels of renal calbindin protein and mRNA were similar to the levels observed in control rats, although 1,25-(OH)2D3 serum levels were markedly elevated, suggesting that factors in addition to 1,25-(OH)2D3 can modulate renal calbindin gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Regulation of calbindin-D28K gene expression by 1,25-dihydroxyvitamin D3 is correlated to receptor occupancy.

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) induces the synthesis of calcium binding protein (calbindin-D28K) and calbindin-D28K-mRNA in the chick intestine. We have examined the relationship between nuclear uptake of 1,25-(OH)2D3, 1,25-(OH)2D3 receptor occupancy levels, and transcription of the calbindin-D28K gene and found all three parameters to be highly correlated. All three events occur rapidly (within 15-30 min) following a single dose of 6.5 nmol of 1,25-(OH)2D3 to vitamin D-deficient chicks, reaching peak values by 1-2 h; by 4 h, values of all three parameters start to decline. Calbindin-D28K-mRNA begins to accumulate by 3-5 h but does not peak until 12 h following hormone administration. The levels of calbindin-D28K start to increase by 5-8 h and do not peak until 48 h after the 1,25-(OH)2D3 dose. These observations suggest that post-transcriptional regulatory mechanisms may be involved. Measurements of basal levels of calbindin-D28K gene transcription show that there is virtually no transcription in the vitamin D-deficient chick intestine, and a 12-fold induction in the intestine of vitamin D-replete chicks. This basal level of transcription in vitamin D-replete chick intestine is not inhibited by cycloheximide pretreatment. These results confirm the thesis that a major component of the mechanism of action of 1,25-(OH)2D3 is functioning as a steroid hormone, effected through the direct action of the seco-steroid-receptor complex on the initiation of transcription of specific genes.

Animals↗
PubMed2004

Lithium selectively increases neuronal differentiation of hippocampal neural progenitor cells both in vitro and in vivo.

Lithium has been demonstrated to increase neurogenesis in the dentate gyrus of rodent hippocampus. The present study was undertaken to investigate the effects of lithium on the proliferation and differentiation of rat neural progenitor cells in hippocampus both in vitro and in vivo. Lithium chloride (1-3 mM) produced a significant increase in the number of bromodeoxyuridine (BrdU)-positive cells in high-density cultures, but did not increase clonal size in low-density cultures. Lithium chloride at 1 mM (within the therapeutic range) also increased the number of cells double-labeled with BrdU antibody and TuJ1 (a class III beta-tubulin antibody) in high-density cultures and the number of TuJ1-positive cells in a clone of low-density cultures, whereas it decreased the number of glial fibrillary acidic protein-positive cells in both cultures. These results suggest that lithium selectively increased differentiation of neuronal progenitors. These actions of lithium appeared to enhance a neuronal subtype, calbindin(D28k)-positive cells, and involved a phosphorylated extracellular signal-regulated kinase and phosphorylated cyclic AMP response element-binding protein-dependent pathway both in vitro and in vivo. These findings suggest that lithium in therapeutic amounts may elicit its beneficial effects via facilitation of neural progenitor differentiation toward a calbindin(D28k)-positive neuronal cell type.

Animals↗
PubMed1994

Differences in nigral neuron number and sensitivity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in C57/bl and CD-1 mice.

The present study demonstrates that the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes significantly greater reductions in striatal dopamine levels in C57/bl mice than in CD-1 mice, thus confirming a greater sensitivity of the C57/bl mice to MPTP. To determine the possible reasons for this difference in MPTP sensitivity between these two mouse strains, we have compared both the organization and the number of substantia nigra (SN) neurons, the primary target of MPTP, in C57/bl and in CD-1 mice using immunostaining for tyrosine hydroxylase (TH) and calbindin-D28k (calbindin). In saline-injected animals, there is a significantly lower number of SN TH-positive and calbindin-positive neurons in C57/bl than CD-1 mice; no significant differences in the numbers of these neurons are found in the ventral tegmental area between the two strains. In MPTP-injected animals, the reductions in SN TH-positive neurons are significantly greater in C57/bl than in CD-1 mice. In contrast, MPTP does not cause any significant changes in the numbers of SN calbindin-positive neurons in either strain. The present study shows that C57/bl mice which have fewer SN TH-positive neurons are more sensitive to MPTP-induced toxicity than CD-1 mice. This observation suggests a possible inverse relationship between SN TH-positive neuron number and MPTP sensitivity. If correct, this hypothesis may be of major importance for Parkinson's disease since it is suggested that individuals at risk of developing this neurodegenerative disorder may have lower numbers of SN TH-positive neurons to start with. The present study also shows that SN calbindin-positive neurons are spared following MPTP administration. However, the observed difference in SN calbindin-positive neuron numbers does not account for the differential sensitivity to MPTP between these two mouse strains.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2000

Altered calcium homeostasis in cerebellar Purkinje cells of leaner mutant mice.

The leaner (tg(la)) mouse mutation occurs in the gene encoding the voltage-activated Ca(2+) channel alpha(1A) subunit, the pore-forming subunit of P/Q-type Ca(2+) channels. This mutation results in dramatic reductions in P-type Ca(2+) channel function in cerebellar Purkinje neurons of tg(la)/tg(la) mice that could affect intracellular Ca(2+) signaling. We combined whole cell patch-clamp electrophysiology with fura-2 microfluorimetry to examine aspects of Ca(2+) homeostasis in acutely dissociated tg(la)/tg(la) Purkinje cells. There was no difference between resting somatic Ca(2+) concentrations in tg(la)/tg(la) cells and in wild-type (+/+) cells. However, by quantifying the relationship between intracellular Ca(2+) elevations and depolarization-induced Ca(2+) influx, we detected marked alterations in rapid calcium buffering between the two genotypes. Calcium buffering values (ratio of bound/free ions) were significantly reduced in tg(la)/tg(la) (584 +/- 52) Purkinje cells relative to +/+ (1,221 +/- 80) cells. By blocking the endoplasmic reticulum (ER) Ca(2+)-ATPases with thapsigargin, we observed that the ER had a profound impact on rapid Ca(2+) buffering that was also differential between tg(la)/tg(la) and +/+ Purkinje cells. Diminished Ca(2+) uptake by the ER apparently contributes to the reduced buffering ability of mutant cells. This report constitutes one of the few instances in which the ER has been implicated in rapid Ca(2+) buffering. Concomitant with this reduced buffering, in situ hybridization with calbindin D28k and parvalbumin antisense oligonucleotides revealed significant reductions in mRNA levels for these Ca(2+)-binding proteins (CaBPs) in tg(la)/tg(la) Purkinje cells. All of these results suggest that alterations of Ca(2+) homeostasis in tg(la)/tg(la) mouse Purkinje cells may serve as a mechanism whereby reduced P-type Ca(2+) channel function contributes to the mutant phenotype.

Animals↗
PubMed1995

1 alpha, 25-dihydroxyvitamin D3 receptor ontogenesis in fetal renal development.

We used immunohistochemical techniques to examine the distribution of 1 alpha, 25-dihydroxyvitamin D3 receptors (VDR) in developing rat and mouse kidneys and murine metanephric organ culture. In vivo, the patterns of expression in the two species were similar despite the slight difference in gestational periods (rat, 22 days; mouse, 19 days). Starting at gestational day 15, epitopes for VDR were found in cells of branching ureteral buds and in surrounding mesenchyme and at later developmental stages in glomerular visceral and parietal epithelial cells and proximal and distal tubules (DT). Epitopes for the 28-kDa calcium-binding protein (calbindin D28k) were found exclusively in DTs starting at gestational day 19. The pattern of VDR expression during in vitro nephrogenesis in serum-free murine metanephric organ culture paralleled that seen in vivo. At the time of explantation into organ culture (gestational day 13), VDR epitopes were not detected. By 3 days of in vitro development, VDR expression was identical to that found in gestational day 15 metanephroi in vivo. VDR expression after 5 days of in vitro development mirrored the pattern of gestational day 17 metanephroi in vivo. No calbindin D28k epitopes were seen at any in vitro developmental stage studied. We demonstrate for the first time that VDR are present in specific areas of the developing rat and mouse kidney early in gestation. Calbindin D28k appears later in developing rat and mouse kidney and is distributed differently than the VDR. Metanephric organ culture may be a useful model for studying the regulation and function of VDR during early renal development.

Animals↗
PubMed1987

Molecular cloning of cDNA to mRNA for a cerebellar spot 35 protein.

The nucleotide sequence of mRNA for rat cerebellar spot 35 protein, a Ca-binding protein, was determined from recombinant complementary DNA (cDNA) clones. The sequence was composed of 1,714 base pairs (bp) which included the 783 bp of the complete coding region, the 130 bp of the 5'-noncoding region, and the 801 bp of the 3'-noncoding region containing a polyadenylation signal. In addition, a polyadenylic acid [poly(A)] tail was also found. Because the size of spot 35 mRNA was estimated to be about 1,900 bases by Northern blot analysis, the longest insert was verified to contain a nearly full-length cDNA sequence including the poly(A) tail. The amino acid sequence of the protein deduced from the nucleotide sequence contains 261 amino acids and at least five Ca-binding domains. There was a high homology in the amino acid sequences (79%) and the nucleotide sequences (77%) between spot 35 protein and chick intestinal Ca-binding protein (28K).

Amino Acid Sequence↗
PubMed1990

Regulation of calbindin-D28K gene expression by 1,25-dihydroxyvitamin D3 in chick kidney.

We report here the use of a cloned cDNA for the avian calbindin-D28K (28 kD, vitamin D-dependent calcium binding protein, CaBP) to investigate the expression of the chick calbindin gene in the kidney. All three cal-bindin-D28K mRNA species (2000, 2600, and 3100 nucleotide transcripts) were present in the kidney tissue of chronically vitamin D-deficient (-D) chicks; this basal constitutive level of expression was, however, enhanced by administration of the vitamin D3 metabolite, 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in both a time- and dose-dependent manner. D-deficient chick renal calbindin-D28K protein levels (measured by ELISA) were maximally (twofold) stimulated by 6.5 nmole per animal of 1,25-(OH)2D3 when measured 48 h later; a concomitant level of augmentation of calbindin-D28K mRNA accumulation was also observed at this time. Time course experiments showed that enhanced renal calbindin-D28K mRNA accumulation (in -D chicks) was significantly stimulated as early as 8 h and were maximal 12 h after a single pharmacologic dose of 1,25-(OH)2D3; this elevated level of gene expression was maintained for at least 72 h. Renal calbindin-D28K protein levels (constitutively expressed in the -D chick) were significantly stimulated (twofold) as early as 12 h following the single dose of steroid hormone; the level of calbindin-D28K also remained elevated for a minimum of 72 h. Collectively, these data indicate that 1,25-(OH)2D3 acts upon the renal calbindin-D28K gene in a manner similar to that operable in the intestine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗