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PubMed2005

Calbindin, calretinin and parvalbumin immunoreactivity in the retina of the chameleon (Chamaeleo chamaeleon).

Apart from the pioneering studies of Ramon y Cajal [1893] and Rochon-Duvigneaud [1943], few studies have been devoted to the detailed study of the cytological and biochemical structure of the chameleon retina. In the present study we analyzed the expression of calbindin (CB), calretinin (CR) and parvalbumin (PV) immunoreactivities in the chameleon retina, and compared their distribution with those found in the retinas of other vertebrate species. CB immunoreactivity is dense in photoreceptors, horizontal and some lower amacrine cells. The most intense immunoreactivity was observed for calretinin; CR-ir amacrine cells are distributed throughout the inner nuclear, inner plexiform, and ganglion cell layers of the retina. Horizontal cells also display immunoreactivity to CR. A few retinal interneurons are weakly PV-ir. Double-labeling shows that all PV-ir or CB-ir cells, except the photoreceptors, are also strongly CR-ir. The distributions of these calcium-binding proteins in the chameleon retina share similarities with those observed in mammalian and avian retinas. In addition, the widespread distribution and co-localization of CB and CR reinforces the idea that these proteins play a general role in buffering the intracellular calcium levels in retinal cells. Furthermore, CB- and CR-immunoreactivities have enabled us to identify for the first time axon-bearing horizontal cells in the peripheral retina of the chameleon, very similar to those described in mammals.

Animals↗
PubMedDate not supplied

Calbindin-D28K localization in the primate inner ear.

The distribution of one of the calcium-binding proteins, calbindin-D28K (CB-D28K), was studied in the adult human and squirrel monkey inner ear by means of immunocytochemical methods. Inner and outer hair cells in the organ of Corti and vestibular hair cells showed CB-D28K immunoreactivity, though some vestibular hair cells were devoid of immunoreactivity. In the spiral and vestibular ganglion, immunoreactive cells were found in both the squirrel monkey and human. The present results indicate that CB-D28K is localized within afferent neuronal components in these sensory organs and may regulate Ca++ levels for optimal neurotransmission in the primate auditory and vestibular systems. This study also provides evidence of two nonneuronal localizations of CB-D28K in the squirrel monkey. Subpopulations of fibrocytes in the spiral ligament and vestibular end organs were enriched with CB-D28K, suggesting that these cells are possibly equipped with the function to regulate Ca++ concentration in the perilymphatic fluid. In the maculae, many CB-D28K-immunoreactive particles were found in the otoconial membrane, indicating that CB-D28K may participate in the formation of otoconia.

Adolescent↗
PubMed2001

Calbindin d28k overexpression protects striatal neurons from transient focal cerebral ischemia.

BACKGROUND AND PURPOSE: Increased intracellular calcium accumulation is known to potentiate ischemic injury. Whether endogenous calcium-binding proteins can attenuate this injury has not been clearly established, and existing data are conflicting. Calbindin D28K (CaBP) is one such intracellular calcium buffer. We investigated whether CaBP overexpression is neuroprotective against transient focal cerebral ischemia. METHODS: Bipromoter, replication-incompetent herpes simplex virus vectors that encoded the genes for cabp and, as a reporter gene, lacZ were used. Sprague-Dawley rats received bilateral striatal injections of viral vector 12 to 15 hours before ischemia onset. With the use of an intraluminal occluding suture, animals were subjected to 1 hour of middle cerebral artery occlusion followed by 47 hours of reperfusion. Brains were harvested and stained with X-gal (to visualize beta-galactosidase, the gene product of lacZ). The number of remaining virally transfected, X-gal-stained neurons in both the ischemic and contralateral striata were counted and expressed as the percentage of surviving neurons in the ischemic striatum relative to the contralateral nonischemic striatum. RESULTS: Striatal neuron survivorship among cabp-injected animals was 53.5+/-4.1% (n=10) versus 26.8+/-5.4% among those receiving lacZ (n=9) (mean+/-SEM; P<0.001). CONCLUSIONS: We conclude that viral vector-mediated overexpression of CaBP leads to neuroprotection in this model of central nervous system injury. This is the first demonstration that CaBP overexpression protects neurons in a focal stroke model.

Animals↗
PubMed1996

Ontogenetic expression of spot 35 protein (calbindin-D28k) in human olfactory receptor neurons and its decrease in Alzheimer's disease patients.

Expression of a calcium-binding protein, spot 35 protein (S-35, calbindin-D28k), was investigated immunohistochemically in the human olfactory mucosa of patients who ranged in age from 16 weeks of fetal development to 98 years old, including some with Alzheimer's disease (AD). S-35 immunoreactivity was observed clearly in olfactory receptor neurons (ORNs) and olfactory nerve bundles that were identified previously with antibodies to olfactory marker protein (OMP) and neuron-specific enolase (NSE). Throughout all ages, the mean number of ORNs immunoreactive for OMP did not change significantly, whereas the mean number of NSE- and S-35-immunoreactive ORNs declined markedly in the postnatal infant, young, and old patients when compared with that of the prenatal fetuses. S-35-immunoreactive ORNs decreased significantly in AD patients when compared with AD control patients. These results indicate that ORNs in humans express S-35 and that there is an age-related trend in the expression of S-35. Furthermore, the marked decrease of S-35 expression in ORNs of AD patients suggests that cell excitability associated with calcium ions and cell protective function against overload of intracellular calcium ions decline in these patients.

Adult↗
PubMedDate not supplied

GDNF increases the density of cells containing calbindin but not of cells containing calretinin in cultured rat and human fetal nigral tissue.

Among the dopaminergic neurons in substantia nigra pars compacta and in the ventral tegmental area, subpopulations express the calcium-binding proteins calbindin (CB) and calretinin (CR), and the CB-containing neurons are supposed to be less prone to degeneration in Parkinson's disease. Glial cell line-derived neurotrophic factor (GDNF) is a potent survival factor for nigrostriatal dopaminergic neurons. Using free-floating roller-tube (FFRT) cultures derived from fetal rat (E14) ventral mesencephalon we found that GDNF (10 ng/ml) significantly increased the number of surviving tyrosine hydroxylase (TH)-immunoreactive neurons. The possible effects of GDNF treatment on CB-immunoreactive (CB-ir) and CR-ir neurons in such cultures were examined in the present study. The neuronal cell densities were measured by quantifying the numbers of CB-ir and CR-ir neurons in areas of sections through the most extensive parts of the spherical cultures. In 4-day-old and 8-day-old cultures GDNF treatment increased the density of CB-ir neurons by 50% and 59%, respectively. Partial co-existence of TH and CB was shown using the method of double immunolabeling. The density of CR-containing neurons was unaffected by GDNF treatment as confirmed by Western blotting for CR. Parallel effects of GDNF treatment were obtained for cultures of human fetal ventral mesencephalon (8 weeks postconception). In conclusion, our findings identify GDNF as a potent factor for fetal rat and human nigral CB-ir neurons able to promote their survival in culture. Referring to a suggested neuroprotective role of CB, the results may be of relevance in the context of neuronal transplantation of patients suffering from severe Parkinson's disease.

Animals↗
PubMed1995

Immuno-localization of the calcitriol receptor, calbindin-D28k and the plasma membrane calcium pump in the human eye.

Using immunohistochemical methods, we detected epitopes of the calcitriol receptor, the ATP-dependent plasma membrane calcium pump and the 28kD vitamin D-dependent calcium-binding protein in sections of the human eye. In retinal photoreceptors, vitamin D receptor, plasma membrane calcium pump and calcium-binding protein epitopes were detected in the outer nuclear layer. Epitopes for the vitamin D receptor and the calcium-binding protein were present in the inner and outer segments of the photoreceptors, where visual transduction occurs. All three proteins were detected in some cells of the ganglion cell layer, the inner nuclear layer, and the retinal pigment epithelium. Epitopes for these proteins also were noted in the ciliary body epithelium. VDR epitopes were seen in lens epithelium. Some immunostaining for VDR, PMCA and calbindin-D28k also was present in the endothelium and in the basal epithelium of the cornea. The presence of these proteins in several tissues of the human eye suggests that the proteins may play a role in the cellular physiology of the eye. Their exact functions in the eye remain undetermined.

Antibodies, Monoclonal↗
PubMed1997

Progressive loss of glutamic acid decarboxylase, parvalbumin, and calbindin D28K immunoreactive neurons in the cerebral cortex and hippocampus of adult rat with experimental hydrocephalus.

The authors investigated functional neuronal changes in experimental hydrocephalus using immunohistochemical techniques for glutamic acid decarboxylase (GAD) and two neuronal calcium-binding proteins: parvalbumin (PV) and calbindin D28K (CaBP). Hydrocephalus was induced in 16 adult Wistar rats by intracisternal injection of a kaolin solution, which was confirmed microscopically via atlantooccipital dural puncture. Four control rats received the same volume of sterile saline. Immunohistochemical staining for GAD, PV, and CaBP, and Nissl staining were performed at 1, 2, 3, and 4 weeks after the injection. Hydrocephalus occurred in 90% of kaolin-injected animals with various degrees of ventricular dilation. In the cerebral cortex, GAD-, PV-, and CaBP-immunoreactive (IR) interneurons initially lost their stained processes together with a concomitant loss of homogeneous neuropil staining, followed by the reduction of their total number. With progressive ventricular dilation, GAD- and PV-IR axon terminals on the cortical pyramidal cells disappeared, whereas the number of CaBP-IR pyramidal cells decreased, and ultimately in the most severe cases of hydrocephalus, GAD, PV, and CaBP immunoreactivity were almost entirely diminished. In the hippocampus, GAD-, PV-, and CaBP-IR interneurons demonstrated a reduction of their processes and terminals surrounding the pyramidal cells, with secondary reduction of CaBP-IR pyramidal and granular cells. On the other hand, Nissl staining revealed almost no morphological changes induced by ischemia or neuronal degeneration even in the most severe cases of hydrocephalus. Hydrocephalus results in the progressive functional impairment of GAD-, PV-, and CaBP-IR neuronal systems in the cerebral cortex and hippocampus, often before there is evidence of morphological injury. The initial injury of cortical and hippocampal interneurons suggests that the functional deafferentation from intrinsic projection fibers may be the initial neuronal event in hydrocephalic brain injury. Although the mechanism of this impairment is still speculative, these findings emphasize the importance of investigating the neuronal pathophysiology in hydrocephalus.

Analysis of Variance↗
PubMed2002

Comparative immunolocalization of the plasma membrane calcium pump and calbindin D28K in chicken retina during embryonic development.

The immunolocalization of the plasma membrane calcium pump (PMCA) was studied in 4-week-old chick retina in comparison with calbindin D28K (CaBP) immunostaining. We have demonstrated that the monoclonal anti-PMCA antibody SF10 from human erythrocyte plasma membrane cross-reacts with a Ca2+ pump epitope of the cells from the neural retina. The immunolocalization of both proteins was also studied during the embryonic development of the chicken retina. At age 4.5 days, the cells of the retina were faintly immunoreactive to PMCA and CaBP antibodies, but the lack of cellular aggregation and differentiation did not allow discrimination between the two proteins. A clear difference in the localization was seen from the tenth day of development through post-hatching with slight variation. PMCA localized mainly in the outer and inner plexiform layers, in some cells in the ganglion layer, in the nerve fiber layer and slightly in the photoreceptor cells. CaBP was intensely stained in cones, cone pedicles and some amacrine cells. The number of CaBP positive amacrine cells declined after hatching. A few ganglion cells and several nerve fibers were CaBP immunoreactive. The role of these proteins in the early stages of retinal development is unknown, but the results suggest that Ca2+ homeostasis in the retina is well regulated, probably to avoid excessive accumulation of Ca2+, which often leads to neurodegeneration.

Animals↗
PubMed2000

Patterns of calretinin, calbindin, and tyrosine-hydroxylase expression are consistent with the prosomeric map of the frog diencephalon.

This paper re-examines a previously published segmental map of the frog diencephalon (Puelles et al. [1996] Brain Behav.Evol. 47:279-310) by means of immunocytochemical mapping of calretinin, calbindin, and tyrosine hydroxylase. The distribution of neuronal populations, axon tracts, and neuropils immunoreactive for these markers was studied in adult specimens of Rana perezi and Xenopus laevis sectioned sagittally or horizontally. Emphasis was placed on study of the relationship of observed chemoarchitectural boundaries with the postulated overall prosomeric organization and the schema of nuclear subdivisions we reported previously, based on acetylcholinesterase histochemistry and Nissl pattern in Rana. The data reveal a large-scale correspondence with the segmental map in both species, although some differences were noted between Rana and Xenopus. Notably, retinorecipient neuropils were generally immunoreactive for calretinin only in Rana. Importantly, calretinin immunostaining underlines particularly well the transverse prosomeric boundaries of the dorsal thalamus. A number of nuclear subdivisions noted before with AChE were corroborated, and some novel subdivisions became apparent, particularly in the anterior nucleus of the dorsal thalamus and in the habenular complex. The mapping of tyrosine hydroxylase clarified the segmental distribution of the catecholaminergic cell groups in the frog forebrain, which is comparable to that observed in other vertebrates.

Animals↗
PubMed2002

Effects of simulated weightlessness on Calbindin D-28K-immunoreactivity in rat soleus muscle spindle.

Objective. To analyze the mechanism involved in muscle spindle deterioration during simulated weightlessness. Method. Using the immunoperoxidase reaction utilizing the ABC (avidin-biotin-complex) method, Calbindin D28K-like immunoreactivity (CaBP-LI) of intrafusal fibres in soleus muscle were detected in 7 d, 14 d tail-suspended rats and compared with control rats. Result. The extrafusal muscle fibres and nerve fibres did not exhibit immunoreactivity to CaBP. CaBP-LI was found in some of the intrafusal muscle fibres in all the muscle spindles. After 14 d suspension, the immunoreactivity to CaBP of the intrafusal fibres decreased markedly. Conclusion. Simulated weightlessness could induce changes in the immunoreactivity of rat soleus muscle spindle to CaBP, which may contribute to the deterioration of muscle spindle.

Animals↗
PubMed2004

Increased calbindin-D28K immunoreactivity in rat cerebellar Purkinje cell with excitatory amino acids agonists is not dependent on protein synthesis.

The calcium binding protein Calbindin-D28K (CaBP) is abundantly expressed in cerebellar Purkinje cells and show increased immunoreactivity (CaBP-IR) when challenged with glutamate or an analog agonist for the ionotropic glutamate receptor (iGluR). Here we report that t-ACPD, a metabotropic glutamate receptor (mGluR) agonist, produced small increases in CaBP-IR which was potentiated by a mGluR antagonist The increase in CaBPIR was not due to de novo protein synthesis because the translational inhibitors (cycloheximide and emetine) or transciptional inhibitors (actinomycine-D and a-amanitine), did not prevent the EAA enhanced CaBP-IR. The CaBP-IR in the PC appears to be coupled to the ionotropic rather than the metabotropic glutamate receptors, but the latter become effective in the presence of their blocker, L-AP3. The results suggest that CaBP may increase its IR through a conformational change of the protein itself.

Animals↗
PubMed1991

Proliferative and degenerative changes in striatal spiny neurons in Huntington's disease: a combined study using the section-Golgi method and calbindin D28k immunocytochemistry.

Dysmorphic alterations of dendritic arbors and spines in spiny striatal neurons were identified in section-Golgi impregnations of moderate and severe grades of Huntington's disease (HD). These alterations could be characterized as either proliferative or degenerative changes. Proliferative changes included prominent recurving of distal dendritic segments, short-segment branching along dendrites, and increased numbers and size of dendritic spines. Degenerative alterations consisted of truncated dendritic arborizations, occasional focal dendritic swellings, and marked spine loss. Proliferative changes were found primarily in moderate grades of HD, while degenerative changes were predominantly found in severe grades. Cytopathologic changes increased with neuropathologic severity. Similar morphologic alterations were observed in calbindin D28k (Calb) stained neurons in HD striatum. The immunoreactive intensity of Calb staining was increased in the distal dendrites of positive neurons in HD striatum. The present findings provide morphologic and quantitative evidence that confirms an early and marked involvement of spiny striatal neurons in HD and suggest that neuronal growth, rather than degeneration, may be the harbinger of cell death in this disorder.

Aged↗
PubMed1990

Transcaltachia, vesicular calcium transport, and microtubule-associated calbindin-D28K: emerging views of 1,25-dihydroxyvitamin D3-mediated intestinal calcium absorption.

Within the past 5 years it has become apparent that the biological actions of the seco-steroid 1,25-dihydroxyvitamin D3 are more complex than previously realized. Many cell types respond in both a classical genomic manner, as well as in a nongenomic fashion to 1,25(OH)2D3. In intestine, the presumptive nongenomic effects of the seco-steroid result in transcaltachia, the rapid, hormonal stimulation of calcium transport. To better understand nongenomic points of regulation in the intestine, studies were undertaken to identify the subcellular components of the 1,25(OH)2D3-stimulated calcium transport pathway. This research has revealed the existence of a vesicular transport mechanism, an involvement of microtubules, and microtubule-associated calbindin-D28K.

Animals↗
PubMed1990

The use of quantitative immunocytochemistry (QICC) to measure calbindin D28k-like immunoreactivity in the rat brain.

We have developed a method of quantitative immunocytochemistry using an iodinated second antibody to visualise the anatomical distribution of primary antibodies in tissue sections, by macroautoradiography. Computer-assisted densitometry was used to analyse the pattern of optical densities within autoradiograms. The amount of antigen present in tissue sections was then quantified by comparison with non-biological standards which were processed in parallel with the tissue sections. Using this technique we have measured calbindin like-immunoreactivity in 4 areas of rat brain and have found that the values obtained are similar to those obtained by radioimmunoassay. A similar approach can be used to quantify autoradiograms by comparison with antigen standards to measure amounts of radiolabelled immunoreactivity and determine concentrations of biologically active molecules in discrete brain areas.

Animals↗
PubMed1990

Corticosterone regulates calbindin-D28k mRNA and protein levels in rat hippocampus.

Corticosterone was administered to normal and bilaterally adrenalectomized rats (250-300 g), and hormonal regulation of brain calbindin-D28k (CaBP28k) levels was investigated by radioimmunoassay for CaBP28k protein and by slot and Northern blot analyses for CaBP28k mRNA. The specificity of the changes observed in CaBP28k mRNA levels was tested by reprobing blots with calmodulin and B-actin cDNAs. Rats were either adrenalectomized, adrenalectomized treated with corticosterone, intact, or intact treated with corticosterone. Chronic corticosterone administration (subcutaneous injection for 7 days, 10 mg/day) to normal intact rats significantly increased levels of CaBP28k immunoreactivity (43%) and mRNA (125%) in the hippocampus. Adrenalectomy (animals were killed 7 days after adrenalectomy) produced a significant decrease in hippocampal CaBP28k immunoreactivity (85%) and mRNA (80%) compared with intact controls. Immunocytochemical analysis of tissue sections inducated a marked depletion of CaBP28k immunoreactivity in the dentate gyrus of the hippocampus 2 weeks after adrenalectomy. When adrenalectomized rats were treated with corticosterone (10 mg/day for 7 days), CaBP28k protein and mRNA levels in hippocampus were restored to levels observed in intact controls. No changes in CaBP28k protein and mRNA in kidney, cerebellum, striatum, or cerebral cortex were noted in adrenalectomized rats or in intact rats treated with corticosterone when compared with controls, indicating the specificity of the effect on CaBP28k for the hippocampus. These studies present the first evidence of a regulator of CaBP28k gene expression in the brain.

Adrenalectomy↗
PubMed1996

Calbindin D28K forms a Ca(2+)-dissociable complex with mellitin in vitro.

Calbindin D28K (CB), a cytosolic calcium binding protein (CBP), forms a macromolecular complex with the polypeptide mellitin (ME) the absence of calcium, which can be reversibly dissociated by the addition of Ca2+. The molar ratio of CB:ME constituted in this complex is 1:4, suggesting that CB interacts with the tetrameric form of ME. Like free tetrameric ME, the CB:ME complex does not migrate into 15% non-denaturing polyacrylamide electrophoretic gels, although both constituents migrate normally after irreversible complex denaturation by heating in sodium dodecyl sulphate (SDS). The interaction of these two proteins can be distinguished from the association of calmodulin (CM) with ME, which forms a reversibly dissociable, equimolar complex in the presence of Ca2+ and a stable non-migrating complex (molar ratio = 1:12) in its absence. Thus, CB and CM appear to bind ME under different Ca2+ regulatory control, suggesting possible roles for CB as a Ca(2+)-dependent regulatory binding protein.

Animals↗
PubMed1996

A population of supramammillary area calretinin neurons terminating on medial septal area cholinergic and lateral septal area calbindin-containing cells are aspartate/glutamatergic.

The excitatory amino acid, aspartate/glutamate content of septal complex calretinin (CR)-, choline acetyltransferase plus substance P-, and Leu-enkephalin (Leu-enk)-containing extrinsic afferents was examined. Experiments were carried out using the transmitter-specific [3H]-D-aspartate retrograde tracer technique in combination with immunostaining for CR, choline acetyltransferase, and Leu-enk. The extrinsic and intrinsic CR innervation of the same brain areas were elucidated on control rats and on animals in which the septum was surgically separated from its ventral afferents. Correlated light and electron microscopic double-immunostaining experiments were used to determine the synaptic connections between CR axon terminals and lateral septal area calbindin (CB)- and medial septal area choline acetyltransferase-immunoreactive neurons. Furthermore, to determine the synaptic power of supramammilloseptal aspartate/glutamatergic neurons on the septal complex, semiquantitative analyses were performed in the supramammillary area on retrogradely (1) [3H]-D-aspartate-radiolabeled and (2) HRP-labeled material. The results demonstrated that a population of the extrinsic CR axons originating in the supramammillary area are aspartate/glutamatergic. These fibers forming asymmetric synaptic contacts terminate on both CB and cholinergic neurons. Intraseptal CR neurons, which establish symmetric synapses, innervate only lateral septal area neurons, including the CB-containing cells. These observations, together with other published data, raise the possibility of a hippocampus-lateral septal (GABAergic CB-containing neurons)-supramammillary area (aspartate/glutamatergic cells)-medial septal (cholinergic neurons)-hippocampus signal loop, which might be involved in the generation and regulation of hippocampal theta rhythm activity.

Animals↗
PubMed1997

Calbindin-D28k immunoreactivity in the rat amygdala.

Calbindin-D28k (CB) is a calcium-binding protein whose exact function has yet to be elucidated. Because CB is contained in distinct cell types in the nervous system, it is a valuable marker for distinguishing specific nuclear subdivisions and neuronal populations. In the present study, immunohistochemical methods were used to localize CB in the rat amygdala. A subpopulation of nonpyramidal neurons in all nuclei of the basolateral amygdala (ABL) exhibited intense CB immunoreactivity (CB-ir). CB-positive puncta resembling axon terminals were observed surrounding pyramidal perikarya in the ABL. Pyramidal neurons in caudal and lateral portions of the ABL exhibited moderate CB-ir. Intensely stained nonpyramidal neurons resembling those of the ABL were also seen in the cortical nuclei, periamygdaloid cortex, and nucleus of the lateral olfactory tract; these nuclei also contained variable numbers of moderately stained pyramidal cells. Numerous CB-positive neurons were observed in all subdivisions of the medial nucleus. The posterodorsal subdivision of the medial nucleus exhibited a centrally located island of small CB-negative neurons and three cell-dense clusters of CB-positive neurons. The distribution of CB-ir in the central nuclear complex was very heterogeneous. The intermediate subdivision of the central nuclear complex exhibited the most robust staining, whereas the lateral subdivision contained relatively few CB-positive cells. Dorsal and ventral portions of the lateral capsular subdivision of the central nuclear complex could be readily distinguished on the basis of differing levels of CB-ir. These results indicate that CB is localized in discrete cell types and nuclear subdivisions in the rat amygdala and suggest that CB immunohistochemistry is a useful technique for identifying specific structural components in this brain region.

Amygdala↗