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PubMed1989

Co-localization of adrenergic receptors and vitamin-D-dependent calcium-binding protein (calbindin) in the dopaminergic amacrine cells of the rat retina.

Using antisera against tyrosine hydroxylase (TH) and purified beta 2-adrenergic receptors (beta 2-AdR), we found that TH- and AdR-like immunoreactivities coexisted in large amacrine cells. These findings indicated an association between dopamine-containing amacrine cells and adrenergic amacrine cells. The present study also showed that amacrine cells with TH-like immunoreactivity have vitamin-D-dependent calcium-binding protein (calbindin, 27,000 kDa)-like immunoreactivity as well, suggesting that calbindin plays an important postsynaptic role in dopaminergic amacrine cells.

Animals↗
PubMed1989

Maintenance of neuronal expression of calbindin by a muscular extract in cultures of chick dorsal root ganglion cells.

Calbindin D-28K is a calcium-binding protein which is expressed by subpopulations of dorsal root ganglion cells cultured from 10-day-old (E10) chick embryos. After 7 or 10 days of culture, more than 20% of the ganglion cells are immunostained by an anticalbindin-antiserum; however, after 14 days of culture, the proportion drops to 10%. This fall can be prevented by addition of muscle extract to cultures at 10 days. Thus the transitory expression of calbindin-immunoreactivity by responsive sensory neurons would be not only induced but also maintained by a differentiation factor of muscular origin.

Animals↗
PubMed1991

The immunocytochemical distribution of calbindin-D28k and parvalbumin in identified neurons of the pulvinar-lateralis posterior complex of the cat.

The calbindin-D28k and parvalbumin immunoreactivities of the neurons of the pulvinar-lateral posterior complex (Pul-LP) were studied in the cat. The neurons of the Pul-LP projecting to the cerebral cortex were identified by a retrogradely transported tracer injected in the suprasylvian gyrus. Two populations of cells were found, a calbindin-D28k-immunoreactive, large-diameter population and a parvalbumin-immunoreactive, small-diameter group. The two kinds of cells are closely intermingled. The former includes the neurons retrogradely marked, and therefore projecting to the suprasylvian gyrus. The latter includes neurons which were not retrogradely marked, and therefore presumably intrinsic elements.

Animals↗
PubMed1992

Localization of gene expression of calbindin in the brain of adult rats.

Localization of gene expression of calbindin, a cytosolic calcium-binding protein, was examined throughout the adult rat brain by in situ hybridization with cDNA probes. The gene was expressed most intensely in the Purkinje cells in the cerebellum, intensely in the granule cells of the dentate gyrus, and moderately in the inferior olivary nucleus, in the nuclei of the trapezoid body, in the medial part of the lateral habenular nuclei, entorhinal cortex and in the mammillary nuclei. In addition, weak expression of the gene was widespread in the forebrain and brainstem gray matter, and also in small cells in the spinal posterior horn as well as the ependymal cells. The widespread and heterogeneous expression of the gene in the brain suggests that calbindin is differentially involved in calcium-regulated phenomena in different neurons.

Animals↗
PubMed1995

Distribution of calbindin D-28k immunoreactivity in the cochlear nucleus of the young adult chinchilla.

Calbindin is a 28 kD calcium-binding protein found in neural tissue. Although its functional role in nerve cell physiological processing is still uncertain, previous investigations have suggested that because of its intracellular calcium buffering and regulation properties, it could influence temporal precision of neuronal firing to subserve temporal processing in the auditory brainstem, or could mediate monaural versus binaural coding, or be involved in synaptic plasticity (learning). The present study demonstrates differential calbindin immunoreactivity in the cochlear nuclear complex of the chinchilla, a rodent with exceptionally good low-frequency hearing. The most intense labeling in the cochlear cochlear nucleus was in somata of cartwheel and fusiform cells of the fusiform cell layer, and somata and process of the molecular layer of the dorsal cochlear nucleus (DCN). Only a relatively few scattered neurons were stained in the deep layers of DCN. In contrast, moderate labeling of neurons and neuropil throughout the ventral cochlear nucleus was seen. For instance, moderately stained spherical and elongate cells of the anteroventral cochlear nucleus were observed in contact with labeled puncta and amidst stained fibers. In the cochlear nerve root region, stained auditory nerve fibers and global cells were noted. In the posteroventral cochlear nucleus, principal cells of elongate and octopus shape were observed, in contact with labeled swellings and surrounded by labeled neuropil.

Animals↗
PubMed1994

Partial colocalization of the GABAA receptor with parvalbumin and calbindin D-28K in neurons of the visual cortex and the dorsal lateral geniculate nucleus of the cat.

Monoclonal antibodies to a synthetic peptide fragment of the beta 1-subunit of the bovine central GABAA/benzodiazepine receptor were used to investigate immunocytochemically the distribution of this receptor in the visual system of the cat. Labeled neurons were observed in all layers of the visual cortex and the dorsal lateral geniculate nucleus. About half of the total cortical or geniculate neuronal population was found to be positive. To further identify immunocytochemically these GABAA receptor expressing cells, double stainings were undertaken with, on one hand, the monoclonal antibodies directed against the receptor complex, and on the other hand polyclonal antisera directed against cat muscle parvalbumin or chicken calbindin D-28K. A high degree of colocalization between either of the two calcium binding proteins and the GABAA receptor was found in the upper layers (I, II and III) of the visual cortex and in the A and C laminae of the dorsal lateral geniculate nucleus; all calbindin D-28K-positive cells were immunoreactive for the GABAA receptor. The parvalbumin-positive cells, scattered throughout all layers of the dorsal lateral geniculate nucleus and the visual cortex, except cortical layer I, were also all positive for the GABAA receptor. However, a large proportion of all GABAA receptor bearing cells were negative for one of the calcium binding proteins.

Animals↗
PubMed2006

Prenatal acoustic stimulation influences neuronal size and the expression of calcium-binding proteins (calbindin D-28K and parvalbumin) in chick hippocampus.

Prenatal auditory enrichment by species-specific sounds and sitar music enhances the expression of immediate early genes, synaptic proteins and calcium binding proteins (CaBPs) as well as modifies the structural components of the brainstem auditory nuclei and auditory imprinting area in chicks. There is also facilitation of postnatal auditory preference of the chicks to maternal calls following both types of sound stimulation indicating prenatal perceptual learning. To examine whether the sound enrichment protocol also affects the areas related to learning and memory, we assessed morphological changes in the hippocampus at post-hatch day 1 of control and prenatally sound-stimulated chicks. Additionally, the proportions of neurons containing calbindin D-28K and parvalbumin immunoreactivity as well as their protein levels were determined. Fertilized eggs of domestic chick were incubated under normal conditions of temperature, humidity, forced draft of air as well as light and dark (12:12h) photoperiods. They were exposed to patterned sounds of species-specific and sitar music at 65 dB for 15 min per hour over a day/night cycle from day 10 of incubation till hatching. The hippocampal volume, neuronal nuclear size and total number of neurons showed a significant increase in the music-stimulated group as compared to the species-specific sound-stimulated and control groups. However, in both the auditory-stimulated groups the protein levels of calbindin and parvalbumin as well as the percentage of the immunopositive neurons were increased. The enhanced proportion of CaBPs in the sound-enriched groups suggests greater Ca(2+) influx, which may influence long-term potentiation and short-term memory.

Acoustic Stimulation↗
PubMed2001

Calcineurin A and calbindin immunoreactivity in the spinal cord of G93A superoxide dismutase transgenic mice.

A qualitative immunohistochemical study was performed on calcineurin A- and calbindin-positive neurons in the spinal cord of transgenic mice, an animal model of amyotrophic lateral sclerosis, carrying the G93A mutation of the Cu/Zn-superoxide dismutase gene. The results show that calcineurin A-immunoreactive motoneurons are affected by the neurodegenerative process; in contrast, calbindin-positive cells are selectively spared. The findings suggest that calcineurin plays a role as an accessory factor responsible for selective vulnerability in the neurodegenerative process of amyotrophic lateral sclerosis.

Animals↗
PubMed1998

Co-expression of p75NTR- and calbindin-immunoreactivity in cholinergic neurons of the raccoon basal forebrain.

The cholinergic system of the basal forebrain is involved in the modulation of sensory information. This has previously been investigated in the raccoon, an animal especially interesting because of its highly developed somatosensory cortex. The present study focused on the co-expression of the low-affinity neurotrophin receptor p75NTR and calbindin in cholinergic neurons of the raccoon basal forebrain and neostriatum. Carbocyanine immunofluorescence double labelling revealed the co-localization of choline acetyltransferase and p75NTR as well as calbindin in a large portion of basal forebrain neurons, but not in the neostriatum. In contrast, immunolabelling of two other calcium-binding proteins, parvalbumin and calretinin, was found exclusively in non-cholinergic neurons.

Animals↗
PubMed1999

FlCRhR/cyclic AMP signaling in myenteric ganglia and calbindin-D28 intrinsic primary afferent neurons involves adenylyl cyclases I, III and IV.

The aims of this study were to improve insight into cAMP signaling in myenteric neurons and glia and identify the adenylyl cyclase (AC) isoforms expressed in myenteric ganglia of the guinea-pig small intestine. An increase in the intracellular cAMP levels was measured indirectly by an increase in the 520 nm/580 nm fluorescence emission ratio of the protein kinase A fluorosensor FlCRhR. Forskolin or pituitary adenylyl cyclase activating peptide caused an increase in cAMP levels in cell somas and neurites and elicited a slow EPSP-like response in myenteric AH/Type 2 neurons, whereas the inactive form of forskolin was without these effects. Glia displayed similar cAMP responses. Immunoblot analysis showed that AC I, III and IV were present in myenteric ganglia, with AC I being detected as two bands of 160 kDa and 185 kDa, AC III as two bands near 220 kDa, and AC IV as two bands of greater than 220 kDa. Pretreatment with N-ethylmaleimide and N-glycosidase F revealed an AC IV band at 115 kDa. Preabsorption with specific blocking peptides prevented detection of AC I or AC IV immunoreactive proteins. In ganglia which expressed strong AC IV immunoreactivity, no immunoreactive bands were detected for AC II, AC V/VI, AC VII or AC VIII. The amount of AC isoforms expressed in myenteric ganglia followed the order of AC IV&z.Gt;III>I. Immunofluorescent labeling studies revealed that AC I, AC III and AC IV were variably expressed in myenteric neurons and glia of the duodenum, jejunum and ileum. In the guinea-pig ileum, AC I, III and IV immunoreactivities were respectively present in 26%, 58% and 89% of calbindin-D28-colabeled myenteric neurons. These findings suggest that (1) AC I, AC III and AC IV variably contribute to cAMP signaling in myenteric ganglia, (2) AC I, AC III and AC IV may be differentially expressed in distinct subsets of calbindin-D28 neurons which may represent intrinsic primary afferent myenteric neurons. Our study also provides direct evidence for activation of cAMP-dependent protein kinase.

Action Potentials↗
PubMed1990

Comparative structural analysis of the calcium free and bound states of the calcium regulatory protein calbindin D9K.

The solution structure of apo calbindin D9K, a member of the calmodulin superfamily of calcium-binding regulatory proteins, has been investigated by 1H nuclear magnetic resonance spectroscopy and the results compared with a corresponding study of the calcium-loaded protein. On the basis of complete sequence-specific assignments, characteristic patterns of short proton-proton distances have been identified in two-dimensional nuclear Overhauser effect spectra, allowing the elements of secondary structure to be determined. It is found that four helices and a short section of antiparallel beta-sheet are present regardless of the calcium content of the protein. In addition, a preliminary analysis of the long-range nuclear Overhauser effects shows that the global folding patterns are the same and that the tertiary structures of the apo protein is very similar to that of the calcium-loaded protein. These results are in stark contrast to a number of very substantial changes in 1H chemical shift. Preliminary studies of protein dynamics show some very large differences in flexibility and internal mobility. This suggests that protein dynamics may play a role more important than was initially realized in the function of calbindin D9K and other homologous calcium-binding regulatory proteins.

Amino Acid Sequence↗
PubMed2001

Steroid hormone influence on brain calbindin-D(28K) in male prepubertal and ovariectomized rats.

Calbindin-D(28K) (CALB), a calcium-binding protein, is thought to buffer intracellular calcium levels in neurons playing several important roles during central nervous system development such as, protecting against apoptosis (programmed cell death), neurodegenerative diseases and influencing sexually dimorphic brain structures. While preliminary research indicates that calbindin levels are modulated by steroids, there has not yet been a comprehensive study to determine the role androgens, androgen metabolites and corticosterone have on CALB expression in males and throughout the estrous cycle in rats. The present study had two main components utilizing Western analysis: (1) examination of the influence of steroid hormones (testosterone, dihydrotestosterone, corticosterone, and estradiol) and aromatase and 5alpha-reductase blockers on rat brain CALB expression in frontal cortex, MBH-POA, and cerebellum of male rats in experiment 1; (2) characterization of CALB abundance in frontal cortex, MBH-POA, and cerebellum throughout the hormonally induced estrous cycle of rats in experiment 2. There were no significant alterations in CALB levels by any of the treatments in experiment 1 or experiment 2 when frontal cortical tissue was examined. In male MBH-POA samples, estradiol treatment significantly increased CALB levels compared to oil-injection and aromatase or 5alpha-reductase blockers. Additionally, DHT treatment significantly increased CALB levels vs. 5alpha-reductase blocker values. In female samples, MBH-POA CALB levels increased from diestrus through proestrus and estrus to metestrus, where metestrus values were significantly higher compared to diestrus levels. In the cerebellum, the only significant alteration in CALB levels, in males, was observed in corticosterone-treated animals where a significant decrease was seen compared to oil injection. In females, cerebellum CALB levels increased from diestrus through proestus, with a slight decrease at estrus. Thereafter, CALB levels increased during metestrus where cerebellar CALB values were significantly higher than diestrus levels. These findings suggest that steroid hormones play an important regulatory role in CALB expression in the brain (except for the frontal cortex) where it potentially influences the development/function and neuroprotective changes of neuroanatomical structures.

Animals↗
PubMed1999

Effect of calbindin D 28K on sodium transport by the luminal membrane of the rabbit nephron.

We previously reported that in the rabbit, the vitamin D-dependent calcium binding protein 28K (CaBP 28K) increases calcium (Ca2+) transport in the distal tubule by opening a high affinity Ca2+ channel in the luminal membrane. Since Na+ and Ca2+ transports are interdependent in this membrane, we questioned whether the calbindin has any influence on Na+ transport. Luminal membranes from rabbit proximal and distal tubules were purified and 22Na uptake by the membrane vesicles was measured using the rapid filtration technique. The vesicles were loaded with 280 mM mannitol and 20 mM Tris-Hepes pH 7.4, with either 3 microM CaBP or the carrier. Incubation medium contained 1 mM 22NaCl, 278 mM mannitol, and 20 mM Tris-Hepes pH 7.4. The presence of 3 microM CaBP 28K in the distal luminal membrane vesicles increased the 0.5 mM Ca2+ uptake from 0.91 +/- 0.21 to 1.84 +/- 0.33 pmol/microg/10 s (P < 0.01) and decreased 1 mM Na+ uptake from 0.62 +/- 0.15 to 0.27 +/- 0.08 pmol/microg/10 s (P < 0.05). A similar decrease of Na+ uptake was observed in proximal luminal membrane experiments. The effect on Na+ uptake by the distal membrane was dose-dependent with a IC50 of 4.5 microM. Addition of 2 mM Ca2+ to the incubation medium decreased 1 mM Na + uptake from 0.62 +/- 0.15 to 0.49 +/- 0.12 pmol/microg/10 s (P < 0.05), but did not influence the effect of CaBP 28K on Na+ uptake. Experiments performed in the presence and absence of ethyl isopropyl amiloride (EIPA) suggest that the effect of calbindin involves the Na+/H+ exchanger activity.

Animals↗
PubMed2001

The retinal input to calbindin-D28k-defined subdivisions in macaque inferior pulvinar.

Several studies have provided evidence for direct retinal input to the pulvinar of macaques monkeys, but there is no general agreement regarding the extent of this projection. Moreover, it is not known how retinal input correlates with chemoarchitectonic subdivisions recently recognized within the large, classical divisions of the pulvinar. The potential implications of this correlation have become more evident after reports that chemoarchitectonic subdivisions of the inferior pulvinar (PI) have specific patterns of connections with cortical visual areas. We have therefore re-examined the retino-PI projection using intraocular injections of horseradish peroxides, and correlated it with pulvinar subdivisions revealed using an antibody for calbindin-D28k. Retinal projections were found preferentially within the medial subdivision of the PI, with some involvement of the posterior and central calbindin-D28k defined subdivisions.

Animals↗
PubMed1998

Chronic morphine alters calbindin D-28k immunostaining patterns in mouse forebrain.

The influence of chronic morphine treatment on the brain of adult mouse has been studied. Female Swiss mice were daily administered saline or morphine (30 or 60 mg/kg body weight) for a period comprising 7 days before mating, during gestation and until 21 days post-partum. Their brains were then perfusion-fixed and examined for histology and calbindin D-28k protein-immunoreactivity. Histological observations revealed no significant changes in the various brain regions; whereas a reduced number of calbindin-positive cells was encountered in the cingulate and parietal cortices and the lateral septal regions of morphine-treated brains compared with those of controls. The alteration in the expression-patterns of this neuroprotective calcium-binding protein in specific regions of the adult brain might be one of the mechanisms by which the addictive drugs modify the functional aspects of the CNS.

Animals↗
PubMed2001

Bone morphogenetic protein-2, but not bone morphogenetic protein-7, promotes dendritic growth and calbindin phenotype in cultured rat striatal neurons.

Bone morphogenetic proteins are members of the transforming growth factor-beta superfamily. They are widely expressed in the mammalian nervous system, where they exert trophic effects on several neuronal populations. We studied the neurotrophic activity of bone morphogenetic protein-2 and bone morphogenetic protein-7 (also called osteogenic protein-1) on cultured striatal cells, previously shown to express bone morphogenetic protein ligands and receptors. Our results indicate that only bone morphogenetic protein-2 promoted the differentiation of GABAergic neurons, especially of the calbindin-positive subpopulation, the subset of projecting striatal neurons that degenerates in Huntington's disease. Bone morphogenetic protein-2 increased the area, perimeter and degree of arborization of GABAergic neurons, promoting calbindin phenotype without altering proliferation or apoptosis. In contrast, neither bone morphogenetic protein-2 nor -7 affected striatal cholinergic interneurons. However, they both increased the number of glial fibrillary acidic protein-positive cells. Suppression of glial proliferation with 5-fluorodeoxyuridine did not abolish bone morphogenetic protein-2 effects on the differentiation of striatal neurons, ruling out an indirect mechanism through astrocytes. In conclusion, our results show that bone morphogenetic protein-2 promotes the differentiation of cultured GABAergic striatal neurons, suggesting that bone morphogenetic proteins are involved in the development of the striatum.

Animals↗
PubMed2003

Light microscopic study of GluR1 and calbindin expression in interneurons of neocortical microgyral malformations.

Rat neocortex that has been injured on the first or second postnatal day (P0-1) develops an epileptogenic, aberrantly layered malformation called a microgyrus. To investigate the effects of this developmental plasticity on inhibitory interneurons, we studied a sub-population of GABAergic cells that co-express the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor GluR1 subunit and the calcium-binding protein, calbindin (CB). Both malformed and control cortex of adult (P40-60) animals contained numerous interneurons double-stained for CB and GluR1. Immunoreactivity (IR) for CB was up-regulated in perikarya of interneurons within supragranular layers of control cortex between P12 and P40. However, in malformed adult (P40) cortex, CB-IR levels were significantly lower than in adult controls, and fell midway between levels in immature and adult control animals. Between P12 and P40, GluR1-IR was down-regulated in perikarya of interneurons in control cortex. Somatic GluR1-IR levels in malformed adult (P40) cortex were not different from adult controls. These neurons formed a dense plexus of highly GluR1-positive spiny dendrites within layer II. The dendritic plexus in the malformation was more intensely GluR1-immunoreactive than that in layer II of control cortex. This was due to apparent changes in thickness and length of dendrites, rather than to significant changes in the number of interneuronal perikarya in the microgyral cortex. Results indicate that the population of GluR1/CB-containing interneurons is spared in malformed microgyral cortex, but that these cells sustain lasting decreases in their somatic expression of calbindin and alterations of dendritic structure. Potential functional implications of these findings are discussed.

Age Factors↗
PubMed1997

Calbindin immunoreactivity delineates the circadian visual centers of the brain of the common marmoset (Callithrix jacchus).

The hypothalamic suprachiasmatic nucleus and the thalamic pregeniculate nucleus (which includes the intergeniculate leaflet) comprise the circadian visual system in the primate brain. In this study, we used intraocular injections of cholera toxin subunit B to identify those nuclei in the common marmoset brain, and demonstrated that calbindin D-28k immunoreactivity apparently labels most neurons in both the suprachiasmatic and pregeniculate nuclei. These data suggest that calbindin D-28k could represent a reliable neuronal marker for structures of the circadian visual system in marmosets and provide anatomical information on the primate equivalent of the rodent intergeniculate leaflet.

Animals↗