Disease relevance of Calb1

• Expression in Escherichia coli of full-length and mutant rat brain calbindin D28. Comparison with the purified native protein [1].
• 1. We have examined the ability of the Ca(2+)-binding proteins (CABP) calbindin D28k and paravalbumin to modulate increases in the intracellular free Ca2+ concentration ([Ca2+]i), produced by brief depolarizations, in rat dorsal root ganglion (DRG) neurones [2].
• We used herpes simplex amplicons to overexpress calbindin D(28k) (CaBP) selectively in dentate gyrus (DG) granule cells [3].
• Immunoreactive staining for the calcium-binding proteins calbindin and parvalbumin in lower brainstem auditory nuclei shows abnormalities in areas susceptible to the effects of hyperbilirubinemia and provides a sensitive new way to assess bilirubin toxicity in the auditory system [4].
• Nonetheless, our data do suggest that calbindin may offer striatal neurons some protection against moderate excitotoxic insults, and this may explain the reportedly slightly greater vulnerability of striatal neurons that are poor in calbindin to ischemia and Huntington's disease [5].

Psychiatry related information on Calb1

• In rats stimulated by novel environmental cues during the period of wakefulness preceding perfusion, Fos-positive neurons increased markedly relative to unstimulated animals, and involved the majority of the calbindin- or parvalbumin-labeled cell populations (60-75% and over 95%, respectively) [6].
• Thirty days after the last of 36 electroconvulsive shocks, the calbindin immunoreactivity was back to normal [7].
• Cytotoxicity in response to calcium ionophore or amyloid beta-peptide (which accumulates in the brain in Alzheimer's disease and has been reported to be neurotoxic) was measured by MTT reduction in vector transfected cells and in calbindin transfected clones [8].

High impact information on Calb1

• Prolonged afferent stimulation of the rat dentate gyrus in vivo leads to degeneration only of those cells that lack immunoreactivity for the calcium binding proteins parvalbumin and calbindin [9].
• Total RNAs were isolated from both duodenum and kidney cortex, and the VDR and calbindin mRNA levels were determined by Northern blot hybridization using specific cDNA probes [10].
• We report that basic fibroblast growth factor is mitogenic for stem cells and is a differentiation factor for calbindin-expressing hippocampal neurons [11].
• In contrast, BDNF elicited small but significant calbindin responses [12].
• We have used a retrovirus containing the full-length cDNA for CB to transfect the pituitary tumor cell line GH3, to generate CB-expressing GH3 cells and to investigate whether ionic channel activities as well as the concentration of intracellular free Ca2+ ([Ca2+]i) homeostasis could be altered by the presence of this Ca(2+)-binding protein [13].

Chemical compound and disease context of Calb1

• Thus, selective vulnerability of GABA-containing neurons and relative resistance of neurons in which PV or CB immunoreactivity is present or is expressed later, occur in the hippocampus after neonatal anoxia [14].
• The influence of kainic acid, which induces status epilepticus, on the expressions of calbindin D28k, parvalbumin and calretinin was examined in the rat striatum by immunohistochemistry and microdensitometry [15].
• In rats that were injected after status epilepticus with bromodeoxyuridine (BrdU) to label newly born cells, and also labeled for calbindin D(28K) (because it normally stains granule cells), many double-labeled neurons were located at the hilar/CA3 border [16].
• Calbindin D28K gene transfer via herpes simplex virus amplicon vector decreases hippocampal damage in vivo following neurotoxic insults [17].
• We now report that brain injury, effected by systemic administration of the excitotoxin kainate or mechanical trauma, induces expression of calbindin in cells of the corpus callosum and subcortical white matter [18].

Biological context of Calb1

• Studies of vitamin D-dependent 28-kilodalton calcium binding protein (calbindin D28) have been hindered by difficulties in purifying large amounts of the protein [1].
• Nucleotide sequence of cDNA to mRNA for a cerebellar Ca-binding protein, spot 35 protein [19].
• Comparing the amino acid sequence to that recently reported for the chicken Calbindin D28 there is 79% homology [20].
• 7. Calbindin D28k caused an 8-fold decrease in the rate of rise in [Ca2+]i and altered the kinetics of decay of [Ca2+]i to a single slow component [2].
• Recent evidence supports a neuroprotective role for calbindin in regulating calcium homeostasis during periods of heightened Ca2+ influx [21].

Anatomical context of Calb1

• In contrast, only a subset of CALB- and CALR-immunoreactive interneurons (24% and 23%, respectively) displayed hybridization signals for NGF [22].
• In the present study, calretinin (CALRET) and CALB patterns were determined by Western analysis in the medial basal hypothalamus (MBH) from male rats along with assaying plasma testosterone levels during postnatal development [23].
• A small percentage of the CA-positive cells in lamina I and in the magnocellular layers were retrogradely labeled from the thalamus [24].
• Parvalbumin, calbindin, or calretinin in cortically projecting and GABAergic, cholinergic, or glutamatergic basal forebrain neurons of the rat [25].
• Postembedding immunostaining demonstrated that CB-containing cells contain GABA, whereas CR-positive axon terminals forming asymmetric synapses are devoid of this labeling [26].

Associations of Calb1 with chemical compounds

• These findings suggest that there is not a clear correspondence between the androgen status in male rats and the calcium-binding proteins (CALRET & CALB) expressed in the MBH [23].
• Calbindin-positive neurons constituted almost 60% of the GABA-containing population in both subdivisions of the basolateral nucleus and more than 40% of the GABA-containing population in the lateral nucleus [27].
• Significant proportions of Calb(+) (>40%) and Calret(+) (>80%) neurons were immunopositive for phosphate-activated glutaminase, the synthetic enzyme for transmitter glutamate [25].
• Most CALB/NGF+ cells were located in the stratum oriens/alveus of the CA3-CA1 regions, suggesting that they may include the population of CALB+, hippocamposeptal, nonpyramidal neurons [28].
• Combined dual-immunofluorescence and confocal microscopy revealed that somatodendritic alpha4 nicotinic acetylcholine receptors colocalized with cortical neurons stained positively for CR, PV or CB [29].

Physical interactions of Calb1

• These data indicate that PA and CA antisera identify two cell populations in whisker-related regions of the V brainstem complex and that PA cells are somatotopically patterned in PrV, SpI, and SpC [24].
• In the lateral septum, 5-HT1A receptor immunoreactivity was colocalized with the calcium-binding protein calbindin D-28k, a marker for septal GABAergic somatospiny neurons [30].
• We tested whether the rat pineal gland controls the expression of a neuropeptide (neuropeptide Y) and a calcium-binding protein (calbindin) in sympathetic postganglionic neurones that innervate it [31].

Co-localisations of Calb1

• From the second week, in addition to labeling vestibular afferents in their specific target areas, parvalbumin was also found colocalized with calbindin in mature Purkinje cell afferents [32].
• Calbindin is largely co-localized with SRIF, and not with VIP [33].
• On the other hand, calbindin was also found in spinal afferents to the esophagus where it was co-localized with calcitonin gene-related peptide [34].

Regulatory relationships of Calb1

• In cortical or diencephalic cultures, CR was rarely coexpressed with GABA or calbindin D-28k [35].
• In layers II to IV of the barrel cortex most PARV-immunoreactive neurons are likely to derive from a subpopulation of CALB-immunoreactive neurons whose CALB immunoreactivity ceases when they begin to express PARV between the second and third postnatal weeks [36].
• In conclusion, all calbindin-containing cortical interneurons seem to be under direct influence of other GABAergic interneurons expressing the peptide VIP [37].
• Glial cell line-derived neurotrophic factor stimulates the morphological differentiation of cultured ventral mesencephalic calbindin- and calretinin-expressing neurons [38].
• A small population of calbindin-positive interneurons and very few calretinin-positive cells express Reln immunopositivity [39].

Other interactions of Calb1

• All of these are PV, CB, SOM and NOS negative [40].
• Combined dual immunofluorescence and confocal microscopy further revealed that CRF-ir puncta made possible pericellular contacts on PV-ir (not CB-, CR- or glutamate-ir) cell bodies [41].
• NC/CB, NC/CR and NC/VIP double-labeled cells were found in all hippocampal regions, and represented 29%, 24% and 18% of the NC-IR cells, respectively [42].
• With the exception of calbindin-positive interneurons, GluR2/3 was absent from hippocampal interneurons in both rat and monkey [43].
• From dual immunostaining for the CBPs and glutamic acid decarboxylase (GAD), it appeared that the vast majority (>90%) of the Parv(+) group was GAD(+), whereas only a small minority (<10%) of the Calb(+) or Calret(+) group was GAD(+) [25].

Analytical, diagnostic and therapeutic context of Calb1

• Parvalbumin and calbindin immunocytochemistry reveal functionally distinct cell groups and vibrissa-related patterns in the trigeminal brainstem complex of the adult rat [24].
• Molecular cloning of cDNA to mRNA for a cerebellar spot 35 protein [44].
• By double immunostaining and correlated light and electron microscopy, we show that calbindin (CB)-containing interneurons located in layers II-VI of rat barrel cortex are targets of symmetric VIP-immunoreactive synapses [37].
• Partial coexistence of neuropeptide Y and calbindin D28k in the trigeminal ganglion following peripheral axotomy of the inferior alveolar nerve in the rat [45].
• We have used fluorescence and circular dichroism (CD) spectroscopy to characterize the effects of calcium binding on the structure and stability of calbindin [46].

References