Disease relevance of Calb1

• In scrapie infected mice, cortical PV+ neurons were severely reduced while CB+ and CR+ neurons were well preserved [1].
• At the chronic stage, i.e. at 2 months after pilocarpine-induced status epilepticus, significant reduction of CCR7-10 expression in CB-, CR- and PV-immunpositive interneurons may suggest the phenotype change of surviving interneurons [2].
• In wildtype mice, the trigeminal ganglion contained abundant parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while the ganglion was almost devoid of calretinin-immunoreactive neurons [3].
• In the midbrain, calbindin is preferentially expressed in those dopamine neurons which are spared from degeneration in Parkinson's disease and its animal models [4].
• Effect of calbindin-D28K on cyclosporine toxicity in cultured renal proximal tubular cells [5].

Psychiatry related information on Calb1

• Recent biochemical data, however, indicate that CB also has characteristics of a Ca(2+) sensor and activates myo-inositol monophosphatase (IMPase), a key enzyme of the inositol-1,4,5-trisphosphate signaling cascade and an assumed target of mood-stabilizing drugs in the treatment of bipolar disorder [6].
• Striatal degeneration in Huntington's disease (HD) is associated with increases in perikaryal calbindin immunolabeling in yet-surviving striatal projection neurons [7].
• Immunoreactivity of calbindin D28K is compared in Alzheimer's disease and age-matched controls [8].

High impact information on Calb1

• We extended the study to the CB-positive facilitating excitatory mossy fiber-CA3 pyramidal cell synapse [9].
• Loading the presynaptic terminals with BAPTA or CB rescued the effect of the CB washout [9].
• The effects of different extracellular Ca2+ concentrations and of EGTA indicated that PPF in CB-containing terminals depended on Ca2+ influx rather than on the initial release probability [9].
• Such supralinear Ca2+ responses were attributed to the saturation of a large concentration (0.36 mM) of a mobile, high-affinity (dissociation constant, 0.37 microM) Ca2+ buffer with cooperative Ca2+ binding sites, resembling calbindin-D28K, and to an immobile, low-affinity Ca2+ buffer [10].
• In normal mice, GAD mRNA is present in four sets of neurons in the cerebellar cortex while calbindin mRNA is present only in Purkinje neurons [11].

Chemical compound and disease context of Calb1

• Neuronal phenotypes in mouse dorsal root ganglion cell cultures: enrichment of substance P and calbindin D-28k expressing neurons in a defined medium [12].
• The calcium-binding protein calbindin-D28k (CB) is located in midbrain dopaminergic (DA) neurons that are less vulnerable to degeneration in Parkinson's disease and in an animal model of the disorder, the MPTP-treated monkey [13].
• Cytochalasin B (CB), administered i.p. to C57B1/6 mice in a single dose as a suspension in carboxymethylcellulose 2%/Tween 20 1%, inhibits in a dose-dependent and time-dependent manner the ability of spleen cells to respond to allogeneic P815 mastocytoma tumor cells in vitro [14].
• To identify the epitope on the type II collagen molecule that induced autoimmune ear disease, electrophysiological and histological studies were carried out in DBA/1J mice immunized with native chick type II collagen (Clln) and cyanogen bromide (CNBr) peptide 1I (CB-I1 peptide) that was cleaved from chicken type II collagen with CNBr digestion [15].
• Significant differences were also observed between the mouse strains in the concentrations of lithium in plasma, heart, liver, kidney and brain 2 hrs. after a subcutaneous injection of 15.1 or 18.2 mmol/kg LiCl, but the lithium concentrations were not related in an obvious manner to LiCl toxicity [16].

Biological context of Calb1

• Calbindin D28 encodes a calcium binding protein that is expressed in the cerebellum exclusively in Purkinje cells [17].
• However, similar to PV, delayed binding by CB leads to biphasic Ca2+ decay kinetics [18].
• Calbindin-positive cells start to be seen very early during embryogenesis and increase dramatically until birth, thus becoming the most abundant cell type during embryonic development, especially in the ventral pallial part of the claustrum [19].
• Calretinin and calbindin D-28k delay the onset of cell death after excitotoxic stimulation in transfected P19 cells [20].
• On the other hand, Purkinje cells in Zones II, IV, and VI were very low in calbindin immunoreactivity and marked by small cell size, ectopia, poorly-developed dendrites and low cell density [21].

Anatomical context of Calb1

• Calbindin D28k targets myo-inositol monophosphatase in spines and dendrites of cerebellar Purkinje neurons [6].
• The Ca(2+)-binding protein calbindin D28k (CB) is vital for the normal function of the central nervous system but its specific functional role is largely unclear [6].
• Ontogeny of calbindin-D28K and calbindin-D9K in the mouse kidney, duodenum, cerebellum and placenta [22].
• In CA1 area and the hilus of the dentate gyrus of the mouse hippocampus, drastic reduction of NeuN, calbindin, calretinin, or parvalbumin immunopositive neurons was shown at 3, 7 and 60 days after pilocarpine-induced status epilepticus [23].
• Many CB+ cells observed in the pallial amygdala appeared to originate in the anterior entopeduncular area/ganglionic eminences of the subpallium [24].

Associations of Calb1 with chemical compounds

• Here, we show that CB interacts with IMPase in cerebellar Purkinje neurons, a cell type well known to rely on inositol-1,4,5-trisphosphate-dependent synaptic integration [6].
• Expression of high levels of exogenous calbindin or calretinin decreased transcription mediated by PCE1 in Purkinje cells 2.5- to 3-fold, whereas the presence of 1 microM ionomycin in the extracellular medium increased expression [17].
• 5. At E16.5, CB+ cells became more abundant in the lateral and basolateral nuclei than in the basomedial nucleus, showing a pattern very similar to that of gamma-aminobutyric acid (GABA)ergic neurons [24].
• Calbindin, calretinin, or parvalbumin and 5-bromo-2'-deoxyuridine (BrdU) double labeling showed that calcium binding protein immunopositive neurons in gliotic CA1 area at 60 days were surviving instead of newly generated neurons [23].
• Undifferentiated P19-cells were stably transfected with the cDNA for CR, CB or PV, induced to differentiate, and then exposed to NMDA, a glutamate-receptor agonist [20].

Co-localisations of Calb1

• VILIP-3 was found to be abundant in distal and collecting ducts where it partly colocalized with calbindin D28K [25].

Regulatory relationships of Calb1

• Overexpression of calbindin-D28K induces neurite outgrowth in dopaminergic neuronal cells via activation of p38 MAPK [26].
• This indicated that calbindin is expressed postmitotically in immature olfactory cells and is lost by mature cells [27].
• Group 1 are Renshaw cells and intensely express calbindin and coexpress parvalbumin and calretinin [28].
• No alterations in the number and distribution were found in the parvalbumin- or calbindin-expressing cell populations of the visual and anterior cingulate cortices of mdx mice [29].
• It is therefore concluded that a defined synthetic medium offers reproducible conditions to culture dorsal root ganglion cells for at least 5 days, stimulates the expression of substance P and enriches preferentially neuronal phenotypes expressing substance P or calbindin D-28k, for a longer period of culture [12].

Other interactions of Calb1

• Numerical simulations indicate that the residual deviation from a single exponential decay in PV/CB-/- is due to saturation of the Ca2+ indicator dye [18].
• Degree and time course of PC loss and the subsequent denervation of DCN neurons were monitored by using Calbindin D-28k (Calb) immunocytochemistry [30].
• In this study, we describe the expression of markers for photoreceptors (recoverin), horizontal cells (calbindin), bipolar cells (protein kinase C; PKC) and cytoskeletal elements pivotal to axonogenesis (beta-tubulin and actin) during perinatal development of mouse retina [31].
• 5. In contrast, interneurons expressed a subpallial transcription factor (Dlx), contained high levels of GABA, were frequently calbindin(+), and were born throughout corticogenesis (from E10.5 to E16.5) [32].
• In contrast, calbindin-positive cells in the MZ do not co-express reelin and are not altered in the Pax6 mutant cortex [33].

Analytical, diagnostic and therapeutic context of Calb1

• Calbindin D-28K immunohistochemistry did not detect any marked changes in CaB IR within Purkinje cells at 4 weeks [34].
• Further, RT-PCR analysis of CaB mRNA in the cerebellum in 6 week old heterozygous TM demonstrated a significant decrease in mRNA in comparison with the aged-matched nTM [35].
• We used in situ hybridization to study the expression of GAD67 and calbindin D28K mRNAs in developing mouse cerebellar Purkinje cells [36].
• To study the possible neuroprotective role of calbindin in vivo, we generated calbindin-deficient mice by gene targeting and assessed the viability of midbrain dopamine neurons in both a chemical and a genetic lesion paradigm [4].
• We identified cytochrome c with Western blotting and monitored cell loss in the cerebellum with Calbindin D-28k immunohistochemistry, Nissl-staining and morphometry [37].

References