Disease relevance of Calb2

• The apparent decrease in the number of PV and CR immunoreactive hilar neurons was correlated with the duration of the SE and was most extensive in rats with a progressive form of epilepsy [1].
• Calretinin and parvalbumin-immunoreactivity was present at a lower level of fluorescence than that of calbindin immunoreactivity in all the neurons of the major pelvic ganglion and this level was unchanged in aged rats [2].
• CR gene is active in some neurons, such as cerebellar granule neurons and in some tumor cells such as colon adenocarcinoma or epithelial mesothelioma [3].
• The present data indicate that the striatal calretinin-positive neurons are less resistant to transient ischemia, suggesting that there may exist vulnerability differences among the striatal interneurons in ischemia-induced neuronal injury [4].
• Calbindin-D28k and calretinin in the rat posterior pituitary; light and electron microscopic localization and upregulation with dehydration [5].

Psychiatry related information on Calb2

• The function of another gene, calretinin, is putatively related to mechanosensation and proprioception [6].
• The unilateral sensory deprivation seemed to induce a permanent asymmetry in the expression of calretinin which was not abolished after vestibular compensation [7].
• These findings suggest that intrinsic characteristics of calretinin cells, possibly including enhanced calcium buffering capacity, underlie the resistance of these cells to A beta toxicity in vitro and perhaps similar insults in Alzheimer's disease [8].

High impact information on Calb2

• Their size as well as staining for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase 67, calretinin and/or calbindin, suggest that new neurons in both regions are GABAergic interneurons [9].
• They consistently co-expressed calretinin and vasoactive intestinal polypeptide [10].
• In addition, double labeling with calretinin and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) revealed that differentiated hair cells underwent apoptosis during normal development at late embryonic and early postnatal stages in vivo and in vitro [11].
• In contrast, no colocalization was found between cortistatin and calretinin, cholecystokinin, or vasoactive intestinal peptide [12].
• Analysis of rat vestibular hair cell development and regeneration using calretinin as an early marker [11].

Chemical compound and disease context of Calb2

• RESULTS: When the adenosine deaminase inhibitor erythro-9-(2-hydroxyl-3-nonyl)adenine (EHNA) was injected into the eye just before ischemia, the ischemia-reperfusion changes in the b-wave and calretinin immunoreactivity were largely prevented [13].
• GDNF also protected striatal CaR-positive neurons against glutamate toxicity [14].
• In contrast, the level of calretinin, a Ca(2+) binding protein was significantly increased with chronic dehydration [15].
• These results indicate that CR may protect dopaminergic neurons from levodopa-induced toxicity [16].

Biological context of Calb2

• Virtually every PARV-positive neuron innervated by GABAergic septohippocampal baskets expressed NGF mRNA (86%), whereas 39-59% of CALR- and CALB-positive interneurons that were contacted by GABAergic septohippocampal axons showed NGF gene expression [17].
• An up-regulation of calretinin and parvalbumin in calyces of Held probably increases the presynaptic Ca(2+) buffering strength during postnatal development, but the unexpected heterogeneity of calretinin expression might cause differences in Ca(2+) signalling and transmitter release probability between calyces of Held [18].
• Calretinin may still buffer calcium at low concentrations or be a component in a calcium-based signal transduction system [19].
• Since we found the Mr 29,000 calcium binding protein to be an abundant protein in rat cerebellum, these results suggest either posttranscriptional regulation of calretinin in cerebellum or species differences.(ABSTRACT TRUNCATED AT 250 WORDS)[20]
• Calbindin, parvalbumin, and calretinin, members of EF-hand calcium-binding proteins, play important roles in buffering intracellular calcium ions [21].

Anatomical context of Calb2

• Mixed-effects statistical models, adapted specifically for these analyses, indicated that perturbations of amygdalar inputs to the hippocampus significantly alter the drive that hippocampal PVB-, CR-, and CB-IR neurons within the dentate gyrus/CA4 region exercise on CCK-IR terminals within the same region as well as in CA3-1 [22].
• The numerical density (Nd) of somata showing immunoreactivity (IR) for parvalbumin (PVB) was decreased in dentate gyrus (DG) and the CA4-2 region, while that of calretinin (CR)-IR was decreased in DG and CA2 [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].
• CR-labelled neurones were bipolar or multipolar with round to ovoid somata (diameters between 8 and 12 microm), and rostrocaudally running dendrites forming a network [24].
• Postembedding immunostaining demonstrated that CB-containing cells contain GABA, whereas CR-positive axon terminals forming asymmetric synapses are devoid of this labeling [25].

Associations of Calb2 with chemical compounds

• The results show that the majority of PV (100%), SOM (89.8%) and CR (93.9%) staining neurons are GABA positive [26].
• Calretinin interneurons were decreased significantly in the strata oriens and radiatum of CA3, in the dentate granule cell and molecular layers, and in the dentate hilus [27].
• Calretinin-containing neurons in cortical primary cultures derived from E14 rat embryos were not resistant to either kainic acid or a brief calcium overload induced by the calcium ionophore A23187 [19].
• Calretinin-containing axons and neurons are resistant to an intrastriatal 6-hydroxydopamine lesion [28].
• 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 [29].

Physical interactions of Calb2

• The nature and the origin of the cell populations that colonize the preplate/marginal zone was studied by means of immunohistochemistry using cell markers for gamma-amino butyric acid (GABA), reelin and the calcium binding proteins calretinin and calbindin [30].
• Using antibodies against the ionotropic glutamate receptor GluR2 and the calcium binding protein calretinin we found two populations of UBCs [31].
• Calmodulin, calbindin-D28k and calretinin are calcium-binding proteins largely distributed in the bipolar olfactory receptor cells [32].

Co-localisations of Calb2

• In neocortex, calretinin is partially co-localized with VIP (especially in the deeper layers) and is not co-localized with SRIF [33].
• Calretinin co-localizes with the NMDA receptor subunit NR1 in cholinergic amacrine cells of the rat retina [34].
• In intraganglionic laminar endings and nodose ganglion cells calretinin was highly co-localized with calbindin but not with calcitonin gene-related peptide [35].
• Both P2X2 and P2X3 receptor immunoreactivities were highly co-localized with calretinin positive IGLEs as shown by confocal laser scanning microscopy [36].

Regulatory relationships of Calb2

• In cortical or diencephalic cultures, CR was rarely coexpressed with GABA or calbindin D-28k [19].
• BDNF also regulates the calretinin content of Cajal-Retzius cells but is not necessary for their survival [37].
• About 80% of the neurons with P2X3 receptor immunoreactivity in the myenteric plexus and about 40% in the submucosal plexus expressed calretinin [38].
• Basic fibroblast growth factor promotes the generation and differentiation of calretinin neurons in the rat cerebral cortex in vitro [39].
• Here, using a culture system of dissociated rat cortical cells, we found that brain-derived neurotrophic factor and neurotrophin-3 promoted the morphological differentiation of one of the calretinin-containing neuronal subpopulations, the Cajal-Retzius cells [39].

Other interactions of Calb2

• 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 [40].
• In addition, the majority of CR and VIP interneurons exhibited colocalization of both neurochemicals [41].
• Calretinin- and parvalbumin-immunoreactive neurons in the rat main olfactory bulb do not express NADPH-diaphorase activity [42].
• They contained CCK, but not CR [43].
• Only a subpopulation of CR-containing cells, the spiny neurons of the dentate gyrus and CA3 region of the hippocampus were characterized by a strong expression of GluR-A and -D subunit mRNAs [44].

Analytical, diagnostic and therapeutic context of Calb2

• In order to gather more information about calcium-binding proteins during development, we analyzed the spatiotemporal distribution of PV and CR in the rat auditory brainstem using immunocytochemistry [45].
• In fact, double in situ hybridization analysis confirmed that most NT-3+ neurons also expressed NGF mRNA, indicating coexpression of both neurotrophins in subpopulations of PARV+ and CALR+ neurons [46].
• In contrast, when the striatal grafts were examined after 30 days survival using confocal microscopy, only 10% of hNT neurons immunopositive for NuMA were PV+; 19% were CB+/NuMA+, approximately the same percentage as was seen in vitro, and 82% of grafted hNT neurons were CR+ [47].
• Chronic NIC exposure for 3 weeks in adolescent rats, either via drinking water (the oral group) or by twice daily subcutaneous injections (the injection group), resulted in the expression of high levels of CR proteins in the ACC but not in the parietal cortex [48].
• Calretinin was also quantified by radioimmunoassay [49].

References