Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Calbindin 2”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1995

Distribution of calretinin mRNA in the vestibular nuclei of rat and guinea pig and the effects of unilateral labyrinthectomy: a non-radioactive in situ hybridization study.

We examined the localization of neurons expressing mRNA for calretinin, a cytosolic EF hand calcium-binding protein, throughout the vestibular nuclei of rat and guinea pig by non-radioactive in situ hybridization, using an alkaline phosphatase labeled oligonucleotide probe. Labeled cells were particularly numerous in the medial vestibular nucleus (mVN) and their distribution was similar in rat and guinea pig, and presented a characteristic rostrocaudal and mediolateral pattern. The effects of hemilabyrinthectomy were assessed at various times post lesion from 10 h to 30 days by comparison of the pattern of labeling in the ipsi- and contra-lateral vestibular nuclei of guinea pig. After up to 48 h no modification in the calretinin mRNA distribution was detected. After 3 to 30 days of survival, there was a decrease (about 30%) of the calretinin expressing neurons in the nucleus on the side of the lesion. The unilateral sensory deprivation seemed to induce a permanent asymmetry in the expression of calretinin which was not abolished after vestibular compensation. These results suggested that the calretinin expression in these neurons depends upon the integrity and activity of sensorineuronal peripheral vestibular influences.

Alkaline Phosphatase↗
PubMed1995

Corticosterone effects on rat calretinin mRNA in discrete brain nuclei and the testes.

Calretinin is an EF-hand calcium binding protein found predominantly in discrete sets of neurons in the central system, and in the sex hormone producing cells of the gonads. Calretinin mRNA levels were measured in discrete brain areas from vehicle and corticosterone treated rats (subcutaneous injections of 0, 0.1, 1, or 10 mg, 7 days) using a micropunch ribonuclease protection assay. Treatment with high dose corticosterone (10 mg) caused a 93% decrease in calretinin mRNA levels in the hypothalamic paraventricular nucleus compared to controls. Two other brain regions, the medial amygdaloid nucleus and the nucleus reuniens, demonstrated an approximately 40% decrease in calretinin mRNA following high dose corticosterone. In separate experiments, adrenalectomy and diurnal corticosterone variations had no effect on calretinin mRNA in the brain areas examined. In the testes, corticosterone treatment decreased calretinin protein in a dose dependent fashion (to 81%, 68%, and 39% of controls at doses of 10, 1, and 0.1 mg/day, respectively). Low dose corticosterone treatments decreased testicular but not neuronal calretinin mRNA, whereas high dose corticosterone reduced calretinin mRNA in testes and several discrete brain areas. This suggests that corticosterone's effects on brain calretinin may be due to its pathological effects, e.g. energy depletion of brain cells or interference with the normal support functions of glia.

Amygdala↗
PubMed1993

Nucleotide sequence of rat calretinin cDNA.

A rat calretinin cDNA clone was selected by antibody screening of a lambda gt11 brain library. The sequence revealed remarkable nucleotide and amino acid homology with human calretinin (91.1% and 98.5%, respectively), with only four amino acid differences. A high degree of homology with chick calretinin was also observed (79.8% and 86.6%, respectively), with 36 amino acid differences. Although the role of this central nervous system protein has not been well characterized, the evolutionarily conserved calcium binding domains and connecting regions, in addition to the limited local changes observed between rat and chick primary structure, lead us to believe that calretinin interacts with other highly conserved constituents of brain cells. This calretinin cDNA clone provides a new probe for the analysis of a specific subset of neurons in the central nervous system. The probe will allow a more detailed analysis of calretinin regulation in the brain and will be useful for screening genomic libraries for the complete chromosomal gene. (GenBank accession No X66974).

Amino Acid Sequence↗
PubMed1996

Antigens associated with specific retinal cells are affected by ischaemia caused by raised intraocular pressure: effect of glutamate antagonists.

Raising the rat's intraocular pressure above the systolic blood pressure for 60 min followed by a reperfusion of 7-10 days caused an ischaemic insult to the retina. The b-wave of the electroretinogram was abolished and the retinal thickness was much reduced, the greatest influence being associated with the inner retinal layers. No obvious histological damage was apparent at the light microscopy level. Immunocytochemistry, however, revealed a clear change in the nature of certain antigens associated with specific cell-types. Thy-1 antigen located to ganglion cell membranes was much reduced, suggesting that the ganglion cells are affected by ischaemia. Calretinin-immunoreactivity associated with amacrine cells is drastically reduced by ischaemia. In contrast, Ret-P1, located to the outer segments of the photoreceptors is unaffected by ischaemia. Ischaemia also caused GFAP-immunoreactivity to be expressed in the Müller cells, which is normally only associated with astrocytes in the ganglion/nerve fibre layer. Injection of a mixture of CNQX and MK-801, kainate and NMDA receptor antagonists, respectively, into the eye just before ischaemia failed to reverse the changes induced by the insult. However, analysis 3 days after reperfusion revealed that when the ischaemic insult was reduced to 45, rather than 60 min, the changes in the calretinin-immunoreactivity were reversed. The results show that immunocytochemistry provides a powerful way of following biochemical changes associated with specific cell types caused by ischaemia.

Animals↗
PubMed1991

Calretinin, a neuronal calcium binding protein, inhibits phosphorylation of a 39 kDa synaptic membrane protein from rat brain cerebral cortex.

The neuronal calcium binding protein calretinin was studied for possible effects on brain protein phosphorylation. Calretinin (100 nM) inhibited the appearance of a calcium stimulated 39 kDa phosphoprotein within a synaptic membrane fraction following sucrose density centrifugation. Calmodulin or a specific protein kinase C inhibitor had no effect on either the phosphorylation of the 39 kDa protein or the inhibition produced by calretinin. At the same concentration, calretinin produced a slight increase in the phosphorylation of several other synaptic membrane proteins which appeared additive with the stimulation produced by either calmodulin or phosphatidylserine in the presence of calcium.

Adenosine Triphosphate↗
PubMed1993

The new monodendritic neuronal type within the adult human cerebellar granule cell layer shows calretinin-immunoreactivity.

The distribution of calretinin immunoreactive structures within the granule cell layer of the adult human cerebellar cortex was studied using the avidin-biotin peroxidase method. Immunoreactivity is found in numerous fibers and glomerular formations, in Golgi- and Lugaro cells as well as in a recently described novel neuronal type, the monodendritic cell. The soma of the monodendritic neuron contains a faintly stained nucleus and issues a single short dendrite terminating in a tuft. Most probably, the tuft contributes to the formation of a glomerulum. Soma and tuft are of about the same size (diameter 10-18 microns). The number of monodendritic neurons is higher in the vermal than in the hemispheric part of the lobulus (lobulus VII) and is higher in lobulus X than in lobulus VII of the vermis.

Adult↗
PubMed1993

Calretinin-immunoreactive neocortical interneurons are unaffected in Alzheimer's disease.

Recent studies have revealed that select neuronal populations may display a differential sensitivity to degeneration in Alzheimer's disease. For example, large pyramidal neurons have been shown to be vulnerable, whereas small, local circuit neurons appear to be resistant to the pathologic process. More significantly, interneurons that contain the calcium-binding proteins parvalbumin and calbindin are particularly resistant to degeneration in Alzheimer's disease. Using a polyclonal antibody to the calcium-binding protein calretinin, we analyzed the possible changes in the subset of interneurons containing this protein in two neocortical areas that are generally devastated in Alzheimer's disease. In the prefrontal cortex as well as in the inferior temporal cortex, we observed no difference in the density of calretinin-immunoreactive neurons in Alzheimer's disease brains as compared to control cases. Moreover, the cellular morphology of these neurons was well preserved in the Alzheimer's disease cases. These data suggest that calretinin-immunoreactive neurons, like other calcium-binding protein-containing interneurons, are resistant to degeneration in Alzheimer's disease. The results support the notion that the pathological process in Alzheimer's disease involves specific cellular populations sharing particular morphological and neurochemical characteristics. In addition, it is possible that the presence of calcium-binding proteins confers a certain degree of resistance to degeneration in specific neuronal subsets.

Aged↗
PubMed1993

Neurogenesis persists in the subependymal layer of the adult mouse brain.

Neurogenesis of olfactory bulb granule cells is known to persist in adult rats where, in some strains, the bulbs grow throughout life. In mice, bulb growth ceases early in adulthood and here we ask if granule cell neurogenesis persists after the bulbs have stopped growing. By injecting adult mice with bromodeoxyuridine (BrdU) and allowing short and long survival times, we found that new cells form in the subependymal layer and that they migrate subsequently into the olfactory bulbs where they acquire the nuclear morphology of granule cells and express neuron-specific markers. Using [3H]thymidine, we found that most of these adult-generated granule neurons persist within the bulbs for at least 16 weeks. This shows the persistence of neurogenesis and neuronal migration in adult animals in which the olfactory bulbs have stopped growing.

Animals↗
PubMed1994

Patches in the striatum of squirrel monkeys are enriched with calretinin fibers but devoid of calretinin cell bodies.

In squirrel monkeys, the calcium-binding protein calretinin (CR) was found to be distributed according to strikingly different patterns in striatal patch/matrix compartments, as visualized on adjacent sections immunostained for another calcium-binding protein, calbindin D-28k. Striatal patches were characterized by a dense CR-immunoreactive neuropil, whereas the matrix contained a moderate number of medium-sized and a small number of large-sized CR perikarya uniformly scattered among a few immunoreactive fibers. Matriceal CR perikarya often closely surrounded striatal patches, but none of them invaded the patches themselves. The CR-neuropil-dense patches were particularly conspicuous in ventromedial sectors of the striatum, including the limbic territory, but much less obvious in the dorsolateral sensorimotor territory. These findings indicate that CR neurons may be involved in patch/matrix intercommunication.

Animals↗
PubMed1995

Ultrastructural associations between dopamine terminals and local circuit neurons in the monkey prefrontal cortex: a study of calretinin-immunoreactive cells.

Dopamine terminals in the monkey prefrontal cortex (PFC) synaptically target the distal dendrites of both pyramidal cells and GABA interneurons. We sought to determine whether the latter input includes the innervation of interneurons that utilize calretinin (CalR) as a calcium-binding protein. Sections through prefrontal area 9 of cynomolgus monkeys were processed by immunoperoxidase for tyrosine hydroxylase (TH) to label dopamine varicosities and by pre-embedding immunogold for CalR. Electron microscopic examination of layers 1-3 revealed numerous TH-immunoreactive (TH-ir) terminals, but few were located in the vicinity of CalR-ir dendrites. Although close appositions were sometimes detected between these labeled processes, no synaptic inputs from TH-ir terminals to CalR-ir dendrites were observed. However, in adjacent sections from the same animals, TH-ir terminals were observed to synapse on GABA-ir dendrites. These findings suggest that dopamine afferents to the monkey PFC target the subclasses of GABA interneurons that do not contain CalR.

Animals↗
PubMed1996

Innervation of rat abdominal paraganglia by calretinin-like immunoreactive nerve fibers.

The extended hepatic pedicle of the rat containing the vagal hepatic branch and associated paraganglia was dissected as whole mount, processed for calretinin immunocytochemistry, and analyzed by laser-scanning confocal microscopy. About half of the 8-12 paraganglia of the region were innervated to a various degree by calretinin-immunoreactive (CAL-IR) nerve fibers that formed basket-like varicose terminals around small clusters of glomus tissue. Neither the numerous capillaries, nor the occasional non-CAL-IR neuron accompanying some paraganglia, were recipients of CAL-IR terminals. In animals with prior left cervical vagotomy the number of CAL-IR fibers was decreased but not abolished. Since about 30% of neurons in the nodose ganglia, a few neurons within the vagal hepatic branch/hepatic hilus area, and numerous neurons in the gastric myenteric plexus were CAL-IR, these neurons represent other potential sources of CAL-IR innervation of the paraganglia.

Animals↗
PubMed1989

Immunoreactivity for calretinin and other calcium-binding proteins in cerebellum.

Two calcium-binding proteins, calbindin and parvalbumin, have been reported to be abundant in Purkinje cells and other cell types in the cerebellum. Immunoreactivity for a related protein, calretinin, is now reported in cerebellum of chick and rat. In the chick, antibodies against calretinin stain mossy fibres throughout, and climbing fibres in a distinct group of folia. They also stain several cell types in the molecular layer. As there is no detectable calretinin mRNA in the cerebellar cortex, this cellular staining may be due to cross-reaction with an unknown antigen. In the rat, antibodies against calretinin stain the Lugaro cells, and some granule cells in lobe X; they also give weak staining of all the granule cells in the other lobes. Thus almost all the neuronal cell types in the cerebellum show immunoreactivity for at least one of the calcium-binding proteins in one or both species.

Animals↗
PubMed1992

Calretinin is present in non-pyramidal cells of the rat hippocampus--I. A new type of neuron specifically associated with the mossy fibre system.

Calretinin-containing cells were visualized with immunocytochemistry in the rat dorsal hippocampal formation. Calretinin immunoreactivity was present exclusively in non-pyramidal cells in all layers of the dentate gyrus and the CA1-3 areas. Calretinin-positive neurons and processes were most abundant in the hilus of the dentate gyrus and in the stratum lucidum of the CA3 region. Several calretinin-immunoreactive cells were located within the hippocampal fissure. A distinct band of calretinin-immunoreactive fibres occupied the superficial part of the granule cell layer and the lowest part of the molecular layer. Closer examination of the calretinin-positive cells revealed that they formed two distinct cell groups. One group of cells, found exclusively in the stratum lucidum of the CA3 area and in the hilus of the dentate gyrus, was covered with numerous spines. Their somata and dendrites were restricted to stratum lucidum and to the hilus. Cells of the other group had smooth, often varicose, radially running dendrites, and were present in all areas and layers of the hippocampal formation. Two to three thick primary dendrites arose from the irregularly shaped cell body of spiny cells and emitted fine secondary branches only distally (70-100 microns) from the soma, where they formed a profuse network. The extensive dendritic tree of the cells spread horizontally within stratum lucidum and span a distance of 400-600 microns both in the septotemporal and in the transverse directions. The layer-specific location of these cells and their processes suggested that the majority of their input may derive from mossy fibres. This presumption has been confirmed by electron microscopic examination. A large number of asymmetrical synapses were found to cover the soma, the dendritic shafts and the spines (four to six synapses/spine) of the cells. A large proportion of the synapses were formed by boutons, which showed the distinctive features of mossy fibre terminals. Three to six primary dendrites arose from the multipolar, bipolar or pyramidal-shaped somata of spine-free cells, which were smaller than the somata of spiny cells. The smooth and frequently varicose dendrites branched proximally and ran primarily radially. Dendrites ascended or descended through several layers and received both asymmetrical and symmetrical synapses. In the CA1 subfield, the vertically running dendrites frequently contacted other calretinin-immunoreactive spine-free dendrites or cell bodies. Two or three calretinin-immunoreactive dendrites were often seen to be attached for over 100 or, occasionally, 200 microns and several puncta adherentia were observed between them using the electron microscope.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Calretinin distribution in the thalamus of the rat: immunohistochemical and in situ hybridization histochemical analyses.

The distribution of calretinin-containing cells was examined by in situ hybridization histochemistry and compared with the immunohistochemical mapping of calretinin in the thalamus of the rat. Results revealed a close correspondence between the immunohistochemical localization of cell bodies and the messenger RNA label produced by the calretinin oligonucleotide probe. Calretinin cells were most prominent in the midline (paraventricular, reuniens, rhomboid) and intralaminar (central medial, paracentral) nuclei and in a group of cells along the rostral central gray which appeared continuous with the caudal extent of the midline nuclei. A subpopulation of calretinin cell bodies was also identified in the reticular nucleus. The mediorostral lateral posterior nucleus, subparafascicular, lateral geniculate and habenular nuclei also contained calretinin messenger RNA probe label. In contrast, no positive cells were found in the anterior, ventral or posterior thalamic nuclei. The distribution of calretinin cells did not correspond directly with that of other histochemical markers. Thus, the in situ hybridization histochemical and immunohistochemical results revealed calretinin as a unique identifying marker for distinct sets of thalamic neurons.

Animals↗
PubMed1993

Selective neuronal death in the contralateral hippocampus following unilateral kainate injections into the CA3 subfield.

Intracerebral or intraperitoneal injections of kainic acid, an agonist at a class of glutamate receptors, have been extensively used to model temporal lobe epilepsy. In the present study we compared the types and distributions of selectively vulnerable neurons in the ipsi- and contralateral hippocampi following unilateral kainate injections into the CA3 subfield in order to examine whether "proximal" or "distant" neuronal damage resembled the pathology, and possibly also the mechanism, of human temporal lobe epilepsy. The degeneration of principal cells in the different hippocampal subfields was visualized by silver impregnation, and the loss of various types of non-principal cells was studied by immunostaining for the calcium binding proteins parvalbumin, calbindin-D28k and calretinin, as well as for somatostatin. In the first series of experiments various concentrations (ranging from 0.1 to 1 mg/ml) and volumes (0.5-2 microliters) of kainate were tested to induce reproducible damage in the contralateral hippocampus. The optimal dose, employed in the subsequent vulnerability studies, was found to be 3 x 0.5-microliter injections (over a period of 10 min) of a concentration of 0.33 mg/ml under ether anaesthesia, which was discontinued immediately after injection. Anaesthesia with equithesin was found to prevent contralateral cell death. Most if not all pyramidal cells in the CA3 region degenerated on the ipsilateral side, whereas the dentate granule cells, and the majority of CA1 pyramidal cells were resistant. A strikingly different pattern was found on the contralateral side, where CA1 pyramidal cells were almost completely lost, but the CA3 region (with the exception of CA3c) and the dentate gyrus remained intact. Three subpopulations of non-principal cells were found to be vulnerable in both hemispheres, the hilar somatostatin cells, spiny calretinin cells and mossy cells, as well as the spiny calretinin cells in stratum lucidum of CA3. The other subpopulations were resistant, except for those within the effective injection site. We propose that the "distant" (contralateral) damage resembles the pattern, and probably also the mechanism, of cell death in human temporal lobe epilepsy, whereas the ipsilateral damage does not.

Anesthetics↗
PubMed1993

Early degeneration of calretinin-containing neurons in the rat hippocampus after ischemia.

The mechanism of delayed death of pyramidal cells in the hippocampal CA1 region and the acute death of various types of hilar neurons after ischemia is still unknown. Excitotoxicity may play a role in ischemic cell death, a prerequisite of which is the development of increased excitability or an enhanced excitatory transmission in the selectively vulnerable subfields of the hippocampus. Such changes may take place upon the loss or malfunction of local inhibitory neurons in the early postischemic period. In the present study we examined the vulnerability of non-pyramidal neurons containing a recently discovered calcium binding protein, calretinin, in the rat hippocampus following 15 min ischemia induced by four-vessel occlusion. Immunostaining for calretinin enabled us to visualize a new type of spiny non-pyramidal cell in the hippocampus specifically associated with the mossy fiber system. This cell type is present exclusively in regions where mossy fiber terminals occur, i.e. in the hilus of the dentate gyrus and in stratum lucidum of the CA3 subfield. A selective loss of immunoreactivity in these neurons was already observed at 12-24 h after ischemia, when the pyramidal cells in the CA1 region showed no signs of damage. At a survival time of two to three days, most if not all spiny calretinin-immunoreactive cells had disappeared from the hippocampus. Other types of calretinin-containing GABAergic neurons were also reduced in number, but only at a time when CA1 pyramidal cells also started to degenerate, i.e. two to three days after ischemia. We speculate that the early loss of spiny calretinin-containing cells, together with other non-pyramidal cells associated with the mossy fiber system (somatostatin-containing neurons and mossy cells of the hilus), may result in pathological network activity in the hippocampus, which may ultimately lead to an increased excitatory transmission and delayed pyramidal cell death in the CA1 region.

Animals↗
PubMed1993

Calretinin immunoreactivity in the monkey hippocampal formation--II. Intrinsic GABAergic and hypothalamic non-GABAergic systems: an experimental tracing and co-existence study.

Our light and electron microscopic studies (Seress L., Nitsch R. and Leranth C. (1993) Neuroscience 55, 775-796.) indicated that in the hippocampus of the African Green monkey, calretinin is exclusively present in non-pyramidal cells. Calretinin-positive axons formed a prominent band at the border of the dentate molecular and granule cell layers and in the pyramidal layer of CA2, and established asymmetric synapses with different postsynaptic targets. The goal of this study is to determine the cells of origin of this presumably extrinsic innervation, and subsequently, the characterization of their neurochemical features. We were able to demonstrate that calretinin-immunoreactive axon terminals in the inner molecular layer of the dentate gyrus and in the pyramidal layer of CA2 disappear 10 days after fimbria-fornix transection. Retrograde tracing revealed their cells of origin to be in the supramammillary nucleus. Co-localization studies employing the cryostat consecutive, semithin section technique provided evidence that these large projecting neurons contained both calretinin and substance-P but lack GABA as an inhibitory transmitter. In contrast, co-localization studies revealed that almost all of the intrinsic calretinin-positive neurons in different areas of the primate hippocampus contained GAD or GABA. These results suggest that there are two separate calretinin-containing systems in the primate hippocampus, i.e. an intrinsic inhibitory and an extrinsic excitatory one, the latter deriving from the supramammillary nucleus of the hypothalamus.

Animals↗
PubMed1993

Degeneration of Purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline.

The indole alkaloids ibogaine and harmaline are beta-carboline derivatives that cause both hallucinations and tremor. Reports that ibogaine may have potent anti-addictive properties have led to initiatives that it be tested for the treatment of opiate and cocaine addiction. In this study, ibogaine-treated rats were analysed for evidence of neurotoxic effects because human clinical trials of ibogaine have been proposed. We recently found that ibogaine induces a marked glial reaction in the cerebellum with activated astrocytes and microglia aligned in parasagittal stripes within the vermis. Based on those findings, the present study was conducted to investigate whether ibogaine may cause neuronal injury or degeneration. The results demonstrate that, after treatment with ibogaine or harmaline, a subset of Purkinje cells in the vermis degenerates. We observed a loss of the neuronal proteins microtubule-associated protein 2 and calbindin co-extensive with loss of Nissl-stained Purkinje cell bodies. Argyrophilic staining of Purkinje cell bodies, dendrites and axons was obtained with the Gallyas reduced silver method for degenerating neurons. Degenerating neurons were confined to narrow parasagittal stripes within the vermis. We conclude that both ibogaine and harmaline have selective neurotoxic effects which lead to degeneration of Purkinje cells in the cerebellar vermis. The longitudinal stripes of neuronal damage may be related to the parasagittal organization of the olivocerebellar climbing fiber projection. Since these drugs produce sustained activation of inferior olivary neurons, we hypothesize that release of an excitatory amino acid from climbing fiber synaptic terminals may lead to excitotoxic degeneration of Purkinje cells.

Animals↗