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PubMed2004

Effects of brain-derived neurotrophic factor on cell survival, differentiation and patterning of neuronal connections and Müller glia cells in the developing retina.

The aim of the present study was to determine the influence of brain-derived neurotrophic factor (BDNF) on survival, phenotype differentiation and network formation of retinal neurons and glia cells. To achieve a defined concentration and constant level of BDNF over several days, experiments were performed in an organotypic culture of the developing rat retina. After 6 days in vitro, apoptosis in the different cell layers was determined by TUNEL staining and cell-type-specific antibodies were used to identify distinct neuronal cell types and Müller cells. Cultured retinas treated with BDNF (100 ng BDNF/mL medium) were compared with untreated as well as with age-matched in vivo retinas. Quantitative morphometry was carried out using confocal microscopy. BDNF promoted the in vitro development and differentiation of the retina in general, i.e. the number of cells in the nuclear layers and the thickness of the plexiform layers were increased. For all neurons, the number of cells and the complexity of arborizations in the synaptic layers were clearly up-regulated by BDNF. In control cultures, the synaptic stratification of cone bipolar cells within the On- and Off-layer of the inner plexiform layer was disturbed and a strong reactivity of Müller cell glia was observed. These effects were not present in BDNF-treated cultures. Our data show that BDNF promotes the survival of retinal interneurons and plays an important role in establishing the phenotypes and the synaptic connections of a large number of neuronal types in the developing retina. Moreover, we show an effect of BDNF on Müller glia cells.

Age Factors↗
PubMed2004

Impaired formation of the inner retina in an AChE knockout mouse results in degeneration of all photoreceptors.

Blinding diseases can be assigned predominantly to genetic defects of the photoreceptor/pigmented epithelium complex. As an alternative, we show here for an acetylcholinesterase (AChE) knockout mouse that photoreceptor degeneration follows an impaired development of the inner retina. During the first 15 postnatal days of the AChE-/- retina, three major calretinin sublaminae of the inner plexiform layer (IPL) are disturbed. Thereby, processes of amacrine and ganglion cells diffusely criss-cross throughout the IPL. In contrast, parvalbumin cells present a nonlaminar IPL pattern in the wild-type, but in the AChE-/- mouse their processes become structured within two 'novel' sublaminae. During this early period, photoreceptors become arranged regularly and at a normal rate in the AChE-/- retina. However, during the following 75 days, first their outer segments, and then the entire photoreceptor layer completely degenerate by apoptosis. Eventually, cells of the inner retina also undergo apoptosis. As butyrylcholinesterase (BChE) is present at a normal level in the AChE-/- mouse, the observed effects must be solely due to the missing AChE. These are the first in vivo findings to show a decisive role for AChE in the formation of the inner retinal network, which, when absent, ultimately results in photoreceptor degeneration.

Acetylcholinesterase↗
PubMed2005

Soluble guanylyl cyclase appears in a specific subset of periglomerular cells in the olfactory bulb.

In the brain, nitric oxide acts as an atypical messenger in cellular nonsynaptic transmission. In the olfactory bulb, this gas is produced at the level of the olfactory glomeruli by a subpopulation of periglomerular cells that participates in the first synaptic relay of the olfactory information between the olfactory nerve and the dendritic tufts of principal cells. It has been proposed that nitric oxide modulates intraglomerular synaptic integration of sensory inputs, but its specific role in the glomerular circuitry remains to be understood. In this article, we demonstrate that, in the glomerular circuits, a specific subset of periglomerular cells, most of them expressing the calcium binding protein calbindin D-28 k, expresses the beta1 subunit of the soluble guanylyl cyclase. These cells could be the targets for the action of nitric oxide at the glomerular level via activation of soluble guanylyl cyclase and production of cGMP.

Animals↗
PubMed2005

Characterization of the rhesus monkey superior olivary complex by calcium binding proteins and synaptophysin.

This study was performed in order to characterize the main nuclei of the rhesus monkey superior olivary complex by means of antibodies against the calcium binding proteins parvalbumin, calbindin and calretinin and the synaptic vesicle protein synaptophysin. These markers revealed the neuronal morphology and organization of nuclei located within the rhesus monkey superior olivary complex. The architectural details included the distribution of axonal terminals on neurons. The medial superior olivary nucleus was present as a column of neurons. No clear segregation of calretinin-positive terminals was noticed on the medial and lateral dendritic fields of these neurons. The lateral superior olivary nucleus was characterized by a distinct nuclear shape. Calretinin-, parvalbumin- or calbindin-positive terminals contacted somata and dendrites. The medial nucleus of trapezoid body could be clearly differentiated as a distinct region in the rhesus monkey superior olivary complex. Somata of that nucleus showed calbindin- and parvalbumin-labelling whereas somatic calyces of Held were reavealed by calretinin and synaptophysin labelling. The results are discussed with respect to the processing of acoustic information in primate species and their ability to hear high and low frequencies, which is reflected by anatomical correlates.

Animals↗
PubMed2004

Chronic cortisol exposure promotes the development of a GABAergic phenotype in the primate hippocampus.

Glucocorticoids regulate plasticity and survival of hippocampal neurons. Aberrant exposure to this steroid hormone can result in neurodegeneration, perhaps secondary to disruption of calcium homeostasis. Calbindin, a calcium-binding protein that buffers excess calcium, may protect against neurodegeneration resulting from overabundance of intracellular calcium. In this study, we examined whether chronic treatment (1 year) with cortisol enhances hippocampal calbindin expression in primates. Calbindin is a marker for inhibitory neurons and the dentate gyrus is known to adopt an inhibitory phenotype in response to extreme conditions such as seizures. Thus, we hypothesized that chronic cortisol exposure may also promote a GABAergic phenotype. Therefore, we examined the expression of the GABA-synthesizing enzyme glutamic acid decarboxylase. The expression of brain-derived neurotrophic factor, which is responsive to glucocorticoids, was also examined. Our results demonstrate significant increases in calbindin, glutamic acid decarboxylase and brain-derived neurotrophic factor in several regions of the primate hippocampus, including the dentate gyrus and CA3, in response to chronic cortisol exposure. These results suggest that chronic cortisol exposure may shift the balance towards a GABAergic phenotype, perhaps as part of a compensatory feedback mechanism to dampen the initial excitatory effects of glucocorticoids in the hippocampus.

Animals↗
PubMed1995

Alteration in levels of expression of brain calbindin D-28k and calretinin mRNA in genetically epilepsy-prone rats.

Variations in the concentration of free calcium in neurons is believed to play a major role in regulating neuronal excitability. Because calcium-binding proteins such as calbindin D-28k and calretinin help to regulate intracellular calcium, we investigated the possibility that the expression of these proteins may be affected in genetically epilepsy-prone rats (GEPRs). The mRNA levels of both proteins were compared across several brain regions using in situ hybridization histochemistry and Northern blot analysis with semiquantitation by optical density measures in autoradiograms from two GEPR strains that differ in the severity of audiogenic seizures (GEPR9 and GEPR3) and from Sprague-Dawley rats. Results revealed a lower level of expression in calbindin D-28k mRNA in the in the caudate putamen-accumbens nuclei in GEPR3 (-30%) and GEPR9 (-60%) relative to controls. The calbindin D-28k mRNA level was also lower in the reuniens nucleus of the thalamus (-41% in GEPR3; -34% in GEPR9). The calretinin mRNA level was lower in the substantia nigra compacta of both GEPR rat strains (-31% in GEPR3 and -34% in GEPR9 relative to controls). No changes in mRNA were detected in other brain regions expressing calbindin D-28k or calretinin mRNA. These results indicate that the expression of these related calcium-binding proteins is altered in the GEPRs before the induction of seizures. This initial defect could alter either the calcium-buffering capacity or regulation of calcium-mediated processes by these proteins and thus play a role in the molecular cascade of events inducing the genetic susceptibility to, and the generalization of, seizures in these rat strains.

Animals↗
PubMed2006

Architectural (Type IA) focal cortical dysplasia and parvalbumin immunostaining in temporal lobe epilepsy.

PURPOSE: We analyzed 26 surgically treated patients operated on for intractable epilepsy associated with type IA (architectural) cortical dysplasia, to investigate neuropathologic and immunocytochemical features, particularly of the gamma-aminobutyric acid (GABA)ergic system, and to compare the findings with those observed in normal cortex. METHODS: Routinely stained slides and serial sections immunostained for neurofilaments (SMI 311), microtubule-associated protein-2 (MAP-2), neuron-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), parvalbumin (PV), calbindin (CB), and calretinin (CR) were processed. Some sections were processed by using single-immunoperoxidase procedures; others were processed for double immunofluorescence labelling and observed by confocal microscopy. The density of inhibitory PV-immunoreactive interneurons was quantitatively assessed in all patients and control cases by using a two-dimensional cell-counting technique on PV immunostained sections. RESULTS: The density of PV-immunoreactive interneurons was significantly reduced in this group of patients, whereas CB- and CR- positivity appeared similar to those in normal cortex. In five cases, architectural abnormalities, in addition to those that defined type 1A dysplasia, were present and characterized by abnormal clusters of neurons and laminar cellular loss in superficial cortical laminate. CONCLUSIONS: The reduction of PV expression in type IA cortical dysplasia suggests an impairment of the GABAergic system as a possible mechanism for the epileptogenicity; in addition, PV immunoreactivity can be helpful in the neuropathologic characterization of this form of cortical dysplasia.

Adolescent↗
PubMed1994

Calbindin-D28k, calretinin, and recoverin immunoreactivities in developing chick pineal gland.

Calbindin-D28k, calretinin, and recoverin, three intracellular calcium-binding proteins belonging to the troponin C/calmodulin superfamily, were immunohistochemically localized in chick pineal during development [from embryonic day 16 (E16) to postnatal day 14 (P14)]. At E18, only calretinin immunoreactivity could be detected in nuclei from follicular pinealocytes. With development, calretinin immunoreactivity expanded from nucleus to cytoplasm, and calretinin immuno-positive cell number increased. At P14 almost al pinealocytes were calretinin positive. Calbindin-D28k immunoreactivity was not detected before E20. During development, many follicular and parafollicular pinealocytes became strongly calbindin-D28k positive, reaching a peak both in intensity and in number at P7; thereafter their number decreased. In addition to pinealocytes, neuron-like cells appeared calbindin-D28k positive at E20 and calretinin positive at P7. Recoverin, a myristoylated protein isolated from vertebrate photoreceptor and which might participate in the inactivation of the phototransduction cascade, was transiently expressed in follicular and parafollicular pinealocytes from P1 to P14 with a maximal expression at P7. This transitory expression may coincide with a transitory light sensitivity period in chick pinealocytes, before complete maturity of the pineal gland.

Animals↗
PubMed1995

Calbindin-D28k, calretinin, and S-100 immunoreactivities in rat pineal gland during postnatal development.

Profound morphological modifications occur during postnatal development of the rat pineal gland. We have immunohistochemically followed those events from postnatal day 1 to 20 by using three cytoarchitectonic markers (S-100, calbindin-D28k, and calretinin) that belong to the calmodulin/troponin C calcium-binding protein family. In the developing rat pineal, anticalbindin-D28k antibody labels three cell types: immature and mature astrocytes and perivascular type II pinealocytes. During development, calbindin-D28k positive cells migrate from the base of the pineal stalk into the superficial part of the pineal. Calbindin-D28k, usually used as a neuronal marker in the central nervous system, recognizes in rat pineal precursor astrocytes 5 days before S-100 and labels a subpopulation somewhat different from S-100 positive astrocytes. Calretinin immunoreactivity appeared in the postero-superior part of the pineal and was abundant until postnatal day 5, then its density dramatically felt to leave, after postnatal day 20, an occasional population of cells whose morphology is compatible with neuron-like cells.

Animals↗
PubMed2004

Hippocampal pathology in the human neuronal ceroid-lipofuscinoses: distinct patterns of storage deposition, neurodegeneration and glial activation.

The neuronal ceroid-lipofuscinoses (NCLs) are recessively inherited lysosomal storage diseases, currently classified into 8 forms (CLN1-CLN8). Collectively, the NCLs constitute the most common group of progressive encephalopathies of childhood, and present with visual impairment, psychomotor deterioration and severe seizures. Despite recent identification of the underlying disease genes, the mechanisms leading to neurodegeneration and epilepsy in the NCLs remain poorly understood. To investigate these events, we examined the patterns of storage deposition, neurodegeneration, and glial activation in the hippocampus of patients with CLN1, CLN2, CLN3, CLN5 and CLN8 using histochemistry and immunohistochemistry. These different forms of NCL shared distinct patterns of neuronal degeneration in the hippocampus, with heavy involvement of sectors CA2-CA4 but relative sparing of CA1. This selective pattern of degeneration was also observed in immunohistochemically identified interneurons, which exhibited a graded severity of loss according to phenotype, with calretinin-positive interneurons relatively spared. Furthermore, glial activation was also regionally specific, with microglial activation most pronounced in areas of greatest neuronal loss, and astrocyte activation prominent in areas where neuronal loss was less evident. In conclusion, the NCLs share a common pattern of selective hippocampal pathology, distinct from that seen in the majority of temporal lobe epilepsies.

Adolescent↗
PubMed2006

Intrauterine exposure to dexamethasone impairs proliferation but not neuronal differentiation in the dentate gyrus of newborn common marmoset monkeys.

Glucocorticoids applied prenatally alter birth weight and the maturation of the lungs. Moreover, glucocorticoids impair neuronal proliferation and differentiation in the hippocampal dentate gyrus. In the present study proliferation and neuronal differentiation in the dentate gyrus were studied in newborn common marmoset monkeys which were intrauterinely exposed to the synthetic glucocorticoid dexamethasone (DEX). Pregnant marmoset monkeys received DEX (5 mg/kg body weight) daily either during early (days 42-48) or late (days 90-96) pregnancy. In the hippocampi of newborn monkeys immunohistochemistry was performed with markers of proliferation (Ki-67), apoptosis (in situ tailing) as well as early and late neuronal differentiation (calretinin and calbindin). Both after early and late intrauterine exposure to DEX, proliferation of dentate gyrus cells was significantly decreased (P < 0.05). The density of apoptotic neurons was not altered by DEX treatment. Quantification of calretinin- and calbindin-immunoreactive neurons showed no significant differences between DEX-exposed and control animals. In conclusion, the proliferation of putative precursor cells but not the differentiation into mature cells was impaired in the dentate gyrus of newborn marmosets exposed intrauterinely to DEX.

Animals↗
PubMed2003

Electrical stimulation reveals complex neuronal input and activation patterns in single myenteric guinea pig ganglia.

The myenteric plexus plays a key role in the control of gastrointestinal motility. We used confocal calcium imaging to study responses to electrical train stimulation (ETS) of interganglionic fiber tracts in entire myenteric ganglia of the guinea pig small intestine. ETS induced calcium transients in a subset of neurons: 52.2% responded to oral ETS, 65.4% to aboral ETS, and 71.7% to simultaneous oral and aboral ETS. A total of 41.3% of the neurons displayed convergence of oral and aboral ETS-induced responses. Responses could be reversibly blocked with TTX (10(-)6 M), demonstrating involvement of neuronal conduction, and by removal of extracellular calcium. omega-Conotoxin (5 x 10(-7) M) blocked the majority of responses and reduced the amplitude of residual responses by 45%, indicating the involvement of N-type calcium channels. Staining for calbindin and calretinin did not reveal different response patterns in these immunohistochemically identified neurons. We conclude that, at least for ETS close to a ganglion, confocal calcium imaging reveals complex oral and aboral input to individual myenteric neurons rather than a polarization in spread of activity.

Animals↗
PubMed2005

Spontaneous activity and properties of two types of principal neurons from the ventral tegmental area of rat.

We investigated the spontaneous activity and properties of freshly isolated ventral tegmental area (VTA) principal neurons by whole cell recording and single-cell RT-PCR. The VTA principal neurons, which were tyrosine hydroxylase-positive and glutamic acid decarboxylase (GAD67)-negative, exhibited low firing frequency and a long action potential (AP) duration. The VTA principal neurons exhibited a calretinin-positive and parvalbumin-negative Ca2+-binding protein mRNA expression pattern. The VTA principal neurons were classified into two subpopulations based on their firing frequency coefficient of variation (CV) at room temperature (21-23 degrees C): irregular-type neurons with a large CV and tonic-type neurons with a small CV. These two firing patterns were also recorded at the temperature of 34 degrees C and in nystatin-perforated patch recording. In VTA principal neurons, the AP afterhyperpolarization (AHP) amplitude contributed to the firing regularity and AHP decay slope contributed to the firing frequency. The AHP amplitude in the irregular-type VTA principal neurons was smaller than that in the tonic-type VTA principal neurons. There was no significant difference in the AHP decay slope between the two-types of VTA principal neurons. Apamin-sensitive small-conductance Ca2+-activated K+ (SK) channels contributed to the AHP and the regular firing of the tonic-type neurons but contributed little to the AHP and firing of the irregular-type neurons. In voltage-clamp tail-current analysis, in both conventional and nystatin-perforated whole cell recording, the apamin-sensitive AHP current density of the tonic-type neurons was significantly larger than that of the irregular-type neurons. We suggest that apamin-sensitive SK current contributes to intrinsic firing differences between the two subpopulations of VTA principal neurons.

Action Potentials↗
PubMedDate not supplied

Calcium binding protein immunoreactivity in nucleus rotundus in a reptile, Caiman crocodilus.

Nucleus rotundus is a prominent nucleus in the dorsal thalamus of nonmammalian amniotes. In one group of reptiles, Caiman crocodilus, previous studies have identified three parts of this neuronal aggregate. The central portion, the rotundal core, which receives visual input from the midbrain and projects to a restricted portion of the telencephalon, contains relay cells only. Previous examinations using Nissl morphology indicated that neurons of the rotundal core were not a homogeneous population of cells. The present investigation utilized another methodology to examine cell populations within the rotundal core, immunoreactivity to the calcium binding proteins, calbindin/calretinin and parvalbumin. Light microscopic observations revealed the following features. First, calbindin/calretinin immunoreactive neurons and parvalbumin immunoreactive neurons were present in the rotundal core. Of these two antibodies, immunoreactivity to calbindin/calretinin was much more robust and calbindin/calretinin immunoreactive neurons were more numerous than parvalbumin cells. Second, neurons immunoreactive to either calbindin/calretinin or parvalbumin were not homogeneous but comprised several populations based on perikaryal shape and size and neuronal process morphology. These results are compared with similar data in other amniotes.

Alligators and Crocodiles↗
PubMedDate not supplied

Co-existence of protein kinase C gamma and calcium-binding proteins in neurons of the medullary dorsal horn of the rat.

Protein kinase C gamma isoform (PKCgamma) is present at high levels in the spinal and medullary dorsal horns and is thought to play a role in the sensitization of dorsal horn neurons in certain pain states. Calbindin-D28k (CB), calretinin (CR) and parvalbumin (PV) are the most commonly expressed calcium-binding proteins and are located abundantly in the medullary dorsal horn (also called the caudal subnucleus of the spinal trigeminal nucleus). In the present study, immunofluorescence histochemical double staining for PKCgamma and CB, CR or PV was performed in the rat medullary dorsal horn. Most of the PKCgamma-, CB-, CR- and PV-immunoreactive neurons were observed in lamina II; some were also encountered in lamina I and lamina III of the medullary dorsal horn. Neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma were also mainly found in lamina II, while in lamina I and lamina III, only a few neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma were encountered. The percentages of neurons co-expressing CB/PKCgamma in the total numbers of CB- and PKCgamma-immunoreactive neurons were 6.7 and 5.9%, respectively. Of the total numbers of CR- and PKCgamma-immunoreactive neurons, 5.0 and 5.6%, respectively, showed both CR and PKCgamma immunoreactivities. The percentages of neurons co-expressing PV/PKCgamma in the total numbers of PV- and PKCgamma-immunoreactive neurons were 25.7 and 4.1%, respectively. Most of these neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma were small (</=15 microm) and medium-sized (16-35 microm) neurons and had round, triangular or fusiform-shaped cell bodies; large (>/=36 microm) multipolar neurons were infrequently seen. The present results indicate that there are some neurons co-expressing CB/PKCgamma, CR/PKCgamma and PV/PKCgamma in the medullary dorsal horn. These neurons might play important roles in the nociceptive modulation from the oro-facial region.

Animals↗
PubMed2003

Parvalbumin-, calbindin-, and calretinin-immunoreactive neurons in the prefrontal cortex of the owl monkey (Aotus trivirgatus): a standardized quantitative comparison with sensory and motor areas.

Recent studies have revealed regional variation in the density and distribution of inhibitory neurons in different cortical areas, which are thought to reflect area-specific specializations in cortical circuitry. However, there are as yet few standardized quantitative data regarding how the inhibitory circuitry in prefrontal cortex (PFC), which is thought to be involved in executive functions such as cognition, emotion and decision making, compares to that in other cortical areas. Here we used immunohistochemical techniques to determine the density and distribution of parvalbumin (PV)-, calbindin (CB)-, and calretinin (CR)-immunoreactive (ir) neurons and axon terminals in the dorsolateral and orbital PFC of the owl monkey (Aotus trivirgatus), and compared them directly with data obtained using the same techniques in 11 different visual, somatosensory and motor areas. We found marked differences in the density of PV-ir, CB-ir, and CR-ir interneurons in several cortical areas. One hundred and twenty eight of all 234 possible between-area pair-wise comparisons were significantly different. The density of specific subpopulations of these cells also varied among cortical areas, as did the density of axon terminals. Comparison of PFC with other cortical areas revealed that 40 of all 66 possible statistical comparisons of the density of PV-ir, CB-ir, and CR-ir cells were significantly different. We also found evidence for heterogeneity in the pattern of labeling of PV-ir, CB-ir, and CR-ir cells and axon terminals between the dorsolateral and orbital subdivisions of PFC. These data are likely to reflect basic differences in interneuron circuitry, which are likely to influence inhibitory function in the cortex.

Animals↗