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PubMed2000

Immunolocalization of the mGluR1b splice variant of the metabotropic glutamate receptor 1 at parallel fiber-Purkinje cell synapses in the rat cerebellar cortex.

Several metabotropic glutamate receptor (mGluR) subtypes have been identified in the cerebellar cortex that are targeted to different compartments in cerebellar cells. In this study, preembedding immunocytochemical methods for electron microscopy were used to investigate the subcellular distribution of the mGluR1b splice variant in the rat cerebellar cortex. Dendritic spines of Purkinje cells receiving parallel fiber synaptic terminals were immunoreactive for mGluR1b. With a preembedding immunogold method, approximately 25% of the mGluR1b immunolabeling was observed perisynaptically within 60 nm from the edge of the postsynaptic densities. Values of extrasynaptic gold particles beyond the first 60 nm were maintained at between 10 and 18% along the whole intracellular surface of the dendritic spine membranes of Purkinje cells. For comparison, the distribution of mGluR1a was studied. A predominant (approximately 37%) perisynaptic localization of mGluR1a was seen in dendritic spines of Purkinje cells, dropping the extrasynaptic labeling to 15% in the 60-120-nm bin from the edge of the postsynaptic specialization. Our results reveal that mGluR1b and mGluR1a are localized to the same subcellular compartments in Purkinje cells but that the densities of the perisynaptic and extrasynaptic pools were different for both isoforms. The compartmentalization of mGluR1b and mGluR1a might serve distinct requirements in cerebellar neurotransmission.

Animals↗

PubMed1980

A light and electron microscopic study of the effects of 3-acetylpyridine intoxication on the inferior olivary complex and cerebellar cortex.

The effects of 3-acetylpyridine (3-AP) intoxication on the inferior olivary complex and cerebellar cortex of the rat were examined at both the light and electron microscopic level. Following intraperitoneal injection of 65 mg of 3-AP per kg body weight, the inferior olivary neurons were observed to undergo a rapid form of electron dense degeneration. A complete bilateral involvement of the nuclear complex was well advanced as early as 12 hours following injection. Marked astrocytic proliferation also occurred by 12 hours and appeared essential for neuronal fragmentation and disintegration. Microglial activity was prominent in the later stages, from 60 hours onwards, and participated in the phagocytic removal of degenerating neuronal fragments. By the end of the second week, all cytoplasmic and nuclear debri was removed. Concurrently, degenerative changes in the cerebellar cortex were evident from 12 hours onwards. All climbing fiber varicosities were observed to be degenerative as early as 24 hours following treatment. Electron microscopic observations revealed that these electron dense fragments were largely phagocytized and cleared by Bergmann glial cells around 7 days. The sensitivity of the olivocerebellar system to 3-AP thus provides a convenient and selective means of eliminating all of the inferior olivary neurons and their axons, the climbing fibers of the cerebellar cortex. In contrast to the more conventionally used electrolytic methods, 3-AP causes a complete bilateral ablation of all olivary neurons while avoiding the problems inherent to electrolytic procedures, such as incomplete destruction of the nucleus and involvement of fibers of passage.

Animals↗

PubMed1990

Immunohistochemical demonstration of glutamate dehydrogenase in the postnatally developing rat hippocampal formation and cerebellar cortex: comparison to activity staining.

Distribution patterns of activity and immunohistochemical staining for glutamate dehydrogenase were compared during the postnatal development of rat hippocampal formation and cerebellar cortex. On postnatal day 5, dendritic layers of the hippocampal formation showed only a very weak enzyme activity. Similarly, when studied at the same age, the external granule cell layer and Purkinje cells of the cerebellar cortex exhibited a very faint and moderate staining, respectively. With advancing age, in both brain regions a marked postnatal increase in glutamate dehydrogenase activity occurred in neuropil area as glutamatergic structures matured. However, compared to activity staining, both brain regions of early postnatal stages showed a relatively high level of glutamate dehydrogenase-like immunoreactivity. In this case, the immunohistochemical staining of hippocampal dendritic layers and of the molecular layer of the cerebellar cortex was rather diffuse, being not very similar to parameters of the maturation of the respective glutamatergic structures. In contrast to the activity staining for the enzyme, the immunohistochemical labelling in adult rats revealed a selective predominance of immunoreactivity in astroglial cells from postnatal day 5 onwards. The Bergmann glia in the cerebellar cortex exhibited the strongest intensity of immunoreactivity. Generally, the patterns of immunoreactivity were found to depend on the fixation procedure adopted. Concluding from our results, glutamate dehydrogenase is demonstrable in glial and in neuronal cell elements as well. Therefore, it is recommended that activity staining and the immunohistochemical procedure be combined to study qualitative and quantitative aspects of glutamate dehydrogenase in nervous tissues.

Aging↗

PubMed1980

Immunocytochemical localization of the prostaglandin-forming cyclooxygenase in the cerebellar cortex.

An indirect immunocytofluorescence technique was used to examine the distribution of the prostaglandin-forming cyclooxygenase in the cerebellar cortex of the pig, guinea, rat, mouse, cow, rabbit and sheep. Cyclooxygenase antigenicity was detected (a) in the cell bodies of Bergman glial cells in the Purkinje cell layer of the porcine, ovine and bovine cerebellar cortex; (b) in small arterioles throughout the cerebellar cortex in the sheep and cow; and (c) in the endothelial cells of large arteries in all the species examined. No cyclooxygenase-positive staining was apparent in neuronal cell bodies of granule, basket, stellate or Purkinje cells. Our results establish that prostaglandin endoperoxides can be synthesized by the arterial vasculature and at least certain glial cells in the central nervous system.

Animals↗

PubMed1987

Regular stripe-like activation and suppression of metabolic activity in the cerebellar cortex following apomorphine administration to haloperidol-pretreated rats.

Alteration of the pattern of metabolic activity in the cerebellar cortex, as produced by apomorphine in rats given chronic pretreatment with haloperidol was studied by means of the [14C]deoxyglucose method. Apomorphine induced a regular stripe-like activation and suppression of metabolic activity in the caudal paravermal area of the cerebellar hemisphere and in the caudal vermis of the cerebellar cortex. This stripe-like pattern, oriented perpendicularly to the cerebellar fissure, suggests the functional organization of the cerebellar cortex in a direction which is parallel to the longitudinal axis of folia.

Animals↗

PubMed2005

Glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of adult rat after prenatal exposure to a low concentration of carbon monoxide.

Glutamic acid decarboxylase and GABA immunoreactivities were qualitatively and quantitatively evaluated in the cerebellar cortex of adult rats prenatally exposed to a low concentration of carbon monoxide (75 parts per million). Carbon monoxide-exposed and control rats were perfused with modified Bouin's fluid and their cerebella were embedded in paraffin. Sections from the vermis of each cerebellum were stained with Toluidine Blue or assayed with anti-glutamic acid decarboxylase 65/67 or with anti-GABA antisera. In the Toluidine Blue-stained sections, no differences were observed in the microscopic structure of the cerebellar cortex between carbon monoxide-exposed rats and controls. The distribution patterns of glutamic acid decarboxylase and GABA immunoreactivities in the cerebellar cortex of the treated animals were qualitatively comparable to those of the controls, and in accordance with previous descriptions of glutamic acid decarboxylase and GABA immunoreactivities in the rat cerebellar cortex. However, quantitative analyses demonstrated a significant reduction of immunoreactivities to both substances in the exposed rats in comparison with the controls. The reduction regarded: in the molecular layer, the number of glutamic acid decarboxylase/GABA-immunoreactive neuronal bodies and of axon terminals and the area they covered; in the Purkinje neuron layer, the number and the area covered by glutamic acid decarboxylase/GABA immunoreactive axon terminals. The differences detected in the prenatally exposed adult rats could be due to carbon monoxide-induced impairment of the differentiation of cerebellar GABA synthesizing neurons. A consequently diminished synthesis of GABA might account for some behavioral disorders detected in adult rats submitted to the same experimental procedure.

Animals↗

PubMed1995

Nitric oxide contributes to functional hyperemia in cerebellar cortex.

We used the parallel fibers (PF) system of the cerebellar cortex as a model to investigate the role of nitric oxide (NO) in the increases in blood flow elicited by neural activation. Rats were anesthetized with halothane and ventilated. The vermis was exposed, and the site was superfused with Ringer (37 degrees C; pH 7.3-7.4). PF were stimulated electrically (100 muA; 30 Hz), and the associated changes in cerebellar cortex blood flow (BFcrb) were monitored by laser-Doppler flowmetry. The field potentials evoked by PF stimulation were recorded using microelectrodes. During Ringer superfusion (n = 7), PF stimulation increased BFcrb (+ 52 +/- 4%). Topical application of the NO synthase (NOS) inhibitor N omega-nitro-L-arginine (L-NNA; 0.1-1 mM) attenuated the increases in BFcrb dose dependently and by 50 +/- 4% at 1 mM (n = 9; P < 0.001; analysis of variance and Tukey's test). L-NNA (1 mM) inhibited NOS catalytic activity, assessed ex vivo using the citrulline assay, by 95 +/- 9% (P < 0.001). L-NNA did not influence the field potentials evoked by PF stimulation. D-NNA (1 mM; n = 6), the inactive stereoisomer of nitroarginine, did not attenuate the BFcrb response (P > 0.05). Methylene blue (1 mM; n = 7) reduced the response by 41 +/- 9% (P < 0.01) without affecting NOS catalytic activity (P < 0.05). The increases in BFcrb were not affected by lesioning the NOS-containing nerve fibers innervating cerebral vessels, indicating that these nerves are not the source of NO. Thus the increases in BFcrb elicited by activation of PF are, in part, mediated by NO produced in the molecular layer during neural activity. The results indicated that NO participates in the coupling of function activity to blood flow and support the hypothesis that NO is one of the mediators responsible for functional hyperemia in the central nervous system.

Amino Acid Oxidoreductases↗

PubMed2003

Antigenic compartmentation of the cerebellar cortex in the syrian hamster Mesocricetus auratus.

Despite the apparent uniformity in cellular composition of the adult cerebellar cortex, a complex heterogeneous pattern can be revealed by using biochemical markers. One example is zebrin II/aldolase C, which is expressed by a subset of Purkinje cells that form a highly reproducible array of stripes. Zebrin II/aldolase C immunohistochemistry has been used in both section and whole mount preparations to analyze the architecture of the hamster cerebellar cortex. As in other species studied, zebrin II immunoreactivity in the hamster cerebellum is restricted to a subset of Purkinje cells and, more weakly, to astrocytes. Based on the distribution of these Purkinje cell subsets the hamster cerebellar vermis was found to consist of four transverse zones-the anterior zone, central zone, posterior zone and nodular zone. Zebrin II/aldolase C is expressed uniformly in the central and nodular zones, and as parasagittal stripes in the anterior and central zones. A similar alternation of homogeneous and striped expression domains is seen in the hemispheres. The topography of the hamster cerebellar cortex as revealed by zebrin II expression domains closely resembles that reported in other mammals. Thus, a cerebellar zone-and-stripe topography appears to be conserved across the Mammalia.

Animals↗

PubMed1984

Distribution pattern of DNA template activity in the developing cerebellar cortex in rats and its alteration after transplacental administration of ethylnitrosourea.

The ultracytochemical acridine orange(AO) method has been employed to demonstrate DNA template activity in the developing cerebellar cortex in rats and its alteration after transplacental administration of ethylnitrosourea (ENU). Electron microscopic studies revealed that AO binds to DNA exclusively within the active extended euchromatin portion of the cell nucleus of the proliferating external granular layer. No or only a few AO reaction products were visible in the non-proliferating cell nuclei of the internal granular layer and of Purkinje cells. With increasing cellular differentiation of granule cells in the cerebellar cortex the number of AO positive cells as well as the number of AO reaction products per cell showed a progressive decrease. A single i.p. injection of 50 mg/kg of ENU in rats on day 15 to 21 of gestation resulted in occasional cell damage to the proliferating external granule cells of developing cerebellar cortex at 4 and 7 days after birth. Damaged cells of the external granular layer were found to have no or only a small number of AO reaction products in their nuclei. In further development from 14 to 28 days the cerebellar cortex of offspring from ENU-treated mother showed no abnormality and exhibited no definite alteration in distribution pattern of AO reaction products.

Acridine Orange↗

PubMed1982

Distribution of dopamine-beta-hydroxylase-like immunoreactive fibers in the rat cerebellar cortex during ontogeny.

Postnatal ontogeny of dopamine-beta-hydroxylase (DBH)-like immunoreactive fibers in the rat cerebellar cortex has been studied by immunofluorescence on sagittal sections of the vermis. Except in the case of unusual thick highly fluorescent fibers noticed in the external granular layer during the first 2 weeks after birth, the arrival of DBH-containing fibers through the cerebellar cortex follows an inside-out gradient: at birth sparse fluorescent axons are observed in the album of the cerebellum. They invade the internal granular layer at postnatal day 2 (P2) and reach the Purkinje cell layer at P5. From P5 to P15, the density of fibers increases in this layer, which becomes the most innervated layer of the cerebellar cortex, as in the adult. When the external grains migrate, DBH-containing fibers extend progressively from depth to surface in the molecular layer and show an adult pattern at P30. The relationship between our results and other morphological and biochemical studies is discussed.

Aging↗

PubMedDate not supplied

A comparative immunocytochemical study of human cerebellar cortex in X-chromosome-linked copper malabsorption (Menkes' kinky hair disease) and granule cell type cerebellar degeneration.

A comparative immunocytochemical study on the cerebellar cortex with X-chromosome-linked copper malabsorption (X-cLCM) and granule cell type cerebellar degeneration (gc-CD) was carried out by using specific monoclonal antibodies to synaptophysin (SY) and glial fibrillary acidic protein (GFAP). In X-cLCM cases, marked depletion of SY-immunoreactivity (IR) and reduction in number of SY-positive glomeruli were seen in the molecular and granular layers, respectively. Abnormal Purkinje cells occasionally showed moderately strong SY-IR having a fine granular pattern. Proliferation of GFAP-positive cells was observed in the granular and Purkinje cell layers. In the gc-CD case, SY-positive materials were coarsely distributed in a less dense fashion in the molecular layer as compared to a normal control. Purkinje cell perikarya did not show SY-IR. In the gc-CD granular layer, SY-IR appeared to have a coarsely punctate pattern, whereas immunoreactive glomeruli were almost completely absent. A number of GFAP-positive Bergmann cells was observed in the Purkinje cell layer and their fibres were densely and irregularly distributed in the molecular layer, whereas the granular layer was devoid of GFAP-positive cells. We present an immunocytochemical study of the X-cLCM and gc-CD cerebellar cortices, discuss the possible pathogenic mechanisms occurring in these diseases and discuss the usefulness of the SY-immunostaining technique for visualization of axon terminal involvement in these pathological conditions.

Brain Diseases, Metabolic↗

PubMed2003

Differential distribution of vesicular glutamate transporters in the rat cerebellar cortex.

The chemical organization of excitatory axon terminals in the rat cerebellar cortex was examined by immunocytochemistry and in situ hybridization histochemistry of vesicular glutamate transporters 1 and 2 (VGluT1 and VGluT2). Chemical depletion of the inferior olivary complex neurons by 3-acetylpyridine treatment almost completely removed VGluT2 immunoreactivity from the molecular layer, leaving VGluT1 immunoreactivity apparently intact. On the other hand, neuronal deprivation of the cerebellar cortex by kainic acid injection induced a large loss of VGluT1 immunoreactivity in the molecular layer. In the cerebellar granular layer, both VGluT1 and VGluT2 immunoreactivities were found in mossy fiber terminals, and the two immunoreactivities were mostly colocalized in single-axon terminals. Signals for mRNA encoding VGluT2 were found in the inferior olivary complex, and those for VGluT1 and VGluT2 mRNAs were observed in most brainstem precerebellar nuclei sending mossy fibers, such as the pontine, pontine tegmental reticular, lateral reticular and external cuneate nuclei. These results indicate that climbing and parallel fibers selectively use VGluT2 and VGluT1, respectively, whereas mossy fibers apply both VGluT1 and VGluT2 together to accumulate glutamate into synaptic vesicles. Since climbing-fiber and parallel-fiber terminals are known to make depressing and facilitating synapses, respectively, VGluT1 and VGluT2 might have distinct properties associated with those synaptic characteristics. Thus, it would be the next interesting issue to determine whether mossy-fiber terminals co-expressing VGluT1 and VGluT2 show synaptic facilitation or depression.

Animals↗

PubMed1995

Effect of treatment with the dihydropyridine-type calcium antagonist darodipine (PY 108-068) on the expression of calbindin D-28K immunoreactivity in the cerebellar cortex of aged rats.

The influence of long term treatment with the dihydropyridine-type Ca2+ antagonist darodipine (PY 108-068) on age-dependent changes in calbindin D-28K immunoreactivity in the cerebellar cortex of male Wistar rats was assessed. In 12-month-old rats used as an adult reference group, specific calbindin D-28K immunoreactivity was found within the cytoplasm of Purkinje neurons and their dendritic processes. The number of Purkinje neurons displaying calbindin D-28K immunoreactivity was decreased in the cerebellar cortex of aged in comparison with adult rats. The pattern of calbindin D-28K immunoreactivity was similar in the cerebellar cortex of 24-month-old rats (aged), although a significant decrease in the intensity of immunoreactivity was noticeable. Treatment of aged rats with darodipine for 6 months increased the percentage of immunoreactive Purkinje neurons and the intensity of calbindin D-28K immunoreactivity in the cytoplasm of Purkinje neurons. Calbindin D-28K is a Ca2+ binding protein probably involved in the modulation of Ca2+ homeostasis. The observation of a positive effect of darodipine treatment on calbindin D-28K immunoreactivity in the cerebellar cortex suggests that manipulation of dihydropyridine-type Ca2+ channels may contribute to counter age-dependent changes of Ca2+ homeostasis.

Aging↗

PubMed2004

Molecular morphology of neuronal apoptosis: analysis of caspase 3 activation during postnatal development of mouse cerebellar cortex.

We have used the mammalian post-natal cerebellar cortex as a model to dissect out the molecular morphology of neuronal apoptosis in a well-defined population of central neurons: the cerebellar granule cells. By immunocytochemistry, in situ labeling of apoptotic cells, and analysis of cerebellar slices following particle-mediated gene transfer (biolistics), we have studied the relationship of cell death and cleavage of caspase 3, a key molecule in the execution of apoptosis, and monitored caspase 3 activation in living cells. Our results demonstrate the existence of caspase dependent and independent apoptotic pathways affecting the cerebellar granule cells at different stages of their life. Apoptosis of proliferating precursors and young pre-migratory cells occurs in the absence of caspase 3 cleavage, whereas cell death of post-mitotic post-migratory neurons is directly linked to caspase 3 activation. Data obtained from cerebellar cortex can be generalized to outline a more comprehensive picture of the cellular and molecular mechanisms of neuronal death not only in development, but also in a number of pathological conditions leading to neuronal loss.

Animals↗

PubMed1987

[Development of dendritic spines in the piriform neurons of the cerebellar cortex in human prenatal ontogeny].

The submicroscopic investigation on developmental peculiarities of the dendritic spines in the piriform neurons of the cerebellar cortex has been performed during the human prenatal ontogenesis. The process of morphogenesis of the spines of the tertiary dendrites in the piriform neurons is demonstrated to start rather early--on the 24th week of embryogenesis and goes through three successive stages: 1) formation of a long cytoplasmic processes deprived of any membranous specialization; 2) formation of the terminal spinal head, making synapses with parallel fibers of the cerebellar cortex; 3) definitive stage. A suggestion is made that differentiation processes of the spines depend on inductive influence of the parallel fibers of the cerebellar cortex.

Cerebellar Cortex↗

PubMed1999

Saccadic dysmetria and adaptation after lesions of the cerebellar cortex.

We studied the effects of small lesions of the oculomotor vermis of the cerebellar cortex on the ability of monkeys to execute and adapt saccadic eye movements. For saccades in one horizontal direction, the lesions led to an initial gross hypometria and a permanent abolition of the capacity for rapid adaptation. Mean saccade amplitude recovered from the initial hypometria, although variability remained high. A series of hundreds of repetitive saccades in the same direction resulted in gradual decrement of amplitude. Saccades in other directions were less strongly affected by the lesions. We suggest the following. (1) The cerebellar cortex is constantly recalibrating the saccadic system, thus compensating for rapid biomechanical changes such as might be caused by muscle fatigue. (2) A mechanism capable of slow recovery from dysmetria is revealed despite the permanent absence of rapid adaptation.

Adaptation, Physiological↗

PubMed2002

Multiple zonal projections of the nucleus reticularis tegmenti pontis to the cerebellar cortex of the rat.

Compartmentalization (alternating labelled and unlabelled stripes) of mossy fibre terminals was found in the cerebellar cortex after iontophoretic injections of biotinylated dextran amine into discrete regions of the nucleus reticularis tegmenti pontis (NRTP). The zonal pattern was only observed when volumes of nuclear tissue ranging from 4.5 x 106 to 17.66 x 106 microm3 were impregnated. Up to nine compartments (i.e. up to five stripes separated by four interstripes) were found in crus I and in vermal lobule VI. Up to seven compartments (four stripes and three interstripes) were found in crus II; up to five compartments (three stripes and two interstripes) were identified in the lobulus simplex, the paraflocculus and vermal lobules IV, V and VII; up to three compartments (two stripes and one interstripe) were identified in the paramedian lobule and, finally, up to two compartments (one stripe and one interstripe) were identified in the copula pyramidis, in the flocculus and in vermal lobules II, III, VIII and IX. The projections of the NRTP are arranged according to a divergent/convergent projection pattern. From single injections in the NRTP, projections were traced to a set of cortical stripes widely distributed over the cerebellar cortex. The set of stripes labelled from different regions of the NRTP partially overlapped but complete overlap was never found. This finding revealed that the topographic combination of the projections of the NRTP to the cerebellar cortex is specific for each region of the NRTP. Finally, the projections to single cortical areas were arranged according to a pattern of compartmentalization that is specific for each cortical area, independent of the site of injection in the NRTP and of the number of stripes evident in the cortex.

Animals↗

PubMed1994

A time course study of the alterations in the development of the hamster cerebellar cortex after destruction of the overlying meningeal cells with 6-hydroxydopamine on the day of birth.

This study is a chronological analysis of 6-hydroxydopamine-induced alterations in development of the hamster cerebellar cortex. This treatment destroys the overlying meningeal cells, the sequelae of which include (i) a thinning of the external granular layer over the folial apices and a thickening in the region of the prospective fissures, reflecting a retardation of the growth of the cerebellar cortex, accompanied by displacement of the normally superficialmost GFAP-positive external granular layer cells into deeper parts of the external granular layer; (ii) a retardation of multiplication of Golgi epithelial cells which colonize the rostral third of the Purkinje cell layer so that their numbers decrease in the rostralmost folia; (iii) disturbed morphological and biochemical differentiation of the Golgi epithelial cells and their processes, the growing radial Bergmann glial fibres which detach from the pial surface and branch within the external granular layer, causing a failure in endfeet formation at the superficial glia limitans, loss of characteristic radial morphology, with the adoption of a multipolar form, and normal or increased GFAP expression and decreased S-100 expression; (iv) fragmentation of the external granular layer beyond P5 to P7 with loss of the regular lamination and foliation of the cerebellar cortex, characterized by a completely random distribution of fragments of Purkinje cell layer, molecular zone and internal granular layer. We conclude that the destruction of meningeal cells interferes with the establishment and stabilization of both the external granular layer and the secondary radial glial scaffold composed of Golgi epithelial cells, whose proliferation, growth and differentiation is subsequently disturbed. The failure to stabilize the external granular layer and to form a normal secondary radial glial scaffold is, in turn, responsible for the disruption of the regular laminar deposition of the neurons of the cerebellar cortex.

Animals↗