PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “CEREBELLAR CORTEX”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 397 records · Page 22Linked to original sources
PubMed1983

Biochemical changes in the rat cerebellar cortex elicited by chronic treatment with methyl mercury.

Long-term (20 days) treatment with methyl mercury (MeHg) increases the total number of benzodiazepine binding sites and decreases essentially the content of cyclic GMP in the cerebellar cortex. In contrast, this treatment fails to modify the content of GABA and cyclic AMP, GAD activity and GABA binding sites in the same brain area. The changes in cyclic GMP and benzodiazepine binding sites in the cerebellar cortex are discussed in relation to the motor disturbances associated with MeHg intoxication.

Animals↗
PubMedDate not supplied

Degeneration of posterior column nucleus, inferior olivary nucleus and cerebellar cortex: system degeneration of paraneoplastic disease?

Degeneration of the posterior column nucleus, inferior olive, and cerebellar cortex is reported in a cancer patient. A 70-year-old man developed an ataxic gait and rapidly progressive disturbance of deep sensation over six months, followed by an abasic state. Early well-differentiated tubular adenocarcinoma was detected and total gastrectomy was performed. He died due to pulmonary tuberculosis about two years and nine months after the operation. Degeneration of the posterior column nuclei was found, explaining the disturbance of deep sensation noted in the clinical course, although there were few changes in the peripheral nerves, dorsal root ganglia, and spinal cord. Degeneration of the inferior olive and cerebellar corte was also found. Metastatic small cell carcinoma was present in the right pulmonary hilar and paratracheal lymph nodes at autopsy without any detectable primary focus. There was neither recurrence nor metastasis of the gastric carcinoma. This is the first case report of this type of central nervous system degeneration in a cancer patient, and its pathogenesis and etiology remain obscure. We discuss whether system degeneration or paraneoplastic degeneration was the etiology.

Adenocarcinoma↗
PubMed1986

Critical analysis on the nature of synapses en marron of cerebellar cortex.

An exotic type of contact was described in the last decade, in the rat cerebellar cortex, under the designation of synapse en marron. The junction was referred as existing between an afferent terminal and the soma of a Golgi cell, establishing an axo-somatic synapse. Nonetheless, according to our studies, the contact is of the axo-dendritic type instead, on account of the nature of the postsynaptic component: a dendrite of the Golgi cell. This was observed in sections where that process may be unequivocally demonstrated, regarding its continuity with the cell body which exhibited a nuclear profile.

Afferent Pathways↗
PubMed1987

The cytoskeleton of the human cerebellar cortex: an immunohistochemical study of normal and pathological material.

Monoclonal antibodies to non-phosphorylated and phosphorylated neurofilaments, as well as monoclonal and polyclonal antibodies to other cytoskeletal elements, were applied to the study of the cerebellar cortex of normal and pathological human material. The methods proved to be applicable to formalin fixed paraffin embedded tissue, provided the period of formalin fixation was short. The main difference between normal and pathological material was found in Purkinje cells and their dendrites. While normal Purkinje perikarya and dendrites expressed only non-phosphorylated neurofilaments, reactive dendrites stained more intensely with antibodies to phosphorylated neurofilaments. Similar observations were made on the abnormal dendritic ramifications of the partially deafferented, hypertrophic, inferior olive. The significance of the appearance of phosphorylated neurofilament epitopes in abnormal dendrites remains unknown and requires further investigation.

Adult↗
PubMed1986

Long-term effects of parallel fiber loss in the cerebellar cortex of the adult and weanling rat.

Short- and long-term effects of parallel fiber deafferentation of adult and weanling cerebellar cortex were investigated following parasagittal transections of the lateral cerebellar hemisphere. Short-term electron microscopic examination revealed that parallel fibers undergo rapid electron-dense degeneration within 5 days of axotomy. These axons were the only neuronal elements immediately affected by the lesion. The continued maintenance of Purkinje cell terminal branchlets and stellate cell dendrites is dependent upon the presence of an adequate parallel fiber milieu. Morphological evidence is provided which suggests that Purkinje cell dendritic spines may be phagocytically removed by Bergmann glial cells following parallel fiber loss. Although a marked decrease was reported in the number of spines projecting from terminal branchlets following deafferentation of both adult and weanling rats, these data suggest that some spines are capable of increasing their length. The elongation of these spines may represent a form of dendritic plasticity. No evidence was found to suggest that deafferentated terminal branchlets are receptive to forming heterologous synaptic contacts. The primary response to parallel fiber deafferentation for both the adult and weanling cerebellum therefore appears to be transneuronal degeneration.

Animals↗
PubMed1995

Immunohistochemical demonstration of taurine in the rat cerebellar cortex. Evidence for its location within mossy fibers and Golgi axons.

Taurine, 2-aminoethanesulfonic acid, is one of the most abundant amino acid present in the Central Nervous System. Nevertheless, its functions are remain uncertain. Taking as a basis the immunocytochemical pre-embedding PAP-techniques for demonstrating Taurine-Like substances on cerebellar cortex of rats we have observed positive immunoreaction within Purkinje cell bodies and their dendrites. Likewise, taurine has been demonstrated within mossy fibers and Golgi axons, as well as in glial processes. Our results demonstrate the wide distribution of Taurine in the cerebellar cortex, justifying its possible involvement as an inhibitory neurotransmitter, neuromodulator or as a gliotransmitter.

Animals↗
PubMed1978

Ultrastructural changes in the rat cerebellar cortex during methionine sulphoximine convulsions.

The ultrastructure of the rat cerebellar cortex and the activity of succinic dehydrogenase were examined during methionine sulphoximine (MSO)-provoked convulsions. The animals were killed 3, 6 and 12 hours after the injection of 600 mg/kg of MSO. Convulsions appeared 4--5 hours, status epilepticus developed 8-9 hours after the injection. Progressive ischaemic changes of Purkinje cells could be observed, with condensation of the nucleus and a density of the cytoplasmic matrix. The cisternae of the Golgi complex and endoplasmic reticulum showed some degree of dilation. The basis of Purkinje cells was surrounded by distorted axons and terminals that had lost in most cases the synaptic vesicles, and by clear spaces due to the swollen glial processes. Three to six hours after MSO injection, succinic dehydrogenase activity increased in the mitochondria of Purkinje cells. After the appearance of seizures the enzyme activity decreased. Twelve hours after the injection the enzyme activity recovered to a certain extent.

Animals↗
PubMed1994

Reduction of GABAA and GABAB receptor densities in the cerebellar cortex from 3-acetylpyridine-induced ataxic rats.

We measured GABAA and GABAB receptor densities in the cerebellar cortex from 3-acetylpyridine-induced ataxic rats using receptor autoradiography. GABAA and GABAB receptor densities were significantly reduced both in the molecular layer and the granule cell layer. Reduction of GABA receptor densities may be induced by loss of GABA receptors on the degenerated climbing fibers or by secondary or compensatory changes of neuronal activities in the cerebellum.

Animals↗
PubMed1994

Immunohistochemical localization of metabotropic glutamate receptors, mGluR2 and mGluR3, in rat cerebellar cortex.

The distribution of the metabotropic glutamate receptors mGluR2 and mGluR3 was immunohistochemically examined in the rat cerebellar cortex at both light and electron microscope levels. An antibody was raised against a fusion protein containing a C-terminal portion of mGluR2. On immunoblot, the antibody reacted with both mGluR2 and mGluR3 in rat brain. mGluR2/3 immunoreactivity was expressed in cell bodies, dendrites, and axon terminals of Golgi cells, as well as in presumed glial processes. Golgi axon terminals with mGluR2/3 immunoreactivity were often encountered in the vicinity of glutamatergic mossy fiber terminals. The results suggest that transmitter glutamate may exert control influences upon Golgi cells not only through dendritic mGluR2/3, but also through axonal mGluR2/3.

Animals↗
PubMed1983

Alterations in the postnatal development of the cerebellar cortex due to zinc deficiency. I. Impaired acquisition of granule cells.

The effects of zinc deficiency on cerebellar development were investigated in suckling rats. In 21-day-old zinc-deficient rats the cerebellum as well as the whole brain was reduced in size. The cerebellar cortex was underdeveloped and showed a persistence of the external granule cell layer, a reduction in the thickness of molecular layer and a decrease in the area of the internal granule cell layer. Lobular variations were present. Along the posterior superior fissure there was approximately a 60% reduction in the number of granule cells and in the number of granule cells per Purkinje cell. It was suggested that the reduction in the number of granule cells was predominantly the result of impaired cell proliferation in the external granule cell layer. Comparisons with undernourished, pair-fed pups indicated that the effects of zinc deficiency could not be mediated totally through the reduced food consumption experienced by zinc deficient dams.

Animals↗
PubMed1976

Differentiation of Purkinje cells and their relationship to other components of developing cerebellar cortex in man.

The differentiation of Purkinje cells and their relationship to other components of the developing cerebellar cortex were analyzed by the Golgi impregnation method and by electron microscopy in human specimens of various pre- and postnatal ages. The three stages of Purkinje cell maturation that have been previously recognized in other species are also evident in man: the first stage occupies primarily the fourth fetal month (12-16 weeks); the second stage lasts through the fifth, sixth and seventh feta months (16-28 weeks); the third stage extends throughout the remaining period of intrauterine life and the first postnatal year and continues at a slow rate thereafter. During the first stage, Purkinje cells are distributed in a layer, several rows deep. Their bipolar somas are relatively smooth and have only a few processes at the apical and basal cell poles. In the 3-month period of the second stage, Purkinje cells become gradually organized into a single row. Their somas become invested with additional randomly oriented dendritic processes and numerous somatic spines (pseudopodia). The first morphologically well-defined synapses appear on the Purkinje cell somatic spines and on their immature dendritic shafts at the beginning of the second stage and become more prominent during the period from 18 to 24 weeks. In the third stage, the dendritic arbor becomes flattened in the plane transverse to the folium and somatic spines disappear. Spines appear on the secondary and tertiary dendrites between the twenty-fourth and twenty-eighth fetal weeks and continue to increase in number during the entire third stage as new dendritic branches develop. These observations indicate that cellular maturation and synaptogenesis in the primate cerebellum differ from these events in non-primate species, with respect to time of birth, in the relative duration of each phase and in the total time necessary for neuronal differentiation. The protracted time of differentiation and the slow growth of Purkinje cell dendrites in man may be due to the numerically complex relationships existing between granule and Purkinje cells. It is probably not simply a reflection of the larger size of human Purkinje cells and their dendrites.

Animals↗
PubMed1995

Developing mossy fiber terminal fields in the rat cerebellar cortex may segregate because of Purkinje cell compartmentation and not competition.

Many mossy fiber afferent projections to the rat cerebellar cortex terminate in parasagittal bands. In particular, the anterior lobe vermis of the cerebellum contains alternating bands of mossy fibers from the spinal cord and external cuneate nuclei. The cerebellar cortical efferents, the Purkinje cells, are also organized in parasagittal bands. These can be revealed by immunochemical staining for the antigen zebrin II, which is selectively expressed by bands of Purkinje cells. In some cases, the boundaries between mossy fiber terminal fields align with identified transitions between zebrin+/- sets of Purkinje cells, whereas others are located within apparently homogeneous Purkinje cell compartments. Two theories can explain the terminal-field topography: In one view, mossy fiber terminals segregate during development, because growth cones from different sources compete for common territory. Alternatively, mossy fiber growth cones directly recognize chemically distinct target territories, and activity-dependent mechanisms play only minor roles. To explore these issues, two sets of experiments were performed. First, the terminal-field map of the neonatal spinocerebellar projection was compared to the Purkinje cell compartmentation as revealed by anticalbindin immunocytochemistry. Second, subsets of spinocerebellar mossy fiber afferents were ablated early in postnatal development, and the consequences for the neighboring cuneocerebellar terminal fields were mapped in the adult with reference to the zebrin II+/- compartments. These experiments revealed no evidence that competitive interactions constrain the mossy fiber terminal-field distribution but, rather, suggest that the organization of the mossy fiber projections follows the compartmentation of the Purkinje cells.

Analysis of Variance↗
PubMed2002

Nicotinic receptor abnormalities in the cerebellar cortex in autism.

Autism is a common developmental disorder associated with structural and inferred neurochemical abnormalities of the brain. Cerebellar abnormalities frequently have been identified, based on neuroimaging or neuropathology. Recently, the cholinergic neurotransmitter system has been implicated on the basis of nicotinic receptor loss in the cerebral cortex. Cerebellar cholinergic activities were therefore investigated in autopsy tissue from a series of autistic individuals. The presynaptic cholinergic enzyme, choline acetyltransferase, together with nicotinic and muscarinic receptor subtypes were compared in the cerebellum from age-matched mentally retarded autistic (eight), normal control (10) and non-autistic mentally retarded individuals (11). The nicotinic receptor binding the agonist epibatidine (the high affinity receptor subtype, consisting primarily of alpha3 and alpha4, together with beta2 receptor subunits) was significantly reduced by 40-50% in the granule cell, Purkinje and molecular layers in the autistic compared with the normal group (P < 0.05). There was an opposite increase (3-fold) in the nicotinic receptor binding alpha-bungarotoxin (to the alpha7 subunit) which reached significance in the granule cell layer (P < 0.05). These receptor changes were paralleled by a significant reduction (P < 0.05) and non-significant increase, respectively, of alpha4 and alpha7 receptor subunit immunoreactivity measured using western blotting. Immunohistochemically loss of alpha(4 )reactivity was apparent from Purkinje and the other cell layers, with increased alpha7 reactivity in the granule cell layer. There were no significant changes in choline acetyltransferase activity, or in muscarinic M1 and M2 receptor subtypes in autism. In the non-autistic mentally retarded group, the only significant abnormality was a reduction in epibatidine binding in the granule cell and Purkinje layers. In two autistic cases examined histologically, Purkinje cell loss was observed in multiple lobules throughout the vermis and hemispheres. This was more severe in one case with epilepsy, which also showed vermis folial malformation. The case with less severe Purkinje cell loss also showed cerebellar white matter thinning and demyelination. These findings indicate a loss of the cerebellar nicotinic alpha4 receptor subunit in autism which may relate to the loss of Purkinje cells, and a compensatory increase in the alpha7 subunit. It remains to be determined how these receptor abnormalities are involved in neurodevelopment in autism and what is the relationship to mental function. Since nicotinic receptor agonists enhance attentional function and also induce an elevation in the high affinity receptor, nicotinic therapy in autism may be worth considering.

Adult↗
PubMed1983

[Harmaline tremor: topography of activity in the cerebellar cortex in rats].

In the Rat under tremorogenic doses of harmaline, Purkinje cells of the vermis of the cerebellar cortex display a regular complex spike activity at 6 to 11 Hz ("harmaline-rhythm"). With increased laterality of the recorded units, the rhythm loses its regularity and then disappears. The intermediate regions thus contain less harmaline sensitive units, while lateral regions and those corresponding to the vestibulo-oculomotor system did not present any such units. These results indicate that the parts of the olivo-cerebellar system activated by harmaline in the Rat are homologous to those already known in the Cat, and do not coincide with those of the inferior olive where a serotonergic innervation has been described.

Animals↗