Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cerebellar Cortex”

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 91 records · Page 5Linked to original sources
PubMed1986

Noradrenergic innervation of the cerebellar cortex in normal and in Purkinje cell degeneration mutant mice: evidence for long term survival following loss of the two major cerebellar cortical neuronal populations.

Purkinje cell degeneration mutant mice were examined during the course of Purkinje cell death (26 and 35 days old) and at 3, 5, 9 and 12 months of age. Glyoxylic acid fluorescence histochemistry for catecholamines was used to investigate possible alterations or reorganization of the noradrenergic fibers from the coeruleo-cerebellar system in response to the degeneration of two major cell types in the cerebellar cortex, of which one, the Purkinje cell, is reported to be the major target neuron. In control mice, noradrenergic fibers traveled in linear and tortuous profiles through the granule cell layer, formed pericellular arrays alongside Purkinje cell somata, and branched profusely into both radially oriented and longitudinally oriented chains. The density of noradrenergic varicosities diminished in the molecular layer, there was with age. In the mutants, concomitant with the progressive shrinkage of the molecular layer, there was a progressive increase in the density of noradrenergic varicosities. This was most conspicuous at 9 and 12 months of age, at which time the molecular layer has been depleted not only of Purkinje cell dendrites, but also of parallel fibers. Noradrenergic fibers in these zones formed dense parallel bundles of varicose profiles whose density reached 621.3 +/- 122.8% (mean +/- SD, n = 4) at 9-12 months of age, compared with age-matched controls. Neurochemical measurement of norepinephrine content in whole cerebellum of the Purkinje cell degeneration mutants revealed no change compared with age-matched controls. We conclude that noradrenergic innervation persists in the cerebellar cortex despite the death of Purkinje cells and most of the granule cells. Although we found an increased density of varicosities in the molecular layer of mutant mice, progressing with age, we believe that this can be explained on the basis of the resultant geometry of the altered cerebellar cortex. It appears that the health of the environment surrounding the noradrenergic fibers in cerebellar cortex has little influence on their anatomical integrity.

Adrenergic Fibers↗
PubMed2004

Latencies of climbing fiber inputs to turtle cerebellar cortex.

Responses of separate regions of rat cerebellar cortex (Cb) to inferior olive (IO) stimulation occur with the same latency despite large differences in climbing fiber (CF) lengths. Here, the olivocerebellar path of turtle was studied because its Cb is an unfoliated sheet on which measurements of latency and CF length can be made directly across its entire surface in vitro. During extracellular DC recordings at a given Cb position below the molecular layer, IO stimulation evoked a large negative field potential with a half-width duration of approximately 6.5 ms. On this response were smaller oscillations similar to complex spikes. The stimulating electrode was moved to map the IO and the CF path from the brain stem to the Cb. The contralateral brain stem region that evoked these responses was tightly circumscribed within the medulla, lateral and deep to the obex. This response remained when the brain stem was bathed in solutions that blocked synaptic transmission. The Cb response to IO stimulation had a peak latency of approximately 10 ms that was not dependent on the position of the recording electrode across the entire 8-mm rostrocaudal length of the Cb. However, for a constant Cb recording position, moving the stimulation across the midline to the ipsilateral brain stem and along the lateral wall of the fourth ventricle toward the peduncle did shorten the response latency. Therefore a synchronous Cb response to CF stimulation seems to be caused by changes in its conduction velocity within the entire cerebellar cortex but not within the brain stem.

Action Potentials↗
PubMed1989

Enzyme histochemistry of glutamate dehydrogenase in ageing rat cerebellar cortex.

The influence of ageing on glutamate dehydrogenase activity was studied in the cerebellar cortex of 3-month-old (young), 12-month-old (adult) and 26-month-old (aged) male Sprague-Dawley rats by using an enzyme histochemical technique. In young rats the enzyme reactivity was observed in the neuropil of the molecular layer as well as in the perikarya of basket cells and of stellate cells; within the cytoplasm of Purkinje neurons and in synaptic glomeruli of the granular layer. Glutamate dehydrogenase activity was significantly increased in the cerebellar cortex of adult rats and decreased in old animals. The synaptic glomeruli of the granular layer were the structures of the cerebellar cortex more remarkably affected by age-related changes. The possibility that decreased glutamate catabolism occurring in the ageing cerebellar cortex may result in an excess of the amino acid and may contribute to the nerve cell loss occurring in the cerebellum of old rats is discussed.

Aging↗
PubMed2006

Feedforward inhibition controls the spread of granule cell-induced Purkinje cell activity in the cerebellar cortex.

Synapses associated with the parallel fiber (pf) axons of cerebellar granule cells constitute the largest excitatory input onto Purkinje cells (PCs). Although most theories of cerebellar function assume these synapses produce an excitatory sequential "beamlike" activation of PCs, numerous physiological studies have failed to find such beams. Using a computer model of the cerebellar cortex we predicted that the lack of PCs beams is explained by the concomitant pf activation of feedforward molecular layer inhibition. This prediction was tested, in vivo, by recording PCs sharing a common set of pfs before and after pharmacologically blocking inhibitory inputs. As predicted by the model, pf-induced beams of excitatory PC responses were seen only when inhibition was blocked. Blocking inhibition did not have a significant effect in the excitability of the cerebellar cortex. We conclude that pfs work in concert with feedforward cortical inhibition to regulate the excitability of the PC dendrite without directly influencing PC spiking output. This conclusion requires a significant reassessment of classical interpretations of the functional organization of the cerebellar cortex.

Action Potentials↗
PubMed1975

Mode of distribution of aminergic fibers in the cerebellar cortex of the chicken.

The cerebellar cortex of adult hens contains a dense plexus of thin varicose nerve fibers which display a formaldehyde-induced green fluorescence. This plexus is not distributed at random in the cortical layers. Within the granular layer the plexus forms a netlike pattern. The fiber branches, which have numerous varicosities, are predominantly oriented in the traverse plane of the folium. In the molecular layer the fluorescent plexus shows some variations in the convex, flat and concave portions of the folia. Many of the fluorescent branches are oriented parallel to the course of the folium. They arise from a T-division of radially oriented axons resembling parallel fibers in Golgi sections. The meshes of the fluorescent plexus in the granular layer measure 10-60 mu. In the molecular layer (top of the folia) there are about 30 fluorescent fibers per 100 mu2. The fluorescent fibers originate from the locus coeruleus and form a rostral and a caudal bundle in the cerebellar peduncle. The mode of distribution of the fluorescent fibers in the cortical layers seems to depend on the organization of the innervated tissue. Light microscopy suggests that the aminergic fibers innervate more than one class of cerebellar neurons.

Amines↗
PubMed2006

Histological and biological developmental characterization of the human cerebellar cortex.

The aim of this study was to investigate the histological and biological features of the human cerebellar cortex development and differentiation. We analyzed 52 brains of fetal and infant death victims, aged from 17 gestational weeks to 12th postnatal month. In particular, in the cerebellar cortex at different ages we evaluated, besides the structural aspects, the expression of several biomarkers implicated in proliferative processes (c-fos, PCNA and apoptosis). We observed morphological patterns progressively evolving every month, from the indefinite structure of the second gestational trimester to the four-layered structure (external granular layer, molecular layer, Purkinje cell layer, internal granular layer) of the late fetal cortex and subsequently to the three-layered postnatal definitive morphology, due to involution of the external granular layer. The evaluation of the biological features of the cerebellar cortex showed high proliferative activity mainly confined to the transient external granular layer in prenatal life, and high apoptotic index after birth. Thus, the histological examination, better with the support of biomarker investigations, allows with accuracy to describe the dynamic sequence of steps that occur in human cerebellar cortex development and to establish in each case the age, namely the pre- or postnatal month of life. Consequently, we can diagnose delayed or altered processes of differentiation during the development of the human cerebellar cortex.

Apoptosis↗
PubMed1992

Actions of acetylcholinesterase in the guinea-pig cerebellar cortex in vitro.

Acetylcholinesterase is released in a calcium-dependent manner when afferents of the cerebellar cortex are stimulated. Since cholinergic transmission is probably insignificant in the cerebellar cortex, the esterase itself might serve as a transmitter or modulator. Therefore, the effect of acetylcholinesterase in the cerebellum was investigated in slices of guinea-pig cerebella during intracellular recording from Purkinje cell somata or dendrites. Addition of acetylcholinesterase (20 U/ml) to the superfusion medium did not change the membrane potential or the input resistance of the Purkinje cells. Thus, esterase does not act like a classical transmitter. The threshold for Na+ spikes generated by intracellular current injection was unaffected, but the threshold for Ca2+ spikes was increased. This increase was abolished by tetrodotoxin (1 microM). Furthermore, when Ca2+ currents were blocked by substituting Mn2+ for Ca2+ (2 mM) a decrease in a Na+ plateau potential was seen in the presence of esterase. The effect of acetylcholinesterase of Ca2+ spikes is therefore most likely due to a reduction of the non-inactivating Na+ current of the Purkinje cell membrane. When present this current contributes to activation of Ca2+ spikes in dendrites. Acetylcholinesterase also enhanced the response of Purkinje cells to the excitatory amino acids glutamate and aspartate thought to be transmitters in the cerebellar cortex. The responses became larger and faster in the presence of esterase. Responses to climbing fibre stimulation were also enhanced by acetylcholinesterase. The late part of this synaptic response was increased. The potentiation by esterase of responses of Purkinje cells to excitatory amino acids and to climbing fibre stimulation may be mediated through interference with transmitter uptake, because it was prevented by treatment with DL-2-amino-4-phosphonobutyric acid (0.5 mM) and di-hydrokainate (0.1 mM). None of the effects of esterase was due to hydrolysis of acetylcholine because irreversible inhibition of the catalytic site of the enzyme with soman did not prevent the actions. The observations were specific for acetylcholinesterase. Butyrylcholinesterase (20-40 U/ml) showed none of the effects. It is concluded that acetylcholinesterase in the cerebellar cortex seems to mediate a novel type of modulation by two separate mechanisms. Esterase reduces the tendency towards Ca2+ spike generation in Purkinje cells. Ca2+ spikes are followed by afterhyperpolarizations and in their absence firing of Na+ spikes at higher frequencies is possible. Secondly, there is an enhancement of the action of excitatory transmitters so that the extended operating range can be utilized.

Acetylcholinesterase↗
PubMed1983

The vascularization of the human cerebellar cortex.

The blood vessels of the cerebellar cortex were studied by two methods of injection: india-ink and low viscosity resin (Mercox). The study is divided into two parts: (a) Pial vessels; few in number at the cerebellar surface, the pial vessels are quite dense, forming vascular laminae, within the sulci. Pial vessels do not frequently anastomose. (b) Intracortical vessels closely resemble those of the cerebral cortex. They may be divided into three categories: short, middle and long. There exist three vascular layers within the cerebellar cortex: superficial, middle and deep. The superficial vascular layer is situated within the molecular layer, the middle within the Purkinje cell layer, and the deep within the granular layer. It is therefore possible to establish a correlation between these vascular layers and the cortical cytoarchitecture. We accorded particular attention to the vascularization of the Purkinje cells. Arteries parallel to the cerebellar surface (parallel arteries) are in close relationship to the Purkinje cells whereas capillaries and veins are scarce. It is highly probable that the majority of Purkinje cells obtain nutritive elements by these parallel arteries. Possible implications in physiology and pathology are subsequently discussed.

Arteries↗
PubMed1996

Glutamate microinjections in cerebellar cortex reproduce cerebrovascular effects of parallel fiber stimulation.

Electrical stimulation of cerebellar parallel fibers releases glutamate and increases local blood flow (BFcrb), an effect in part mediated by glutamate-induced nitric oxide (NO) production. We studied whether local microinjection of glutamate into the cerebellar cortex would produce increases in BFcrb comparable to those elicited by parallel fiber stimulation. In halothane-anesthetized rats equipped with a cranial window, glutamate was microinjected into the cerebellar molecular layer, and BFcrb was monitored by laser-Doppler flowmetry. Glutamate microinjections increased BFcrb dose dependently (2-200 pmol in 200 nl) (n = 9) and by 55 +/- 6% at 200 pmol (mean +/- SE). The magnitude and temporal profile of the increases in BFcrb compared favorably with the increase in flow produced by parallel fiber stimulation. The glutamate-induced BFcrb increase was attenuated by superfusion with the Na2+ channel blocker tetrodotoxin (10 microM; -50 +/- 10%; n = 5; P < 0.05; t-test) or by blocking synaptic activity by treatment of the cerebellar cortex with Ringer containing 20 mM Mg2+ and 0 mM Ca2+ (-80 +/- 4%; n = 6; P < 0.05). The glutamate-receptor antagonist kynurenate (10 mM) attenuated the increase in BFcrb by 59 +/- 6% (P < 0.05; n = 5). The relatively selective inhibitor of neuronal NO synthase 7-nitroindazole (100 mg/kg ip) reduced the flow response evoked by microinjection of glutamate (-46 +/- 7%; n = 5; P < 0.05) but not acetylcholine (10 microM; P > 0.05; n = 6). We conclude that glutamate microinjections increase local BFcrb via activation of glutamate receptors. The glutamate-induced vasodilation is mediated, in part, by neurally derived NO. The striking similarities between the vascular responses evoked by parallel fiber stimulation and that produced by microinjection of glutamate support the hypothesis that the increase in BFcrb produced by parallel fiber stimulation is mediated by glutamate release and activation of glutamate receptors. The data also strengthen the hypothesis that glutamate and NO are important mediators in the mechanisms linking synaptic activity to BFcrb in cerebellar cortex.

Acetylcholine↗
PubMed1983

Decrease of [14C]2-deoxyglucose uptake at the intracerebellar nuclei during cerebellar cortex stimulation.

The effect of electrical stimulation of the cerebellar cortex at 10-30 c/s on metabolism in the intracerebellar nuclei has been studied using the [14C]2-deoxyglucose method. The experiments, performed on anesthetized or immobilized animals did not produce any detectable changes in the radioautographic labeling of the intracerebellar nuclei compared with controls. Experiments were also performed in animals pretreated with 3-acetylpyridine neurotoxin which selectively destroys the inferior olive and produces an intense labeling of the intracerebellar nuclei. Less marking was observed in restricted regions of the intracerebellar nuclei receiving the axon terminals of the stimulated Purkinje cells if the experiments were done within the first few hours. Following 3-acetylpyridine intoxication, in this early phase, destruction of the inferior olivary cell bodies occurs, but the climbing fibers remain intact. At 2 days or more following 3-acetylpyridine, changes in marking with stimulation could no longer be obtained. The finding is interpreted as being due to an actual reduction of the Purkinje cell activity upon stimulation of the cerebellar cortex, leading to a reduction of the metabolic activity at their presynaptic terminals.

Animals↗
PubMed2004

Morphological characteristics of Lugaro cells in the cerebellar cortex.

Two types of Lugaro cells were identified in the cat cerebellar cortex using sections impregnated with silver nitrate by the Golgi-Kopsch method; these cells were fusiform and triangular and their bodies were located at different levels in the granular layer. Their processes were directed horizontally, vertically, or obliquely to the axis of the leaf; axons never left the cerebellar cortex. These cells should therefore be regarded as interneurons. The processes of Lugaro cells were very extended, with the result that these cells formed numerous axosomatic and axodendritic contacts with all cerebellar cortical neurons and fibers. The structural and topographical characteristics of Lugaro cells and the features of their contacts with other cells in the cerebellar cortex, taken together with data on their neurotransmitter contents, show that they function as inhibitory interneurons.

Animals↗
PubMed1989

Histochemical localization of Ca2+, Mg2+-ATPase of the rat cerebellar cortex during postnatal development.

In order to investigate the membrane activities underlying development of neural cells, a histochemical localization of Ca2+-ATPase, Mg2+-ATPase and alkaline phosphatase (AlPase) activities in the rat cerebellar cortex during postnatal development was carried out. In the developing cerebellar cortex, ATPase activity was mainly associated with the plasma membranes of Purkinje and granular cells. This activity appeared in the immature Purkinje cells at birth and was proportionally increased throughout postnatal development. It was observed that the ATPase activity of migratory granular cells during a critical period from 3 and 15 postnatal days was increased in a funicular pattern in the developing cerebellar cortex. Conversely, peak AlPase activity in the developing cerebellar cortex was localized in the proliferative external granular cells until 7 postnatal days. Apparently, these phosphatase activities were not present in Bergmann glial fibers during the course of granular cell migration. The present findings were taken to indicate that neuronal cells in the cerebellar cortex have acquired a membrane-bound ATPase which can participate in Ca2+ transport or ATP metabolism during the course of early postnatal development.

Alkaline Phosphatase↗
PubMed1984

Projections of phrenic afferences to the cat cerebellar cortex.

Evoked phrenic potentials were recorded on the cerebellar cortex of anesthetized adult cats after electrical stimulation of both cervical branches (C5 and C6) of the right phrenic nerve. In this case phrenic stimulation evoked a surface positive response with a mean amplitude (+/- S.D.) of 13.4 +/- 5.2 microV. The mean latency and the mean duration of this phase were, respectively, 9.5 +/- 1.2 ms and 19.4 +/- 2.1 ms. This response was found only in the ipsilateral intermediate cortex and in the ipsilateral and, to a less extent, in the contralateral vermis of the posterior part of the anterior lobe (Larsell's lobule V); these areas corresponding to the forelimb projection zones. The phrenic afferences projecting to the cerebellar cortex were essentially conducted in the contralateral ventro-lateral spinal tracts.

Afferent Pathways↗
PubMed1999

Age-related changes of glial fibrillary acidic protein immunoreactive astrocytes in the rat cerebellar cortex.

Age-related changes of glial fibrillary acidic protein (GFAP) immunoreactivity were investigated in the cerebellar cortex of young (3 months), adult (12 months) and old (24 months) rats using immunohistochemical techniques associated with image analysis. In young rats, cell bodies of GFAP-immunoreactive astrocytes were found in the white matter and in the granular layer of cerebellar cortex. Radially-oriented branches of astrocytes which are sited in the granular layer were also observed in the molecular layer. The number of GFAP-immunoreactivity astrocytes of white matter was decreased in adult and old rats in comparison with young cohorts, whereas their size increased progressively from 3 to 24 months old. The number and the size of GFAP-immunoreactive astrocytes of the granular layer was similar in young and adult rats. An increased number and size of GFAP-immunoreactive astrocytes was noticeable in old rats in comparison with younger cohorts. The number of radially oriented branches of the molecular layer was the same in the three age groups investigated. The above results indicate that GFAP-immunoreactive astrocytes of rat cerebellar cortex undergo age-related changes. The not homogeneous sensitivity to aging of cerebellar astrocytes suggests that evaluation of changes of different cell populations of cerebellar cortex should represent an important step of research on aging cerebellum.

Aging↗
PubMed1977

Pharmacologically induced changes in the 3':5'-cyclic guanosine monophosphate content of rat cerebellar cortex: difference between apomorphine, haloperidol and harmaline.

Harmaline increases cerebellar 3':5'-cyclic guanosine monophosphate (cGMP) content in a dose-related manner; this increase is prevented by a pretreatment with 3-acetylpyridine (3-AP) (0.66 mmol/kg) which destroys climbing fibers and inhibits harmaline-induced tremor. The cerebellar cGMP content increases after isoniazid; this response remains unchanged in rats pretreated with 3-AP. Since isoniazid decreases cerebellar gamma-aminobuturic acid (GABA) levels, the increase in cGMP content might reflect a reduction in the availability of GABA at the level of postsynaptic receptors. Apomorphine (a dopamine receptor agonist) and haloperidol (a dopamine receptor blocker) increase or decrease the cGMP content of cerebellar cortex, respectively. Neither drug changes the guanylate cyclase activity of cerebellar homogenates; moreover their action on cerebellar cGMP content persists after 3-AP. Chloropromazine, like haloperidol, decreases the cerebellar cGMP content. The increase in cerebellar cGMP content elicited by apomorphine can be differentiated from that elicited by harmaline or isoniazid; presumably apomorphine indirectly activates mossy fibers. The decrease in cerebellar cGMP content elicited by haloperidol can be differentiated from that elicited by diazepam; perhaps haloperidol reduces the mossy fiber input to the cerebellum. We suggest that the cGMP content of cerebellar cortex fluctuates in response to changes in the afferent stimulatory input to the cerebellum; it increases when the activity of either climbing or mossy fibers is increased; it decreases when either of these two stimulatory inputs is reduced.

Alkaloids↗
PubMed1978

The myelination of the cerebellar cortex in the cat.

The myelination of the cerebellar cortex of the cat was investigated in 61 cats aged from 3 hrs post partum to two and a half years. The first myelinated fibers appear at the time of birth in the central medullary ray. Before the onset of myelination, all fibers reach a critical diameter of about 1 micrometer. About the 14th day of life the number of oligodendrocytes in the prospective while matter increases markedly. Thereafter, the oligodendrocytes invade the inner granular layer. It therefore seems that the myelination of the cerebellar cortex proceeds from the central medullary ray towards the granular layer. At the 60th day of postnatal life, most of the afferent and efferent fiber systems are myelinated. These findings are discussed in relation to the development of function and the maturation of the electrical activity of the cerebellar circuit.

Animals↗
PubMed1990

Learning causes synaptogenesis, whereas motor activity causes angiogenesis, in cerebellar cortex of adult rats.

The role of the cerebellar cortex in motor learning was investigated by comparing the paramedian lobule of adult rats given difficult acrobatic training to that of rats that had been given extensive physical exercise or had been inactive. The paramedian lobule is activated during limb movements used in both acrobatic training and physical exercise. Acrobatic animals had greater numbers of synapses per Purkinje cell than animals from the exercise or inactive groups. No significant difference in synapse number or size between the exercised and inactive groups was found. This indicates that motor learning required of the acrobatic animals, and not repetitive use of synapses during physical exercise, generates new synapses in cerebellar cortex. In contrast, exercise animals had a greater density of blood vessels in the molecular layer than did either the acrobatic or inactive animals, suggesting that increased synaptic activity elicited compensatory angiogenesis.

Animals↗
PubMed1998

Novel receptor protein tyrosine phosphatase (RPTPrho) and acidic fibroblast growth factor (FGF-1) transcripts delineate a rostrocaudal boundary in the granule cell layer of the murine cerebellar cortex.

We have identified a novel receptor-like protein tyrosine phosphatase (RPTPrho) transcript whose expression in the cerebellar cortex is restricted to the granule cell layer of lobules 1-6. Acidic fibroblast growth factor (FGF-1) mRNA follows a similar cerebellar expression pattern. Together, the two markers define a sharp boundary in lobule 6, slightly caudal to the primary fissure. Anterior and posterior compartments became discernible only during postnatal weeks two and six, for RPTPrho and FGF-1, respectively. A rostrocaudal boundary in lobule 6 of the murine cerebellar cortex has also been identified morphologically by the effects of the meander tail mutation. The position of the RPTPrho and FGF-1 boundary on the rostrocaudal axis of the cerebellar cortex was close to, but not coincident with, the caudal extent of the disorganized anterior lobe of meander tail and the rostral extent of Otx-2 expression. The restricted pattern of FGF-1 and RPTPrho implies that these molecules may have specific signaling roles in the tyrosine phosphorylation/dephosphorylation pathway in the anterior compartment of the adult cerebellar cortex.

Animals↗