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PubMed2006

Immunohistochemical localization of cannabinoid type 1 and vanilloid transient receptor potential vanilloid type 1 receptors in the mouse brain.

Cannabinoid type 1 receptors and transient receptor potential vanilloid type 1 channels have been proposed to act as metabotropic and ionotropic receptors, respectively, for two classes of endogenous polyunsaturated fatty acid amides, the acylethanolamides and the acyldopamides. Furthermore, we and others have shown that functional crosstalk occurs between these two receptors when they are expressed in the same cell. Although demonstrated in sensory neurons of the dorsal root ganglia, spinal cord and myenteric neurons, co-expression of cannabinoid type 1 and transient receptor potential vanilloid type 1 has not yet been studied in the brain. In the present study, we addressed this issue by using commercially available specific antibodies whose specificity was confirmed by data obtained with brains from cannabinoid type 1(-/-) and transient receptor potential vanilloid type 1(-/-) mice. Double cannabinoid type 1/transient receptor potential vanilloid type 1 immunofluorescence and single cannabinoid type 1 or transient receptor potential vanilloid type 1 avidin-biotin complex immunohistochemistry techniques were performed and both methods used point to the same results. Cannabinoid type 1/transient receptor potential vanilloid type 1 expression was observed in the hippocampus, basal ganglia, thalamus, hypothalamus, cerebral peduncle, pontine nuclei, periaqueductal gray matter, cerebellar cortex and dentate cerebellar nucleus. In particular, in the hippocampus, cannabinoid type 1/transient receptor potential vanilloid type 1 expression was detected on cell bodies of many pyramidal neurons throughout the CA1-CA3 subfields and in the molecular layer of dentate gyrus. In the cerebellar cortex, expression of cannabinoid type 1/transient receptor potential vanilloid type 1 receptors was found surrounding soma and axons of the vast majority of Purkinje cell bodies, whose cytoplasm was found unstained for both receptors. Cannabinoid type 1 and transient receptor potential vanilloid type 1 immunoreactivity was also detected in: a) the globus pallidus and substantia nigra, in which some intensely transient receptor potential vanilloid type 1 immunopositive cell bodies were found in dense and fine cannabinoid type 1/transient receptor potential vanilloid type 1 positive and cannabinoid type 1 positive nerve fiber meshworks, respectively; b) the cytoplasm of thalamic and hypothalamic neurons; and c) some neurons of the ventral periaqueductal gray. These data support the hypothesis of a functional relationship between the two receptor types in the CNS.

Animals↗

PubMed1991

Noradrenergic agents into the cerebellar anterior vermis modify the gain of vestibulospinal reflexes in the cat.

The noradrenergic (NA) afferent projection to the cerebellar cortex, which originates mainly from the locus coeruleus (LC), may act on the target neurons by utilizing both alpha- and beta-adrenoceptors. Experiments performed in decerebrate cats have shown that unilateral injection into the vermal cortex of the cerebellar anterior lobe of 0.25 microliter of the alpha 1-adrenergic agonist metoxamine or the alpha 2-agonist clonidine (at 2-8 micrograms/microliters of saline) as well as of the non-selective beta-agonist isoproterenol (at 8-16 micrograms/microliters) decreased the postural activity in the ipsilateral forelimb, while the extensor tonus either remained unmodified or slightly increased on the contralateral side. The same agents also increased the gain of the vestibulospinal (VS) reflexes elicited by recording the multiunit EMG responses of the ipsilateral and the contralateral triceps brachii to roll tilt of the animal (at 0.15 Hz, +/- 10 degrees), leading to sinusoidal stimulation of labyrinth receptors. The crossed effects were more prominent for the alpha 2- than for the alpha 1- and beta-agonists. Only slight changes in the phase angle of the responses were observed. The effects described above appeared 5-10 min after the injection, reached the peak values after 15-30 min and disappeared within 2 h. The effective area was located within the third and/or the fourth folium of the culmen rostral to the fissura prima, 1.4-1.8 mm lateral to the midline. This area corresponded to zone B of the cerebellar cortex, which projects to the ipsilateral lateral vestibular nucleus (LVN), on which it exerts a prominent inhibitory influence. In fact, monopolar stimulation of this area with three negative pulses (at 300/sec) performed prior to the local injection inhibited the spontaneous EMG activity of the ipsilateral triceps brachii. The effects described above were dose-dependent; injection of an equal volume of saline was ineffective. All changes in posture and reflexes elicited by metoxamine or clonidine were impaired by previous injection into the same corticocerebellar area of the corresponding alpha 1- or alpha 2-adrenergic antagonist prazosin or yohimbine, respectively (0.25 microliters at 8-16 micrograms/microliters). However, cross-interactions between alpha 1- and alpha 2-adrenergic agonists and antagonists were also observed. In fact, injection of the alpha 2-adrenergic antagonist yohimbine prevented the occurrence of all the metoxamine effects, while administration of the alpha 1-adrenergic antagonist prazosin prevented the occurrence of the ipsilateral, but not of the contralateral effects induced by clonidine injection.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1999

Levels of amino acid neurotransmitters during mouse cerebellar neurogenesis and in histotypic cerebellar cultures.

The variation in the levels of excitatory (glutamate and aspartate) and inhibitory (GABA, glycine and taurine) neurotransmitters during neurogenesis in mouse cerebellum, from embryonic day (E) 15 until the young adult stage, was analyzed by high-pressure liquid chromatography. Between E15 and E21, high contents of GABA, glutamate and aspartate were detected, with the GABA levels approximately 2- to 3-fold higher than those of glutamate and aspartate. After birth, the levels of GABA remained high during the first 2 postnatal weeks and then reached a plateau comparable to adult values by the third week. The levels of glutamate and aspartate increased gradually from birth to the young adult stage, showing peak values at postnatal days (P) 3 and P11. Glycine and taurine were present at relatively low concentrations during the prenatal period, then rose significantly by about 4-fold after birth; their levels decreased by the end of the first postnatal week but increased gradually thereafter until reaching adult values by the third week. To determine the endogenous neurotransmitter production in the cerebellar cortex, primary histotypic cerebellar cultures prepared at P10 were analyzed and the in vitro transmitter contents were compared with the adult in situ values. The cultures showed about the same levels of glutamate and aspartate; however, their concentrations were lower by half than in vivo, suggesting that both play an equally important role in the excitatory neurotransmission of the cerebellar cortex internal circuitry pathways and that in mature cerebellum, about 50% of the excitatory synaptic inputs derive from the afferent climbing and mossy fibers. The in vitro GABA and glycine contents were comparable with the in vivo levels, whereas the taurine concentrations were about 5-fold lower in vitro than in vivo. These findings indicate that most of the GABA and glycine transmitters are produced intrinsically while a high proportion of taurine in the cerebellum comes from extracerebellar afferents. This study provides data on the changing levels of the amino acid neurotransmitters in developing mouse cerebellum and the relative proportions of neurotransmitter contents that are produced by intrinsic neurons in contrast to those derived from extrinsic afferent fibers.

Aging↗

PubMed1996

Astrocytic processes compensate for the apparent lack of GABA transporters in the axon terminals of cerebellar Purkinje cells.

The aim of the present study was to evaluate the expression of two high affinity GABA transporters (GAT-1 and GAT-3) in the rat cerebellum using immunocytochemistry and affinity purified antibodies. GAT-1 immunoreactivity was prominent in punctate structures and axons in all layers of the cerebellar cortex, and was especially prominent around the somata of Purkinje cells. In contrast, the deep cerebellar nuclei showed few if any GAT-1 immunoreactive puncta. Weak GAT-3 immunoreactive processes were present in the cerebellar cortex, whereas GAT-3 immunostaining was prominent around the somata of neurons in the deep cerebellar nuclei. Electron microscopic preparations of the cerebellar cortex demonstrated that GAT-1 immunoreactive axon terminals formed symmetric synapses with somata, axon initial segments and dendrites of Purkinje cells and the dendrites of granule cells. Astrocytic processes in the cerebellar cortex were also immunolabeled for GAT-1. However, Purkinje cell axon terminals that formed symmetric synapses with neurons in the deep cerebellar nuclei lacked GAT-1 immunoreactivity. Instead, weak GAT-1 and strong GAT-3 immunoreactivities were expressed by astrocytic processes that enveloped the Purkinje cell axon terminals. In addition, GAT-3-immunoreactivity appeared in astrocytic processes in the cerebellar cortex. These observations demonstrate that GAT-1 is localized to axon terminals of three of the four neuronal types that were previously established as being GABAergic, i.e. basket, stellate and Golgi cells. GAT-1 and GAT-3 are expressed by astrocytes. The failure to identify a GABA transporter in Purkinje cells is consistent with previous data that indicated that Purkinje cells lacked terminal uptake mechanisms for GABA. The individual glial envelopment of Purkinje cell axon terminals in the deep cerebellar nuclei and the dense immunostaining of GAT-3, and to a lesser extent GAT-1, expressed by astrocytic processes provide a compensatory mechanism for the removal of GABA from the synaptic cleft of synapses formed by Purkinje cell axon terminals.

Animals↗

PubMed1993

Long-term depression of glutamate-induced gamma-aminobutyric acid release in cerebellum by insulin-like growth factor I.

We tested the possibility that insulin-like growth factor I (IGF-I) acts as a neuromodulator in the adult cerebellar cortex since previous observations indicated that IGF-I is located in the olivo-cerebellar system encompassing the inferior olive and Purkinje cells. We found that conjoint administration of IGF-I and glutamate through a microdialysis probe stereotaxically implanted into the cerebellar cortex and deep cerebellar nuclei greatly depressed the release of gamma-aminobutyric acid (GABA), which normally follows a glutamate pulse. This inhibition was dose-dependent and long-lasting. Moreover, the effect was specific for glutamate since KCl-induced GABA release was not modified by IGF-I. Basic fibroblast growth factor, another growth-related peptide present in the cerebellum, did not alter the response of GABA to glutamate stimulation. In addition, electrical stimulation of the inferior olivary complex significantly raised IGF-I levels in the cerebellar cortex. Interestingly, when the inferior olive was stimulated in conjunction with glutamate administration, GABA release by cerebellar cells in response to subsequent glutamate pulses was depressed in a manner reminiscent of that seen after IGF-I. These findings indicate that IGF-I produces a long-lasting depression of GABA release by Purkinje cells in response to glutamate. IGF-I might be present in climbing fiber terminals and/or cells within the cerebellar cortex and thereby might affect Purkinje cell function. Whether this IGF-I-induced impairment of glutamate stimulation of Purkinje cells underlies functionally plastic processes such as long-term depression is open to question.

Animals↗

PubMed1994

Visual pontocerebellar projections in the macaque.

The cerebellum plays an important role in the visual guidance of movement. In order to understand the anatomical basis of visuomotor control, we studied the projection of pontine visual cells onto the cerebellar cortex of monkeys. Wheat germ agglutinin horseradish peroxidase was injected into the dorsolateral pons two monkeys. Retrogradely labelled cells were mapped in the cerebral cortex and superior colliculus, and orthogradely labelled fibers in the cerebellar cortex. The largest number of retrogradely labelled cells in the cerebral cortex was in a group of medial extrastriate visual areas. The major cerebellar target of these dorsolateral pontine cells is the dorsal paraflocculus. There is a weaker projection to the uvula, paramedian lobe, and Crus II, and a sparse but definite projection to the ventral paraflocculus. There are virtually no projections to the flocculus. There are sparse ipsilateral pontocerebellar projections to these same regions of cerebellar cortex. In nine monkeys, we made small injections of the tracer into the cerebellar cortex and studied the location of retrogradely filled cells in the pontine nuclei and inferior olive. Injections into the dorsal paraflocculus or rostral folia of the uvula retrogradely labelled large numbers of cells in the dorsolateral region of the contralateral pontine nuclei. Labelled cells were found ipsilaterally, but in reduced numbers. Injections outside of these areas in ventral paraflocculus or paramedian lobule labelled far fewer cells in this region of the pons. We conclude that the principal source of cerebral cortical visual information arises from a medial group of extrastriate visual areas and is relayed through cells in the dorsolateral pontine nuclei. The principal target of pontine visual cells is the dorsal paraflocculus.

Animals↗

PubMed2005

Functional localization in the human cerebellum based on voxelwise statistical analysis: a study of 90 patients.

The aim of the present study was to examine somatotopy in the cerebellar cortex and a possible differential role of the cerebellar cortex and nuclei in functional outcome. Clinical findings and 3D MRI-based cerebellar lesions site were compared in a group of 90 patients with focal cerebellar lesion using International Cooperative Ataxia Rating Scale (ICARS) and voxel-based lesion-symptom mapping (VLSM). Separate analysis was performed in patients with acute and chronic ischemic lesions (n=43) and patients with acute and chronic surgical lesions (n=47). Thirty-eight patients were included after resection of a cerebellar tumor in childhood or adolescence. The most significant lesion symptom correlations were observed in the subgroup with acute ischemic lesions. Limb ataxia was significantly correlated with lesions of the interposed (NI) and part of the dentate nuclei (ND), ataxia of posture and gait with lesions of the fastigial nuclei (NF) including NI. Correlations with cortical lesions were less significant and present in the superior cerebellum only. Upper limb ataxia was correlated with lesions of vermal, paravermal and hemispheral lobules IV-V and VI, lower limb ataxia with lesions of vermal, paravermal and hemispheral lobules III and VI, dysarthria with lesions of paravermal and hemispheral lobules V and VI and ataxia of posture and gait with lesions of vermal and paravermal lobules II, III and IV. In the subgroups with chronic focal lesions, similar correlations were observed with lesions of the cerebellar nuclei, but significantly less correlations with lesions of the cerebellar cortex. Functional localization based on VLSM backs findings in previous animal and functional brain images studies in healthy human subjects. The lesion site appears to be critical for motor recovery. Lesions affecting the cerebellar nuclei are not fully compensated at any age and independent of the pathology in humans.

Adult↗

PubMedDate not supplied

Developmental localization of noradrenergic innervation to the rat cerebellum following neonatal 6-hydroxydopa and morphine treatment.

In order to demonstrate the influence of morphine on the developmental localization of regenerated noradrenergic fibers in rat cerebellum, a glyoxylic histofluorescent method and radiometric assay for norepinephrine (NE) were utilized. An initial reduction of NE in the cerebellum after 6-hydroxydopa [6-OHDOPA; 60 micrograms/g intraperitoneally (i.p.)] was followed by a return to control levels at 3 days, and an elevation above control levels at 7 days. The initial rates of recovery of NE in the cerebellum of the 6-OHDOPA group of rats and the group receiving morphine (20 micrograms/g i.p.) in combination with 6-OHDOPA were identical up to 7 days. However, by 14 days NE content was further elevated in the cerebellum of the morphine +6-OHDOPA group. Histofluorescent microscopic observations of the cerebellar cortex correlated with the biochemical findings. A reduction in cerebellar NE content at 3 days was associated with a reduction in the number of visible histofluorescent fibers in the cerebellar cortex. By 7 days the relative number of fibers in the 6-OHDOPA groups was similar to that seen in the control group, but by 9 days the relative number of fluorescent fibers in the cerebellar cortex was increased above control. By 13 days there was a further increase in the relative number of fluorescent fibers in the cerebellar cortex of the morphine +6-OHDOPA group, as compared to the group treated with 6-OHDOPA alone. These findings provide an anatomic correlate for recovery of noradrenergic fibers after 6-OHDOPA, and demonstrate an action of morphine in enhancing regenerative sprouting.

Aging↗

PubMed1991

Combined lead acetate and disulfiram treatment-induced alterations of glial fibrillary acidic protein (GFA) immunoreactive astrocytes in brain smears.

Dithiocarbamates are known to form lipid-soluble complexes with lead and greatly increase brain lead levels. The present study was undertaken to investigate whether lead acetate, when administered together with disulfiram (Antabuse, metabolite of dithiocarbamate) during development, would induce morphological changes in brain astrocytes. Female Sprague-Dawley rats were given 0.25% lead acetate in the drinking water from day one of pregnancy and this treatment was continued after birth until the litters were 4 weeks old. In addition, some dams received disulfiram in a dose of 0.1 mmol/kg p.o. twice weekly and after parturition this dose was given s.c. directly to the offspring twice a week. Lead acetate and disulfiram treatments were discontinued at weaning and animals sacrificed 3 weeks later. Samples of parietal cortex, hippocampal formation and cerebellar cortex were dissected out and smeared onto glass-slides and astrocytes were visualized in toto using immunohistochemistry with antibodies against glial fibrillary acid protein (GFA), enabling morphometric analysis with a computerized image analyser. Animals treated with lead acetate showed a minor increase in the size of the GFA-immunoreactive astrocytes in parietal cortex smears, while animals treated with disulfiram showed no difference in size or form compared to controls. However, in combined lead acetate and disulfiram-treated animals a profound increase in astrocyte size and an increase in the number of processes of the individual GFA-immunoreactive astrocytes could be demonstrated in parietal cortex. No significant changes were noted in GFA-immunoreactive astrocytes of hippocampal smears following the different treatments, while GFA-immunoreactive astrocytes in cerebellar cortex smears were significantly smaller and had reduced number or processes following the combined lead acetate and disulfiram treatment compared to lead acetate treatment or controls. It is concluded that combined exposure to lead acetate and disulfiram during development induces regionally specific changes in GFA-immunoreactive astrocyte morphology. Furthermore, the present study demonstrates the usefulness of smear preparations combined with computerized image analysis to study the morphology of GFA-immunoreactive astrocytes as an index of toxic effects in CNS.

Animals↗

PubMed1998

Morphological forms and localization of microglial cells in the developing human cerebellum.

There are relatively few studies on microglia of human developing brain thus function and location of these cells at this period of life are unknown. Moreover, all of them concentrated on the cells in very early period of fetal life. To achieve further insight into the participation of microglial cells in the development of the central nervous system the brains of fetuses, newborns and infants were examined by means of immunological markers: Ricinus communis agglutinin-1 (RCA-1) and ferritin antiserum. Brains of 12 fetuses and infants ranging in age from 14 weeks of gestation to 5 months after birth were used in the study. The fetuses were derived following spontaneous abortions. In pre-term and term newborns the cause of death was of maternal origin (placental insufficiency) or accidental sudden death. Coronal blocks of cerebellum cut into 5 microns thick sections were used in the study. The developing microglial cells were detected by both markers (RCA-1 and anti-ferritin). Ricinus communis agglutinin recognizes carbohydrate residues on the surfaces of microglial and endothelial cells. Therefore, in the sections incubated with this lectin brain vessels as well as microglia were visualized. The second microglial marker anti-ferritin serum detected precisely all morphological subpopulations of microglia including ameboid and ramified cells but endothelial cells remained immunonegative. Therefore, in 14 weeks of gestation only round ameboid microglia were ferritin-immunopositive in cerebellum. These cells were localized at the periphery of the periventricular, germinal matrix and were surrounding a group of nerve cells of the developing dentate nucleus. In 16 week-old fetuses ameboid cells were present in the hilus and between gyri of the dentate nucleus. The ferritin-positive microglial cells on the convolutions of the dentate nucleus gyri manifested as the cells with short fine branched processes and scanty cytoplasm. In cerebellum of the 20 week-old fetuses the subpopulation of branched (ramified) microglia were more numerous than ameboid cells. Ameboid cells were present mainly in the intermediate zone of the future white matter and ramified cells penetrated the inner (at the one third of its thickness) part of the developing internal granular layer of cerebellar cortex. The upper part of cerebellar cortex was colonized by microglia between 24-28 weeks of gestation. In cerebellum of fetuses over 28 weeks of gestation numerous microglial cells infiltrated mainly the Purkinje cell layer, first in the vermis, later in the hemispheres. From 36 weeks of gestation to the birth ferritin-immunopositive microglial cells gradually disappeared from the cerebellar cortex. The microglia of the term newborns and of a 5 month-old child manifested mainly as ramified cells located in the white matter. The results of our study lead to the conclusion that the localization of microglial cells in the brain structure and their morphological forms correlate precisely with the appropriate stages of the brain development.

Cell Death↗

PubMed1989

GABAA/benzodiazepine receptor-like immunoreactivity in rat and monkey cerebellum.

The cellular and subcellular localization of GABAA/benzodiazepine receptor-like immunoreactivity in the rat and monkey cerebellum has been studied with a monoclonal antibody (E9) directed against the alpha-subunit of purified GABAA/benzodiazepine receptors. At both the light and electron microscopic level E9 immunoreactivity is located in all 3 layers of the cerebellar cortex and within the deep cerebellar nuclei. The reaction product accumulates within the cytoplasm of neurons and their dendrites but axons are not immunoreactive. Glial cells in the white matter and the cortical layers are also unlabeled, although in some instances Bergmann glia do contain reaction product. The overall distribution and cellular and subcellular localization of E9 immunoreactivity is identical for both monkey and rat cerebellum. On the basis of cell size, morphology, and location it is evident that E9 immunoreactivity occurs in examples of all 5 neuronal types in the cerebellar cortex: Purkinje cells, Golgi type II cells, granule cells, and stellate and basket cells. However, the distribution of the reaction product within the cells is more selective. For example, electron microscopy demonstrates that axonal processes and terminals are not E9 immunoreactive with the single exception of the mossy fiber terminals in the granular layer. Also, examples of unlabeled axon terminals resembling those derived from Golgi type II cells, basket cells, and stellate cells form synapses with immunoreactive dendrites and cell bodies in the cortical layers. Finally, in the deep cerebellar nuclei unreactive axon terminals make symmetric synapses with immunostained neurons and dendrites. These results show that E9 monoclonal antibodies label neurons and portions of their processes which are postsynaptic in GABA-mediated inhibitory circuits, and demonstrates that this antiserum can be used as a morphological marker for cells which make GABAA/benzodiazepine receptors.

Animals↗

PubMed1981

Neurotransmitter amino acids in dominantly inherited cerebellar disorders.

We measured amino acid contents in the brains of 11 patients with dominantly inherited cerebellar disorders. Despite clinical similarities, three biochemically different disorders were found. One disorder, with demonstrated HLA linkage in one pedigree, was characterized by moderate reduction of aspartate and glutamate contents in cerebellar cortex alone. In a second disorder, aspartate and glutamate contents were reduced markedly in other brain areas as well as in cerebellar cortex. Aspartate and glutamate contents were normal in cerebellar cortex in the third disorder. GABA content in cerebellar cortex and dentate nucleus was reduced in some patients with each disorder, whereas cerebellar taurine content was normal in all patients. Aspartate deficiency in cerebellar cortex did not result from lack of aspartate aminotransferase or pyruvate carboxylase activity. These amino acid abnormalities probably imply loss of specific cerebellar neurons.

Amino Acids↗

PubMed1992

Immunocytochemical evidence for the involvement of glycine in sensory centers of the rat brain.

Glycine-like immunoreactivity was localized to a number of sites in the rat brain which are involved in processing sensory information. In the auditory and vestibular systems, glycine immunoreactivity was seen in dorsal and ventral cochlear nuclei, superior olive, trapezoid body, medial and lateral vestibular nuclei, and inferior colliculus. Staining in the visual system was seen in retina, dorsal lateral geniculate nucleus, and superior colliculus. The olfactory system exhibited staining in the olfactory bulb and accessory olfactory formation. Somatosensory centers with glycine immunoreactivity included the dorsal column nuclei, spinal trigeminal nucleus, principal sensory nucleus of V, reticular formation, and periaqueductal gray. Glycine-immunoreactive neurons were also seen in cerebellar cortex, deep cerebellar nuclei, hippocampus, cerebral cortex, and striatum. The distribution of staining indicates that glycine plays a major role in sensory centers with actions at both strychnine-sensitive and strychnine-insensitive receptors.

Animals↗

PubMed2003

Distribution of mGluR1alpha and SMI 311 immunoreactive Lugaro cells in the kitten cerebellum.

The Lugaro cell is a feedback interneuron of the cerebellar cortex, recognizable by its characteristic morphology. Postnatal neuronal migration to the cortex has been described for several cerebellar interneurons. Since in our previous studies we observed Lugaro-like cells (LCs) in the white matter (WM) and internal granular layer (IGL) of the cerebellum of young cats, we assumed that a proportion of these cells migrate also postnatally to their destination. In the present study using and immunostaining for the metabotropic glutamate receptor mGluR1alpha and neurofilament protein SMI 311 the number and spatial distribution of LCs at different postnatal days were investigated. We found that the number and distribution of both mGluR1a-immunoreactive (ir) and of SMI 311-ir LCs changed with age in the developing cerebellar cortex of kittens: developing LCs express mGluR1alpha already in the newborn, while expression of SMI 311-ir in LCs appears only about a week later. At postnatal day 1 (P1) relatively few mGluR1-ir LCs were detected in the WM and at the border of WM and IGL. Later, their number increased sharply until P15 (6-7 fold) and decreased continuously between P15 and P135. SMI 311-ir LCs were not present at P1 and even at P8 only a few were observed in the WM or in infraganglionic positions. Their number increased gradually (12-14 fold) until adulthood when their number was stabilized at 8.000-10.000/cerebellum. At the same time the number of probably ectopic SMI 311-ir LCs decreased with age: at P22 about one third of them was found in "ectopic" position, whereas in the adult cat only about 10-12% of LCs's was either in the WM or scattered in the whole depth of the granular layer. These results suggest that: (1) most LCs appear in the cerebellar cortex postnatally; and (2) postnatal migration and incorporation of LCs to the cortex is a much longer process than previously expected, occurring even after the cytoarchitectonic built-up (about P65-P70 in cat) of the cerebellum.

Aging↗

PubMed2001

The role of the dura in conditioned taste avoidance induced by cooling the area postrema of male rats.

Experiments were designed to assess the contribution of the dura mater to the formation of conditioned taste avoidance induced by cooling the area postrema. The results of the first experiment verified that the temperature of the dura showed a temperature gradient at various distances from the tip of the cold probe. In the second and third experiments, a circle of dura was cut away so that different amounts of the area postrema could be cooled without cooling the overlying dura. Cooling the dura plus the area postrema did not produce a stronger avoidance than just cooling the area postrema. In the fourth experiment, the cerebellar cortex was cooled with and without cooling the dura. Cooling the cerebellar cortex produced conditioned taste avoidance, and cooling the dura plus the cerebellar cortex did not produce a stronger avoidance. Taken together, these results suggest that cooling the dura mater does not contribute to the conditioned taste avoidance induced by cooling the area postrema. The results of the fifth experiment showed that cooling the area postrema produced a stronger conditioned taste avoidance than cooling the cerebellar cortex. It is suggested that the avoidance induced by cooling both of these structures is the result of physiological changes occurring when neurons in these structures are inactivated and when the subdural meninges are cooled. Furthermore, these changes are more severe when the area postrema is cooled.

Animals↗

PubMed2001

Long-term adaptation to dynamics of reaching movements: a PET study.

Positron emission tomography (PET) was used to examine changes in the cerebellum as subjects learned to make movements with their right arm while holding the handle of a robot that produced a force field. Brain images were acquired during learning and then during recall at 2 and 4 weeks. We also acquired images during a control task where the force field was not learnable and subjects did not show any improvements across sessions. During the 1st day, we observed that motor errors decreased from the control condition to the learning condition. However, regional cerebral blood flow (rCBF) in the posterior region of the right cerebellar cortex initially increased from the control condition and then gradually declined with reductions in motor error. Correspondingly, rCBF in the ipsilateral deep cerebellar nuclei (DCN) initially decreased from the control condition and then increased with reductions in motor error. If measures of rCBF mainly reflect presynaptic activity of neurons, this result predicts that DCN neurons fire with a pattern that starts high in the control task then decreases as learning proceeds. Similarly, Purkinje cells should generally have their lowest activity in the control task. This pattern is consistent with neurophysiological recordings that find that cerebellar activity during early learning of a motor task may mainly reflect changes in coactivation of muscles of the limbs, rather than a learning specific signal. By the end of the first session, motor errors had reached a minimum and no further improvements were observed. However, across the weeks a region in the anterior cerebellar cortex showed gradual decreases in rCBF that could not be attributed to changes in motor performance. Because patterns of rCBF in the cortex and nuclei were highly anti-correlated, we used structural equation modeling to estimate how synaptic activity in the cerebellar cortex influenced synaptic activity in the DCN. We found a negative correlation with a strength that significantly increased during the 4 weeks. This suggests that, during long-term recall, the same input to the cerebellar cortex would produce less synaptic activity at the DCN, possibly because of reduced cerebellar cortex output to the DCN.

Adaptation, Biological↗

PubMed1976

A note on the method of retrograde transport of horseradish peroxidase as a tool in studies of afferent cerebellar connections, particularly those from the inferior olive; with comments on the orthograde transport in Purkinje cell axons.

1. Injections of horseradish peroxidase (HRP) suspension were made in the cerebellar cortex of cats (most often the paramedian lobule). The staining of the cerebellar cortex and the ensuing labeling of neurons in the inferior olive were studied in experiments with variations of concentration of HRP, amounts of fluid injected, survival time and age of the animals. Light microscopical studies were supplemented with electron microscopical observations. The folded cerebellar cortex offers particular difficulties with regard to obtaining a predictable extent of stained tissue, and the spreading of the fluid within the cortex shows great variations even with the same amounts and concentrations of HRP suspension. Diffusion of fluid appears to occur most easily within the molecular layer. Often there are unstained parts of folia between stained parts. Staining of the cortex is barely visible after 7 days, but appreciable shrinking of the stained area does not appear to occur until after 4 days. 2. The first signs of labeling of olivary neurons are seen after 5-10 hours, after 7 days there are no labeled cells. The rate of retrograde transport in olivocerebellar fibers is calculated to be between 50 and 100 mm/day. Labeling of cells appears to require staining of the molecular layer of its projection areas in the cerebellum. 3. For studies of the olivocerebellar projection survival times of 2-3 days and injections of 0.5 mul of a 50% HRP suspension seem in general to be well suited. Best results are obtained with animals weighing 1-3 kg. There is a clearcut correlation between the site of staining of the cortex of a particular part of the cerebellum and the site(s) and extension of olivary area(s) containing labeled cells. 4. Anterograde transport in axons of Purkinje cells has been observed. Electron microscopically the axons of these fibers contain HRP labeled tubules and vesicles as do their terminal boutons in the nuclei. 5. In cases where the injected fluid has spread to the cerebellar nuclei, localized parts contain neurons which are labeled as are the cells in the injected cerebellar cortex.

Afferent Pathways↗

PubMed1993

Shapes and sizes of different mammalian cerebella. A study in quantitative comparative neuroanatomy.

The shape of the cerebellar cortex in fourteen mammalian species and one bird was studied by careful dissection, counts of the numbers of folia, and measurement of their length. All mammalian cerebella conformed to the same general plan, with an anterior region where folia are continuous between right and left, and three separate posterior appendages. There were, however, considerable differences between species, both in the relative length of the posterior appendages and in the relative abundance of folia on the midline compared to the lateral portions. In order to discover general laws referring to the width and length of the cerebellar cortex in their relation to body weight, cerebellar weight, and area of cerebellar cortex, an allometric analysis was performed. By plotting the values for the various species on log-log diagrams, the following statements can be inferred: 1. The weight of the cerebellar cortex is proportionate to the body weight to the power of 0.72, well comparable to the classical proportionality between brain weight and body weight to the power of 2/3 (Jerison 1973). 2. Cerebellar area and cerebellar weight are proportionate in larger animals, but in the smaller species the thickness of the cerebellar cortex varies and therefore a different dependence is valid. 3. The width of the cerebellar cortex increases with body size in the smaller species but tends to remain constant in the larger ones. 4. The longest anterior-posterior extension in our collection was measured in the bovine cerebellum. 5. The position of man in our collection of species is particular in several ways. The width of the human cerebellum is far greater than allometric relations established for the other species would suggest. Also, the vermal length of man falls short of the allometric rule established for the other species.

Animals↗