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PubMed1985

Localization of serotonin immunoreactivity in the opossum cerebellum.

We have used the indirect antibody peroxidase-antiperoxidase technique to analyze the course of serotonin (5-hydroxytryptamine; 5HT) fibers to the deep cerebellar nuclei; the distribution of serotonin within the nuclei; the continued course of 5HT fibers to the cerebellar cortex; and the lobular and laminar distribution of this indoleamine in the cerebellar cortex. Only rarely are fibers found in either the restiform body or the brachium pontis. However, a distinct bundle of serotoninergic axons is present in the medial aspect of the brachium conjunctivum. Axons arise from this bundle and course dorsally into the neuropil of the deep cerebellar nuclei. The densest immunostaining is present in posterior and ventral regions of all four cerebellar nuclei. Within the nuclei large (24% of total) and small (76% of total) varicosities are present. The average distance between varicosities on individual axons is 3.85 micron (S.D. = 1.2). The innervation of the cerebellar cortex is derived primarily from fibers that course through the deep nuclei. At levels caudal to the deep nuclei a single midsagittal band courses into lobules VIII and IX. In the cerebellar cortex, serotoninergic axons and varicosities are present in all lobules; however, the fiber density is not uniform. The densest distribution is present in vermal lobule VIII and the dorsal folia of lobule IX. Within the granule cell layer of lobules VIII and IX, immunoreactive elements form a midsagittal band, and to a lesser degree, two parasagittal bands. Beaded serotoninergic fibers course through the deep and middle portion of the granule cell layer and give rise to a plexus at the border between the Purkinje cell and granule cell layers. Within this plexus axons extend long distances in the transverse and sagittal planes. Long beaded axons oriented in the transverse plane of the folia are also present in the deep molecular layer. A few radial serotoninergic fibers ascend to the pial surface and give rise to very short tangential branches. In all three cortical layers, both large (19% of total) and small (81% of total) varicosities are present. The average distance between varicosities on individual fibers is 5.3 micron (S.D. = 2.2).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2000

Effects of unilateral labyrinthectomy on the norepinephrine content in forebrain and cerebellar structures of albino rats.

Albino (Wistar) rats were used to investigate whether unilateral labyrinthectomy (UL) modified the concentration of norepinephrine (NE) as well as of dopamine (DA) and the corresponding metabolite 3, 4-dihydroxyphenylacetic acid (DOPAC) in different areas of the cerebral and the cerebellar cortex and the striatum. The results obtained in 38 rats submitted to UL were compared to those of 18 rats submitted to sham-operation. The animals were operated under sodium pentobarbital anesthesia and sacrificed 1.5, 3 and 6 h after surgery. All rats submitted to UL showed phenomena of deficit (1.5-3 h after the lesion) followed by partial vestibular compensation (3-6 h after the lesion). Significant changes in the content of NE were neither found in different areas of the cerebral and the cerebellar cortex, nor in the striatum of rats sacrificed 1.5 h after UL. Three h after the lesion a bilateral increase in the NE content occurred in all the explored areas of the cerebral cortex (i.e., frontal, parieto-temporal and occipital) and the cerebellar cortex (i.e., the vermis and flocculus), as well as in the striatum. This increase, however, was more prominent in the parieto-temporal areas of the neocortex of the intact side, in all the explored areas of the cerebellar cortex of that side, as well as in the striatum of the lesioned side. This asymmetric increase in NE content could not be attributed, at least exclusively, to a generalized activation of the noradrenergic LC nuclei of both sides, due to waking and/or stress which may occur after UL, but did rather depend on asymmetric changes in unit discharge of the vestibular nuclei projecting to the LC of both sides, following UL. In particular, the increased discharge of the vestibular nuclei of the intact side would lead to activation of noradrenergic neurons projecting particularly to the parieto-temporal cortex and the cerebellar cortex of the intact side, as well as to the striatum of the lesioned side. A bilateral increase in NE content was still observed in different areas of the cerebral and cerebellar cortex of rats sacrificed 6 h after UL. This increase, however, was of smaller entity than that observed in the same areas 3 h after UL and quite symmetric. The content of DA and its metabolite DOPAC decreased bilaterally in the striatum of rats sacrificed 1.5 h after UL. This effect was attributed to a reduced synthesis and release of DA, which probably resulted from a reduced facilitatory influence that the deafferented vestibular nuclei exert on the dopaminergic, nigrostriatal system of both sides, although mainly on the intact side. The corresponding values, however, bilaterally recovered to slightly increase with respect to the control values in rats sacrificed 3 and 6 h after UL. In these experiments the content of both DA and DOPAC remained symmetric on both sides after UL, in contrast with the bilateral but asymmetric increase in NE concentration observed in the same structure 3 h the lesion. The present results integrate and extend those of previous experiments showing that: 1) albino rats sacrificed 6 h after UL displayed an increased synthesis of NE, which affected particularly the LC of the intact side as well as the medial vestibular nuclei of both sides (21); and 2) the structures which showed an increased content of NE at given time intervals after UL also displayed an increase in the expression of the immediate early gene c-fos (cf. 16 for ref.). These findings suggest that bilateral but asymmetric activation of the noradrenergic LC neurons following UL may lead to an asymmetric increase in c-fos expression in several target structures, thus contributing to the plastic changes responsible for vestibular compensation. In conclusion, it appears that UL induces in several brain structures of albino rats a short-term increase in synthesis and release of NE. (ABSTRACT TRUNCATED)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1993

The use of magnetic resonance imaging in diagnosing infantile neuroaxonal dystrophy.

We used MRI to investigate the brains of four children ranging from 3 to 10 years of age with infantile neuroaxonal dystrophy. T2-weighted imaging revealed characteristic findings of marked cerebellar atrophy and diffuse hyperintensity of the cerebellar cortex. At autopsy, one child had extensive astrogliosis and neuronal loss with shrinkage of the cerebellar cortex, in addition to typical widespread changes of neuroaxonal dystrophy. The characteristic hyperintensity of the cerebellar cortex on T2-weighted imaging probably is secondary to the extensive gliosis and shrinkage of the cerebellar cortex. These cerebellar findings on MRI may permit early diagnosis of infantile neuroaxonal dystrophy.

Atrophy↗
PubMed1995

Projections from the central cervical nucleus to the cerebellar nuclei in the rat, studied by anterograde axonal tracing.

Projections from the central cervical nucleus (CCN) to the cerebellar nuclei were examined following injections of Phaseolus vulgaris-leucoagglutinin or cholera toxin subunit B into the C1-C3 segments in the rat. Labeled axons and terminals were immunohistochemically demonstrated. Labeled spinocerebellar fibers arising from the CCN entered the cerebellum through the inferior and the superior cerebellar peduncles. Labeled mossy fiber terminals were seen in lobules I-VI, sublobule VIIb, lobules VIII and IX, and the copula pyramidis of the cerebellar cortex. Labeled axons ran toward the cerebellar cortex, through and between the medial and the interpositus nuclei, and gave off collateral axons and terminal axons to the cerebellar nuclei. The projections to the cerebellar nuclei were predominantly contralateral to the cells of origin. Labeled terminals were distributed from the medial to the ventrolateral part of the middle subdivision of the medial nucleus throughout its rostrocaudal extent. Labeled terminals were also seen in the lateral part of the medial nucleus and in the border region between the medial nucleus and the interpositus nuclei, which corresponds to the rostromedial extension of the posterior interpositus nucleus. In the anterior interpositus nucleus, labeled terminals were distributed dorsoventrally in the middle third of the mediolateral extent. They were more numerous in the rostrodorsal part of this area. Labeled terminals were distributed dorsally and caudally in the medial third of the posterior interpositus nucleus. No labeled terminals were seen in the caudomedial subdivision and the dorsolateral protuberance of the medial nucleus, the dorsolateral hump region and the lateral nucleus. The present study demonstrates that the CCN projects to specific areas of the cerebellar cortex and the medial and the interpositus nuclei.

Afferent Pathways↗
PubMed1983

6-OHDA-induced ectopia of external granule cells in the subarachnoid space covering the cerebellum. Genesis and topography.

The present report describes the genesis, development and topographical distribution of ectopic cells of the external granular layer in the subarachnoid space covering the rat cerebellum. Following one intracisternal injection to newborn rats of 100 micrograms 6-hydroxydopamine (6-OHDA), the meningeal cells degenerate and are removed by phagocytosis within 24 h post injection (p.i.), leaving the cerebellar cortex without a pia-arachnoid cover. Defects appear in the basal lamina investing the cerebellar cortex 3 to 5 days p.i., and both external granule cells and 'sprouts' from Bergmann-glia endfeet grow into the subarachnoid space. The latter form large, flat glial lamellae and cover extensive areas of the denuded cerebellar surface, although they do not form a glial scar over the exposed neuropil of the cerebellar cortex. The numbers of ectopic external granule cells increase within the subarachnoid space both by proliferation and a continuous efflux of cells from the cerebellar cortex. They migrate, aggregate, and ultimately develop into granule, stellate and basket cells, the morphology of which is indistinguishable from their counterparts in situ; they make specific afferent and efferent connections, both among themselves and with the underlying cerebellar cortex and brainstem. The distribution of ectopic external granule cells and their derivatives is restricted to the anterior vermal fissures and the vermal-hemispheric junctions. The present results indicate that external granule cells and their derivatives are capable of both differentiating normally and surviving in the subarachnoid space if they become associated with glial cells and establish synaptic connections.

Animals↗
PubMed1977

The intracerebellar nucleocortical projection in a primate.

Experiments were performed to determine if a nucleocortical system, a projection from the cerebellar nuclei to the cerebellar cortex, was present in primates. Both electrophysiological and neuroanatomical techniques were employed to investigate this question. It was shown that neurons within the dentate and interposed nuclei were antidromically activated by stimuli applied to the cerebellar cortex. In addition, cells in these nuclei were retrogradely labelled following injections of small amounts of horseradish peroxidase in the cerebellar cortex. The injection of tritiated leucine in the deep nuclei resulted in the labelling of fibers projecting from these structures to the cerebellar cortex which appeared to terminate within the granular layer. Additional electrophysiological studies showed that neurons projecting to the cerebellar cortex could also be antidromically activated from the ventrolateral thalamic nucleus, indicating that the nucleocortical projection in the primate arises at least in part as collaterals from neurons in the deep cerebellar nuclei which also project to extracerebellar structures, as was shown in the cat.

Action Potentials↗
PubMed1993

Partition of the human cerebellum in sensory-motor activities, learning and cognition.

The circuitry of the cerebellum is quite well understood. The computation takes place in the cerebellar cortex, which functions in synchronized strips to provide excellent timing signals to the cerebral cortex and the spinal cord. The cerebellar cortex is also the site where error signals from other parts of the central nervous system are incorporated. For voluntary limb movements the cerebellar cortex is important for the timing of the innervation of the agonist and antagonist anterior horn neurons. It is also important for the temporal order of and precision in the execution of motor programs. As will be apparent, the cerebellum is not only a computer taking care of motor programs.

Cerebellum↗
PubMed1989

Distribution of beta-adrenergic receptors in different cortical and nuclear regions of cat cerebellum, as revealed by binding studies.

In addition to mossy fibers and climbing fibers, the cerebellum receives NE-containing fibers originating particularly from the locus coerulus complex. Since the neurotransmitter of the coeruleo-cerebellar afferents acts mainly on Purkinje cells through beta-receptors, experiments were performed in cats to study the regional distribution and properties of the beta-adrenoceptors at corticocerebellar level; moreover, attempts were made to identify also the presence of beta-adrenoceptor binding in the cerebellar nuclei underlying the different zones of the cerebellar cortex. (-)-[3H]Dihydroalprenolol, a very potent beta-adrenergic antagonist, was used to characterize the beta-adrenergic receptors. (-)-[3H]DHA bound specifically to membrane preparations from all the cortical and nuclear zones of the cerebellum. In particular, beta-adrenergic receptors showed a high density and affinity in the cerebellar cortex with no significant difference in the medial with respect to the intermediate-lateral cortical area. The cerebellar nuclei showed a lower density of beta-adrenoceptors with a comparable or slightly lower affinity with respect to the cerebellar cortex. However, no difference was observed between the fastigial nucleus and the interposite-dentate nuclei. Scatchard analysis of saturation data revealed the presence of a single population of high affinity binding sites in all the examined regions, while the Hill plots excluded the presence of cooperative effects among the binding sites. Attempts to differentiate in the cerebellum beta 1- and beta 2-receptors by using agents which act as selective beta 1 and beta 2 ligands indicated that (-)-[3H]DHA specific binding in cerebellar cortex and nuclei affects predominantly the beta 2 subtype of adrenoceptors. A comparison between results obtained from the cerebellar cortex and those obtained from the whole cerebral cortex was also made. The whole cerebral cortex showed a lower density but a higher affinity than the cerebellar cortex. Moreover, inhibition of (-)-[3H]DHA binding by selective beta 1 and beta 2 ligands indicated the prevalence of the beta 1 subtype of adrenoceptors at this level.

Alprenolol↗
PubMed1997

[(Neurological CPC.55). A 60-year-old woman with progressive cerebellar ataxia, myoclonus, and dementia].

We report a 60-year-old woman with progressive ataxia, myoclonus, choreoathetosis, and dementia. She was well until 27 years of the age when she noted an onset of gait disturbance and speech disturbance. She noted abnormal involuntary movements in her four limbs at 42 years of the age. Her symptoms had progressively become worse and she fell down frequently by her 52 years of the age. In addition, her family members noted gradual decline in her intelligence. She was admitted to our hospital in February of 1993 when she was 57-year-old. On admission, she showed dementia, scanning speech, ataxic gait, limb ataxia, action myoclonus, and choreic movements which involved her four limbs. Deep tendon reflexes were slightly exaggerated in the lower limbs; no Babinski sign was noted. Sensation was intact. Laboratory findings were unremarkable. Cerebral MRI revealed atrophy of the cerebellar cortex, superior cerebellar peduncle, brain stem, and the cerebral cortex; the third ventricle and the lateral ventricles were dilated; furthermore, T2-high signal lesions were seen in the cerebral white matter and in the pontine base. Her clinical course was one of the progressive deterioration of her ataxia, involuntary movements, and dementia. She expired on April 24, 1996 when she was 60-year-old. She was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had dentatorubral-pallidoluysian atrophy. A minor opinion was that she might have had myoclonus epilepsy with ragged-red fibers. Postmortem examination revealed atrophy, gliosis, and neuronal loss in the external segment of the globus pallidus, subthalamic nucleus, red nucleus, and in the dentate nucleus. In addition, the gracil and cuneiform nuclei showed neuronal loss and spheroid formation; the spinocerebellar tracts were retained. The substantia nigra and the locus coeruleus were intact. No ragged-red fibers were seen in the muscle biopsy specimen taken in February, 1993. The neuropathologic findings were consistent with the diagnosis of dentatorubral-pallidoluysian atrophy.

Atrophy↗
PubMed2002

Cerebellar mechanisms in eyeblink conditioning.

A recent model of cerebellar learning in eyeblink conditioning predicts two sites of plasticity, the cerebellar cortex and cerebellar nuclei, which store information relating to timing and driving the movement, respectively. Consistent with this idea, lesions of the cortex or reversible "disconnections" of Purkinje cell output to the nuclei have been shown to disrupt response timing to produce short-latency conditioned eyeblinks. To better characterize potential cortical and nuclear plasticities, we analyzed the effects upon nictitating membrane (NM) and eyeblink conditioned responses (CRs) of different drugs administered to the cortex and to the nuclei. When either excitatory or inhibitory inputs to the cerebellar cortical lobule HVI were blocked by infusions of the AMPA receptor antagonist CNQX or the GABA-A receptor antagonists picrotoxin or SR95531, CRs were abolished. Similarly GABA-A receptor antagonists in the cerebellar nuclei abolished CRs. CR latencies were never shortened. However, blockade of AMPA/kainate receptor-mediated excitatory transmission to the nuclei had no effect upon CR frequencies or latencies. These results suggest that normal cortical and nuclear function is required for performance of NM and eyeblink CRs. We saw no evidence that CRs can be driven by AMPA/kainate receptor-mediated transmission from mossy fiber afferents to the cerebellar nuclei. So, although plasticity in the cerebellar nuclei is not ruled out, it is unlikely that a long-term change in AMPA receptor-mediated transmission from mossy fiber inputs to the nuclei is an essential mechanism in eyeblink conditioning. Our findings indicate that a fully functional olivo-cortico-nuclear loop is required to express all characteristics of associatively conditioned responses.

Animals↗
PubMed1995

Distribution of beta amyloid associated proteins in plaques in Alzheimer's disease and in the non-demented elderly.

Recent studies have shown that cerebral beta amyloid (A beta) protein deposition is a necessary, but not sufficient, factor to develop the pathology of Alzheimer's disease (AD). In the present immunohistochemical study, we have investigated in AD the distribution of A beta associated proteins in the cerebral neocortex, in the cerebellar cortex where A beta plaques are mainly of the diffuse type, and also in the cerebral neocortex of non-demented patients with A beta plaques. Results show that immunolabeling for C1q, C4c, C3d, alpha 1-ACT and Apolipoprotein E (ApoE) occurs in the great majority of A beta plaques in all groups. ApoJ is present in A beta plaques of the cerebral neocortex in AD and in non-demented elderly, but is almost absent from those of the AD cerebellar cortex. C4Bp and P-component, in contrast to AD, rarely occurs in A beta plaques of the cerebral neocortex in the non-demented elderly. Heparan sulphate proteoglycan (HSPG) core protein and intercellular adhesion molecule-1 (ICAM-1) are absent in the diffuse A beta plaques in the AD cerebellum. These differences in distribution and expression of A beta associated proteins may be determined by brain region specific factors (cerebral cortex versus cerebellar cortex) and clinical state (demented versus non-demented cases). We suggest that, besides A beta peptide, certain A beta associated proteins are required for both amyloid plaque formation and for the induction of neurofibrillary changes.

Aged↗
PubMed1983

Specific messenger RNA changes in Joseph disease cerebella.

Joseph disease is an autosomal-dominant, spinocerebellar degeneration characterized at the biochemical level by elevations in the steady-state levels of several abundant proteins (H, J, and L) in affected brain areas such as the cerebellar cortex. The increased levels of these proteins could either be a consequence of a relative increase in their de novo synthesis or result from altered rates of proteolysis in degenerating brain cells. These alternatives can be distinguished by comparing the in vitro protein-synthetic capacities of the messenger ribonucleic acid populations isolated from cerebellar cortex of control subjects and patients with Joseph disease. Protein H (glial fibrillary acidic protein) is synthesized at detectable levels by all messenger ribonucleic acid isolates, and the levels of its translatable messenger ribonucleic acid are reproducibly increased in ribonucleic acids isolated from cerebellar cortex of patients with Joseph disease as compared with those isolated from cerebellar cortex of control subjects. Thus, the increased level of protein H in Joseph disease is a consequence of an increase in its de novo synthesis and is correlated with the increased number of cerebellar glial cells. In contrast to these results, there is no detectable synthesis of proteins J and L by messenger ribonucleic acid populations isolated from cerebellar cortex of either Joseph disease patients or control subjects, suggesting that the increased levels of these proteins in affected cerebellar cortex are a consequence of posttranslational protein modifications.

Adult↗
PubMed2005

Nicotinic receptor modulation of neurotransmitter release in the cerebellum.

Nicotinic ACh receptors (nAChRs) are formed by pentameric combinations of alpha and beta subunits, differentially expressed throughout the central nervous system (CNS), where they have been shown to play a role in the modulation of neurotransmitter release. nAChRs are also important during neuronal differentiation, regulating gene expression and contributing to neuronal pathfinding. The cerebellum, which is involved in the maintenance of balance and orientation as well as refinement of motor action, in motor memory and in some aspects of cognition, undergoes a significant process of development and maturation of its neuronal networks during the first three postnatal weeks in the rat. Autoradiographic as well as in situ hybridization and immunocytochemical studies have shown that several nicotinic receptor binding sites and subunits are expressed in the rat cerebellum from embryonic stage through to adulthood, with the highest expression levels seen during the development of the cerebellar cortex. A diffuse cholinergic afferent projection to all lobules of the cerebellar cortex has been described, with the uvulanodulus, flocculus and lobules I and II of the anterior vermis regions receiving a particularly dense projection. Low levels of nAChR subunit transcripts and immunoreactivity, particularly during adulthood, and the scattered distribution of immunoreactivity between neurons in the cerebellar cortex, can explain the difficulty in assessing electrophysiologically the presence of functional nAChRs in the cerebellar cortex and some contradictory results reported in the early-published papers. In recent years, several groups have shown that also in the cerebellum different nAChR subtypes modulate release of glutamate and GABA at different synapses. The possible role of these mechanisms in synaptic consolidation during development, as well as on plasticity phenomena and network activity at mature synapses, are discussed.

Animals↗
PubMed1992

Direct and indirect "cortico"-rubral and rubro-cerebellar cortical projections in the pigeon.

In birds the red nucleus is the most rostral cell group in the brain having projections to all levels of the spinal cord (Cabot et al., Prog. Brain Res., 57:79-108, 1982), but its sources of afferents are incompletely known. In order to determine these, a series retrograde and anterograde tracing experiments was carried out, largely with cholera toxin B-chain conjugated to horseradish peroxidase. The results show that a sparse and diffuse projection to the red nucleus arises from deep regions of the hyperstriatum accessorium (HA) of the anterior Wulst, and that a much more dense projection arises from the caudal part of the nucleus principalis precommissuralis and the medial part of the medial spiriform nucleus (SpMm). These last two sources were themselves shown to receive a substantial projection from HA of the anterior Wulst. The red nucleus was also shown to project upon the cerebellar cortex of lobule VI, and SpM upon the cerebellar cortex of lobules VI through IX (Karten and Finger, Brain Res., 102:335-338, 1976; Clarke, J. Comp. Neurol., 174:535-552, 1977). Double retrograde labelling experiments with fluorescein and rhodamine labelled latex microspheres injected into the cerebellar cortex and spinal cord showed that the rubrocerebellar cortical neurons are a different population from, although intermixed with, the rubrospinal neurons.

Animals↗
PubMed2002

Computational study on monkey VOR adaptation and smooth pursuit based on the parallel control-pathway theory.

Much controversy remains about the site of learning and memory for vestibuloocular reflex (VOR) adaptation in spite of numerous previous studies. One possible explanation for VOR adaptation is the flocculus hypothesis, which assumes that this adaptation is caused by synaptic plasticity in the cerebellar cortex. Another hypothesis is the model proposed by Lisberger that assumes that the learning that occurs in both the cerebellar cortex and the vestibular nucleus is necessary for VOR adaptation. Lisberger's model is characterized by a strong positive feedback loop carrying eye velocity information from the vestibular nucleus to the cerebellar cortex. This structure contributes to the maintenance of a smooth pursuit driving command with zero retinal slip during the steady-state phase of smooth pursuit with gain 1 or during the target blink condition. Here, we propose an alternative hypothesis that suggests that the pursuit driving command is maintained in the medial superior temporal (MST) area based on MST firing data during target blink and during ocular following blank, and as a consequence, we assume a much smaller gain for the positive feedback from the vestibular nucleus to the cerebellar cortex. This hypothesis is equivalent to assuming that there are two parallel neural pathways for controlling VOR and smooth pursuit: a main pathway of the semicircular canals to the vestibular nucleus for VOR, and a main pathway of the MST-dorsolateral pontine nuclei (DLPN)-flocculus/ventral paraflocculus to the vestibular nucleus for smooth pursuit. First, we theoretically demonstrate that this parallel control-pathway theory can reproduce the various firing patterns of horizontal gaze velocity Purkinje cells in the flocculus/ventral paraflocculus dependent on VOR in the dark, smooth pursuit, and VOR cancellation as reported in Miles et al. at least equally as well as the gaze velocity theory, which is the basic framework of Lisberger's model. Second, computer simulations based on our hypothesis can stably reproduce neural firing data as well as behavioral data obtained in smooth pursuit, VOR cancellation, and VOR adaptation, even if only plasticity in the cerebellar cortex is assumed. Furthermore, our computer simulation model can reproduce VOR adaptation automatically based on a heterosynaptic interaction model between parallel fiber inputs and climbing fiber inputs. Our results indicate that different assumptions about the site of pursuit driving command maintenance computationally lead to different conclusions about where the learning for VOR adaptation occurs. Finally, we propose behavioral and physiological experiments capable of discriminating between these two possibilities for the site of pursuit driving command maintenance and hence for the sites of learning and memory for VOR adaptation.

Adaptation, Physiological↗
PubMed1998

Axonal collateral-collateral transport of tract tracers in brain neurons: false anterograde labelling and useful tool.

It is well established that some neuroanatomical tracers may be taken up by local axonal terminals and transported to distant axonal collaterals (e.g., transganglionic transport in dorsal root ganglion cells). However, such collateral-collateral transport of tracers has not been systematically examined in the central nervous system. We addressed this issue with four neuronal tracers--biocytin, biotinylated dextran amine, cholera toxin B subunit, and Phaseolus vulgaris-leucoagglutinin--in the cerebellar cortex. Labelling of distant axonal collaterals in the cerebellar cortex (indication of collateral-collateral transport) was seen after focal iontophoretic microinjections of each of the four tracers. However, collateral-collateral transport properties differed among these tracers. Injection of biocytin or Phaseolus vulgaris-leucoagglutinin in the cerebellar cortex yielded distant collateral labelling only in parallel fibres. In contrast, injection of biotinylated dextran amine or cholera toxin B subunit produced distant collateral labelling of climbing fibres and mossy fibres, as well as parallel fibres. The present study is the first systematic examination of collateral-collateral transport following injection of anterograde tracers in brain. Such collateral-collateral transport may produce false-positive conclusions regarding neural connections when using these tracers for anterograde transport. However, this property may also be used as a tool to determine areas that are innervated by common distant afferents. In addition, these results may indicate a novel mode of chemical communication in the nervous system.

Animals↗
PubMed2001

Confocal laser scanning, conventional scanning and transmission electron microscopy of vertebrate cerebellar granule cells.

Confocal laser scanning microscopy of hamster cerebellar granular layer showed in montages of z-series the presence of small, medium and large granule cells. A granule cell Golgi cell ratio of 50/4 was observed surrounding glomerular regions. Field emission high resolution scanning electron microscopy of mouse cerebellar granular and molecular layers showed SE-I images of the outer and inner surfaces of nuclear and cytoplasmic compartments of chromium coated granule cells and the axo-spinodendritic synapses of parallel fibers with Purkinje cell dendrites. Conventional scanning electron microscopy of teleost fish cerebellar cortex showed three dimensional morphology of granule cell soma and processes and the synaptic relationship with mossy and climbing fibers, Golgi cell axonal ramifications and dendrites of stellate neurons, by means of SE-II and SE-III signal image mode, in sagittally and transversally cryofractured cerebellar cortex. SE-II images of the non-synaptic segments and synaptic varicosities of parallel fiber outer surface were characterized in the molecular layer. Ultrathin sections of transmission electron microscopy (TEM) revealed somato-somatic, dendro-somatic and dendro-dendritic like-desmosomal and like-hemidesmosomal junctions in human cerebellar granule cells. Freeze-etching replicas of mouse cerebellar cortex displayed granule cell intramembrane morphology, cytoplasmic fractured face and the Bergman glial cell cytoplasm completely surrounding the parallel fibers in the molecular layer. The mossy fiber-granule cell dendrite synaptic relationship was observed in sagittally and transversally cryofractured cerebellar cortex and correlated with TEM images. SE-II images of the climbing fiber synaptic connections with granule cell dendrites were obtained in teleost fish cerebellar cortex. One to one axo-dendritic synaptic contacts between Golgi cell axonal ramifications and granule cell dendrites were also seen. The above findings provide new vistas for future studies dealing with intracortical circuits and information processing in the cerebellar cortex.

Animals↗