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PubMed1998

Patches of synchronized activity in the cerebellar cortex evoked by mossy-fiber stimulation: questioning the role of parallel fibers.

The discrepancy between the structural longitudinal organization of the parallel-fiber system in the cerebellar cortex and the functional mosaic-like organization of the cortex has provoked controversial theories about the flow of information in the cerebellum. We address this issue by characterizing the spatiotemporal organization of neuronal activity in the cerebellar cortex by using optical imaging of voltage-sensitive dyes in isolated guinea-pig cerebellum. Parallel-fiber stimulation evoked a narrow beam of activity, which propagated along the parallel fibers. Stimulation of the mossy fibers elicited a circular, nonpropagating patch of synchronized activity. These results strongly support the hypothesis that a beam of parallel fibers, activated by a focal group of granule cells, fails to activate the Purkinje cells along most of its length. It is thus the ascending axon of the granule cell, and not its parallel branches, that activates and defines the basic functional modules of the cerebellar cortex.

Animals↗

PubMed2005

Axonal and synaptic remodeling in the mature cerebellar cortex.

By blocking electrical activity in the cerebellar cortex the Purkinje cell dendrites become a uniform territory with a high density of spines all bearing the glutamate receptor delta2 subunit (GluRdelta2) and being mainly innervated by parallel fibers. Such a subunit, which is constitutively targeted specifically to the parallel fiber synapses, appears in the spines contacted by the climbing fibers before they disconnect from the target. A similar pattern of hyperspiny transformation and innervation occurs a few days after a subtotal lesion of the inferior olive, the source of climbing fibers. During the climbing fiber reinnervation process which follows the removal of the electrical block or by collateral sprouting of surviving inferior olive neurons, the new active climbing fibers establish synaptic contacts with proximal dendritic spines that bear GluRdelta2s. After, they repress these subunits and displace the parallel fibers to the distal dendritic territory. These findings suggest the following operational principle in the axonal competition for a common target. The Purkinje cells have an intrinsic phenotypic profile which is compatible with the parallel fiber innervation, this mode being operational in targets innervated by a single neuronal population, like the neuromuscular system. An additional input, the climbing fibers, in order to achieve its own territory on the proximal dendrite needs the ability to displace the competitor. Such an inhibition is activity-dependent and the activity needs to be present in order to allow the climbing fiber to maintain its territory, even when the developmental period is over.

Age Factors↗

PubMed1987

The cardiovascular responses elicited from the posterior cerebellar cortex in the anaesthetized and decerebrate rabbit.

1. In this study the posterior cerebellar cortex has been electrically stimulated and changes in heart rate, arterial blood pressure, regional blood flows and renal sympathetic nerve discharge have been recorded in both the anaesthetized and the decerebrate unanaesthetized rabbit. 2. Specifically, lobules VII, VIII, IX and X of the posterior cerebellar vermis were stimulated but the only region which elicited cardiovascular changes was lobule IX (the uvula). The responsive area of the uvula was localized to the medial regions of sublobules a, b and c and was identical in both anaesthetized and decerebrate animals. 3. Under urethane anaesthesia, uvula stimulation evoked a small bradycardia, a fall in arterial pressure, a transient inhibition of renal sympathetic nerve activity, with no change in renal vascular conductance, and an increase in femoral vascular conductance. 4. Stimulation of an identical area in the decerebrate rabbit evoked a marked tachycardia, an increase in blood pressure, maintained increase in renal sympathetic nerve discharge, and decreases in both renal and femoral conductances. 5. The response evoked from the decerebrate rabbit could be reversed by a small dose of anaesthetic to a pattern of response which was essentially identical to that seen in the urethane-anaesthetized rabbit. 6. This influence of anaesthetics on the pattern of cardiovascular responses that may be elicited from the cerebellar cortex indicates that caution should be exercised when making physiological inferences on the basis of stimulation experiments in anaesthetized preparations. 7. In the light of the cardiovascular changes that may be evoked from the uvula, and recent neuroanatomical and neurophysiological data concerning afferent and efferent connexions of this cerebellar region, we discuss the possibility that the uvula plays a role in the alerting reaction of the rabbit.

Anesthesia, General↗

PubMed2006

Caytaxin deficiency disrupts signaling pathways in cerebellar cortex.

The genetically dystonic (dt) rat, an autosomal recessive model of generalized dystonia, harbors an insertional mutation in Atcay. As a result, dt rats are deficient in Atcay transcript and the neuronally-restricted protein caytaxin. Previous electrophysiological and biochemical studies have defined olivocerebellar pathways, particularly the climbing fiber projection to Purkinje cells, as sites of significant functional abnormality in dt rats. In normal rats, Atcay transcript is abundantly expressed in the granular and Purkinje cell layers of cerebellar cortex. To better understand the consequences of caytaxin deficiency in cerebellar cortex, differential gene expression was examined in dt rats and their normal littermates. Data from oligonucleotide microarrays and quantitative real-time reverse transcriptase-PCR (QRT-PCR) identified phosphatidylinositol signaling pathways, calcium homeostasis, and extracellular matrix interactions as domains of cellular dysfunction in dt rats. In dt rats, genes encoding the corticotropin-releasing hormone receptor 1 (CRH-R1, Crhr1) and plasma membrane calcium-dependent ATPase 4 (PMCA4, Atp2b4) showed the greatest up-regulation with QRT-PCR. Immunocytochemical experiments demonstrated that CRH-R1, CRH, and PMCA4 were up-regulated in cerebellar cortex of mutant rats. Along with previous electrophysiological and pharmacological studies, our data indicate that caytaxin plays a critical role in the molecular response of Purkinje cells to climbing fiber input. Caytaxin may also contribute to maturational events in cerebellar cortex.

Animals↗

PubMed1988

Age-related changes of the metabolic profile of rat cerebellar cortex: enzyme histochemical study.

The influence of aging on the metabolic profile of cerebellar cortex was studied in young (3-month-old), adult (12-month-old) and aged (26-month-old) male Sprague-Dawley rats using enzyme histochemical techniques. The following enzymatic activities related to energy transduction were examined: lactate-(LDH) and succinate-(SDH) dehydrogenases; NADH2-tetrazolium reductase (NADHD) and alpha-glycerophosphate-dehydrogenase (GPDH). The intensity of enzymatic staining within the neuropil of molecular and granular layers as well as within the cytoplasm of Purkinje neurons of young, adult and aged animals was assessed microphotometrically. In the molecular layer LSH, SDH and NADHD levels were reduced in old rats; GPDH was decreased both in adult and old animals. In Purkinje neurons no age-related changes of the enzymatic activities under study were observed. In the granular layer LDH and GPDH showed an age-dependent loss; SDH and NADHD were unchanged. The possibility that age-related changes of the enzymatic activities under study may be due to impaired energy production mechanisms and/or represent the consequence of reduced energetic needs resulting from the documented age-dependent loss of synapses in the molecular or in the granular layers of cerebellar cortex is discussed.

Aging↗

PubMed1988

Autoradiographic localization of insulin-like growth factor II receptors in cerebellar cortex of weaver and Purkinje cell degeneration mutant mice.

Autoradiography was used to visualize insulin-like growth factor II (IGF-II) receptors in the cerebellar cortex of weaver and Purkinje cell degeneration (pcd) mice. These mutants were selected for their respective absence of granule or Purkinje cells. Histological preparations confirmed a severe loss of granule cells in the cerebella of weaver mutants and an absence of Purkinje cells in those of pcd mutants. Autoradiographs showed specific IGF-II binding to the granule cell layer of the cerebellar cortex in control mice, and in pcd mutants. No specific [125I]human IGF-II binding was observed in the cerebellar cortex of weaver mutants. These studies suggest that specific IGF-II receptor sites are located on the granule cells of the cerebellum.

Animals↗

PubMed1994

Expression of neurofilament proteins in the rat cerebellar cortex as a function of age: an immunohistochemical study.

The present study was designed to assess changes in the expression of cytoskeletal proteins in the cerebellar cortex of rats of different ages using immunohistochemical techniques associated with image analysis. Male Wistar rats of 3 months (young), 12 months (adult) and 24 months (old) were used. Neuronal cytoskeleton was investigated using monoclonal antibodies to phosphorylated neurofilament (NF) proteins of high (H), medium (M) and low+H+M molecular weight (NF triplet). In young and adult rats in which the expression of phosphorylated NF immunostaining was similar, a dark-brown immunoreactivity was observed primarily in axons of the white matter and of basket neurons which surround Purkinje neurons and enter in the molecular layer. In adult rats a NF-H immunoreactivity was sometimes observed within the dendritic tree of Purkinje neurons. A significant decrease in the density of NF immunoreactivity involving the three different subunits investigated was found in the cerebellar cortex of old rats. This suggests that cytoskeletal abnormalities occur not only in senile dementia, but also in the so called 'physiological aging'. The cerebellar cortex may represent an interesting model for evaluating age-dependent changes of cytoskeleton.

Aging↗

PubMed1989

[Electric responses evoked by C-fiber input from saphenous nerve in cat cerebellar cortex].

When the A-fibers of the saphenous nerve were stimulated at a lower intensity which elicited the A-fiber input only, an evoked potential (A-CEP) which consisted of an early component with latency of 11.8 +/- 3.5ms and a late component with latency of 312.1 +/- 17.5ms could be recorded on the surface of the cerebellar cortex in cat. When A- and C-fibers were activated by stimulation at the strength of C-fiber suprathreshold, the latency and configuration of the evoked potential had no significant difference from one of the A-CEP. After A-fibers were blocked by the polarizing current, stimulation at the strength of C-fiber suprathreshold could evoke a characteristic C-CEP with latency of 134.2 +/- 18.4ms. In general, C-CEP whose maximal amplitude was recorded on the vermain lobule VI was a positive-negative potential and its phases were reversed in the deep layer of the cerebellar cortex. C-CEP had a smaller amplitude, a longer latency and a lower following frequency than A-CEP had. In comparison with A-CEP, C-CEP had a high susceptibility to the morphine. The results showed that C-CEP which was evoked by the selective C-fiber input and generated in the cerebellar cortex seemed to be a response to the information of the slow pain input. It was suggested that C-fiber input could reach the cerebellar cortex and elicited an evoked potential. When A- and C-fiber were activated at the same time, C-CEP might be inhibited by the A-fiber input.

Animals↗

PubMed1996

Expression and immunohistochemical localization of eight phospholipase C isoforms in adult male mouse cerebellar cortex.

By means of specific polyclonal or monoclonal antibodies we have investigated the expression and the localization of phospholipase C isoforms in the adult mice cerebellar cortex. Western-blot analysis revealed that mouse cerebellum expressed eight phospholipase C isozymes: -beta 1, -beta 2, -beta 3, -beta 4, -gamma 1, -gamma 2, -delta 1, -delta 2. Immunohistochemical analysis carried out on cryosections showed a distinct pattern of expression for each of the isoforms. Purkinje cells had high levels of -beta 1, -beta 3, -gamma 2 and -delta 2 isotypes. The -gamma 2 isozyme was the only one that was identified also in the dendrites of Purkinje cells. In the molecular layer we detected mostly -beta 1 and -gamma 1 isozymes whereas in the granular layer -gamma 1 and -gamma 2 isoforms prodominated. These results indicate a heterogeneity of the phospholipase C isoforms expressed in the layers of mouse cerebellar cortex conceivably due to the fact that these enzymes are coupled to different receptors and perform selective tasks in regulating cell signalling events taking place in the cerebellar cortex of mice.

Amino Acid Sequence↗

PubMed1978

Calcium and potassium changes in extracellular microenvironment of cat cerebellar cortex.

1. Local stimulus-evoked changes in concentration of extracellular calcium ions, [Ca2+]0, and potassium ions, [K+[0, were measured in the cerebellar cortex of the cat using paired ion-selected micropipettes. 2. Repetitive stimulation of 30 s duration decreased [Ca2+]0 from a base line of 1.2 mM to as low as 0.8 mM and increased [K+]0 from 3 mM to as much as 8 mM. The magnitude of the changes was directly related to stimulus frequency. Laminar analysis showed that the greatest ion changes occurred at the level of maximum parallel fiber-Purkinje cell dendrite stimulation, but that the [Ca2+]0 changes were more localized than the [K+]0 changes. 3. Combining real-time current-source density measurement with [K+]0 determination and local manganese application, showed that the Mn blocked parallel fiber-Purkinje cell synaptic transmission, but that much of the [K+]0 changes persisted. Thus, a large part of the [K+]0 flux most probably originated in the parallel fibers. In contrast, [Ca2+]0 changes were abolished by the Mn, indicating that the decrease in this ion was probably associated with synaptic transmission or dendritic events. 4. In a few cases, spreading depression occurred in the cat cerebellar cortex. This could be accompanied by decreases in [Ca2+]0 to as low as 0.12 mM and increases in [K+]0 in excess of 48 mM. 5. These results show that significant changes in [Ca2+]0 and [K+]0 occur during cerebellar stimulation and indicate possible origins of the ion fluxes in terms of neuronal elements. This work also shows that the cerebellar cortex of the cat can support spreading depression. The present results, together with those of earlier studies on [Ca2+]0 and [K+]0 changes in the presence of aminopyridine in the cat cerebellum, suggest that synaptic or dendritic electroresponsive properties may play a role in the observed [Ca2+]0 and [K+]0 changes.

Animals↗

PubMed1990

Dysplastic granulo-molecular hypertrophy of the cerebellar cortex (L'hermitte-Duclos disease): report of three cases.

In this paper three cases with peculiar disease of the cerebellar cortex are presented. The disease is well known as L'hermitte-Duclos disease (LDD), but nowadays it is also called "dysplastic granulo-molecular hypertrophy of the cerebellar cortex" according to the modern theories of its etiology. Curious changes of the cerebellum in LDD are probably the result of a combination of delayed migration of Purkinje cells which occurs during the intrauterine period of cerebellar development, and of reactive hypertrophy of granular cells. Presented cases of L'hermitte-Duclos disease are, according to the literature, more or less typical by their clinical appearance and by their histological findings. Our electromicroscopical data support the findings of those authors who found only axodendritic sinapses on the hypertrophied ganglion cells, according to the idea that those cells are originally granular cells of the cerebellar cortex. CT scan of all our patients revealed parallel, worm-like, hyperdense formations in a hypodense process of the cerebellum. The same picture existed in some other described patients, but attention was paid to it. We consider this picture on the computed tomography to be characteristic, if not even patognomonic for the L'hermitte-Duclos disease, which gives us an entirely new scientific contribution in the process of the diagnosis of this peculiar disease.

Adult↗

PubMed1994

Inhibition of classically conditioned eyeblink responses by stimulation of the cerebellar cortex in the decerebrate cat.

The purpose of the present study was to test the hypothesis that neurones in the anterior interpositus nucleus, under the control of Purkinje cells in the c1 and c3 zones of the cerebellar cortex, exert some control over classically conditioned responses. In particular, the experiments were designed to determine whether the cerebellar control of conditioned and unconditioned responses is different. The experiments were performed on cats decerebrated rostral to the red nucleus under halothane anaesthesia. The cats were conditioned using either a 1000 Hz tone or trains of stimuli through the skin of the proximal forelimb as the conditioned stimulus, and periorbital electrical stimulation as the unconditioned stimulus. A large proportion of the animals acquired conditioned responses at normal rates. It could be shown that these were true conditioned responses and did not result from sensitization or pseudoconditioning. For instance, unpaired presentations of conditioned and unconditioned stimuli caused rapid extinction. Cerebellar areas controlling eyeblink were identified by recording climbing fibre responses in the cerebellar cortex and recording EMG activity in the eyelid evoked by stimulation of the cerebellar cortex. When single shocks of 40-70 microA were applied to these areas during the emission of conditioned eyeblink responses, the latter were strongly inhibited. The inhibition had a latency of about 10 ms and a duration of 25-75 ms. It was shown that this inhibition of the conditioned responses was topographically specific and could only be evoked from cortical sites identified as controlling eyeblink. Stimulation of the periphery of an eyeblink area caused little or no inhibition. The effect of cortical stimulation on unconditioned reflex responses in the orbicularis oculi muscle was also tested. Some inhibition of unconditioned responses was observed, but quantitative analysis showed that this inhibition was considerably weaker than the corresponding inhibition of conditioned responses. The magnitude of the inhibition was determined for unconditioned responses of different sizes including responses which were weaker than the conditioned responses. It is concluded that conditioned eyeblink responses are under strong cerebellar control from areas in the c1 and c3 zones receiving climbing fibre input from the periorbital area. This effect is not likely to be due to a reduction in the background facilitation of facial motoneurones. In contrast, the weak inhibition of the unconditioned response was probably due to this mechanism. The results, therefore, suggest that the conditioned responses are dependent on the cerebellum in a way that is not true of unconditioned responses.

Animals↗

PubMed1990

The prevalence of amyloid (A4) protein deposits within the cerebral and cerebellar cortex in Down's syndrome and Alzheimer's disease.

The extent of amyloid deposition within the cerebellum and the cerebral cortex was assessed and compared, using anti-amyloid protein (A4) immunostaining and a novel methenamine silver method, in 20 patients aged between 60 and 77 years with Alzheimer's disease (AD), 29 patients aged between 13 and 71 years with Down's syndrome (DS), 26 demented patients with disorders other than AD and DS and in 20 non-demented elderly individuals of age range 60-102 years. In AD, amyloid deposits were noted in the cerebellar cortex in 90% of patients and in the meningeal vessels of the cerebellum in 80% of patients. In DS, amyloid deposits were seen in the cerebellar cortex in 82% of patients over 30 years of age and was universal in patients over 50 years of age. Overall, in DS, amyloid deposits were present in the meningeal vessels of the cerebellum in 79% of patients, but were present in 94% of those patients over 50 years of age. The sites of amyloid deposition in the cerebellar cortex were (poorly) detected by lectin histochemistry (Concanavalin A binding) in only 40% of patients with AD and 43% of all patients with DS (69% of those over 50 years of age). No amyloid deposits were seen in either the cerebellar cortex or its meningeal vessels in any of the 20 non-demented elderly individuals nor in any of the non-Alzheimer demented patients. The cerebellar amyloid deposits were never associated with a neuritic change [i.e. as characterised by the presence of (tau-positive) paired helical filaments (PHF)] and neurofibrillary tangles were seen only in a few cells of the dentate nucleus in a single patient with AD and in three of the elderly DS patients. Amyloid deposits were numerous in the cerebral cortex of all patients with AD and in all, except the 13-year-old patient, with DS. In all the AD patients and in most of the DS patients over 30 years of age, many of the cerebral cortical amyloid deposits were associated with neurites and were strongly recognised by lectin histochemistry. Amyloid deposits were present within the meningeal vessels of the cerebral cortex in 75% patients with AD and 72% of patients, over 30 years of age, with DS (82% of those over 50 years of age). These data indicate that the process of amyloidosis in AD and in elderly DS patients is not restricted to the cerebral cortex and may affect other grey matter regions, particularly the cerebellum.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1979

Mossy and climbing fibre mediated responses evoked in the cerebellar cortex of the cat by trigeminal afferent stimulation.

1. The trigeminal input to the cerebellar cortex was studied by recording mass and unitary resonses evoked by electrical stimulation of individual trigeminal cutaneous and muscle nerve branches, in cats lightly anaesthetized with sodium thiopentone. 2. The trigeminal projection area of the cerebellar cortex comprised essentially lobule HVI, but included adjacent folia of lobules HV and HVIIA. 3. Each trigeminal branch had a 'patchy' representation throughout the projection area and there was extensive convergence of individual afferents at each site. Exact combinations of convergent inputs varied between loci, the projection from the muscle nerve being weaker. No other differential representation of individual trigeminal branches was evident. 4. Responses were evoked by stimulation of both ipsi- and contralateral trigeminal afferents but contralateral projections were present at fewer sites. 5. Mass responses to stimulation of individual trigeminal branches comprised mossy fibre and climbing fibre-mediated potentials, although both components were not always present. Latencies for mossy and climbing fibre responses, evoked by ipsilateral nerve stimulation, were in the ranges 5--8 msec and 11--29 msec respectively. 6. Unitary responses of Purkinje cells activiated by trigeminal inputs also revealed convergence from individual ipsilateral afferent sources (28% influenced by one ipsilateral trigeminal branch, 48% by two branches, 17% by three branches and 7% by four branches). 7. Response patterns comprised one or more of the following: short latency (3--8 msec) simple, mossy fibre-mediated spikes, 'delayed' (10--25 msec) simple spikes and climbing fibre-mediated multiple spike bursts (9--35 msec).

Afferent Pathways↗

PubMed1992

The Effect of Kainic Acid Lesions of the Cerebellar Cortex on the Conditioned Nictitating Membrane Response in the Rabbit.

In previous studies we have shown that aspiration lesions centred on lobule HVI in the cerebellar cortex of rabbits produce a profound loss of conditioned nictitating membrane (NM) responses. Because aspiration lesions of the cerebellar cortex cause retrograde degeneration in precerebellar nuclei we tested in rabbits whether excitotoxic lesions of the cerebellar cortex that spare these precerebellar nuclei also cause a loss of conditioned NM responses. Following discrete injections of kainic acid into HVI and rostral regions of the adjacent folia of crus I and crus II, we observed an immediate loss of conditioned NM responses. Following extensive retraining several subjects showed a gradual recovery of conditioned responses. But subjects with the most complete lesions never recovered more than a few conditioned responses. Kainic acid lesions did not change ipsilateral unconditioned reflex responses to a range of stimulus intensities. The kainic acid injections caused obvious degeneration of Purkinje and granule cells but not of the precerebellar nuclei. We conclude that HVI and parts of crus I and crus II are essential for normal retention of conditioned NM responses.

Journal Article↗

PubMed2000

Analysis of protein pool of neuronal populations of cerebellar cortex in rodents of different species.

The protein pool of neuronal population of the cerebellar cortex was studied by interference cytometry in rodents occupying different ecological niches and differing by life style, nutrition habits, and motor activity. In all cell populations protein concentrations in the cytoplasm were higher than in the nucleus in all studied rodents and did not depend on the functional characteristics of neurons. The extreme values of protein content were determined for populations of granular and ganglion cells. High protein concentrations per volume unit of cell structure were detected in functionally different cerebellar neurons of gray rats, characterized by high motor activity and a certain degree of synanthropy, while low values were detected in mole rats, slow-moving underground rodents. Therefore, the specific protein pool of neuronal populations of the cerebellar cortex of rodents can be regarded as adaptation to habitation conditions.

Animals↗

PubMed1977

Ultastructural analysis on acetylcholinesterase localization in the cerebellar cortex of teleosts.

The histochemical localization of acetylcholinesterase (AChE) was studied by electron microscopy in the cerebellar cortex of the goldfish and the catfish. The patterns of enzyme distribution show noticeable differences in the two teleost species at the level of the corresponding cerebellar structures. Among the most distinctive features is the prevailing intracellular localization of enzyme activity in the goldfish and the prevailing extracellular localization in the catfish in the molecular layer and, to a lesser extent, the granular layer. Only quantitative differences in the ability to synthesize AChE can be recorded among the different cerebellar neurons in the two species, since all these neurons exhibit different amounts of enzyme activity linked to their cytoplasmic structures. Comparing the results obtained with those of previous histochemical, experimental and developmental researches, the hypothesis seems well founded that the embryonic pool of cerebellar neurons is made up of AChE-synthesizing nruroblasts which, during development, loss or maintain to a different the mechanisms for AChE synthesis. In addition the light and electron microscope histochemistry reveals at different levels of resolution that the final pattern of AChE distribution in the cerebellar cortex is the sum of different degress of AChE synthesis by cerebellar neurons and different degrees of enzyme release in extracellular spaces.

Acetylcholinesterase↗

PubMed1981

Role of the Staggerer gene in determining Purkinje cell number in the cerebellar cortex of mouse chimeras.

Staggerer (sg) is a mutation in mice which causes severe cerebellar atrophy. Virtually all of the granule cells degenerate by the end of the first postnatal month. The Purkinje cells are also affected. They are reduced in number, ectopic in location, reduced in size and show a regional variation in their cytological appearance. The appearance of the cerebellar cortex of Staggerer in equilibrium wild-type chimeric mice has demonstrated that the reduced size, ectopia, and regional variation are always traits of cells whose nucleus is of sg/sg genotype and thus are due to factors intrinsic to the affected cell. This report is a quantitative analysis of the cerebellar cortex of two Staggerer chimeras. Sections were chosen from serially sectioned half cerebella. Using beta-glucuronidase activity as an independent marker of a cell's genotype, cells were scored as belonging to 1 of 3 cell classes: wild-type Purkinje cell, wild-type Golgi cell, and Staggerer medium-to-large neuron. The results confirm that the total number of cells in the chimera (all 3 classes) is greater than that found in a homozygous Staggerer but less than that found in a wild-type. Further, the distribution of the two genotypes strongly suggests that the decreased number of cells in Staggerer and in the chimera is due to an intrinsic defect in the Staggerer cells and not to a general (extrinsic) compromising of cerebellar development. Possible implications for normal cerebellar development are discussed.

Animals↗