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R Hawkes

Publications and source records attributed to R Hawkes.

At least 73 records · Page 4Linked to original sources
PubMed1990

Expression of compartmentation antigen zebrin I in cerebellar transplants.

The mammalian cerebellum is divided into multiple parasagittal compartments as defined by the organization of afferent and efferent projections and by the pattern of expression of several biochemical markers. One such marker is the antigen zebrin I, a 120 kD polypeptide of unknown function that is expressed differentially by a subset of Purkinje cells. Zebrin I+ Purkinje cells are grouped into an array of 14 parasagittal bands interposed by zebrin I- compartments. This Purkinje cell compartmentation corresponds to compartments in the olivocerebellar projection. The afferent axon compartments are present prior to the expression of the mature zebrin I phenotype, thus raising the possibility that differential afferent input regulates the zebrin I phenotype of the target of that input. Lesion studies in the neonate preclude a role for afferent inputs in the regulation of zebrin I expression postnatally, but a prenatal role in commitment still remains open. To explore this possibility, cerebellar anlagen were dissected from embryos at embryonic days 12-15, that is, prior to any contact with afferents, and transplanted ectopically into adult hosts. In the first series of experiments, the grafts were placed into the anterior chamber of the eye, and in the second series, into cavities prepared in the neocortex. Grafts were allowed to mature and then were immunoperoxidase or immunofluorescence stained for zebrin I immunoreactivity. Zebrin I was expressed by grafted Purkinje cells in cortico and in oculo. Double-labelling experiments confirmed that both the zebrin I+ and the zebrin I- phenotypes were present. The zebrin I immunoreactivity revealed that the zebrin I+ Purkinje cells resemble those in situ with an extensive dendritic arborization that extends through the molecular layer perpendicular to the long axes of the folia. In conclusion, the present data suggest that afferent input does not play a role in the determination of the zebrin I phenotype of Purkinje cells.

Animals↗
PubMed1990

Zebrin II: a polypeptide antigen expressed selectively by Purkinje cells reveals compartments in rat and fish cerebellum.

Monoclonal antibody mab-zebrin II was generated against a crude homogenate of cerebellum and electrosensory lateral line lobe from the weakly electric fish Apteronotus leptorhynchus. On Western blots of fish cerebellar proteins, mab-zebrin II recognizes a single polypeptide antigen of apparent molecular weight 36 kD. Immunocytochemistry of apteronotid brains reveals that zebrin II immunoreactivity is confined exclusively to Purkinje cells in the corpus cerebelli, lateral valvula cerebelli, and the eminentia granularis anterior. Other Purkinje cells, in the medial valvula cerebelli and eminentia granularis posterior, are not zebrin II immunoreactive. Immunoreactive Purkinje cells are stained completely, including dendrites, axons, and somata. The antigen seems to be absent only from the nucleus. A similar distribution is seen in catfish, goldfish, and a mormyrid fish. Zebrin II immunoreactivity is also found in the rat cerebellum. Western blotting of rat cerebellar proteins reveals a single immunoreactive polypeptide, with apparent molecular weight 36 kD, as in the fish. Also as in the fish, staining in the adult rat cerebellum is confined to a subset of Purkinje cells. Peroxidase reaction product is deposited throughout the immunoreactive Purkinje cells with the exception of the nucleus. No other cells in the cerebellum express zebrin II. At higher antibody concentrations, a weak glial cross reactivity is seen in most other brain regions: we believe that this is probably nonspecific. Zebrin II+ Purkinje cells are clustered together to form roughly parasagittal bands interposed by similar nonimmunoreactive clusters. In all there are 7 zebrin II+ and 7 zebrin II- compartments in each hemicerebellum. One immunoreactive band is adjacent to the midline; two others are disposed laterally to each side in the vermis; there is a paravermal band; and finally three more bands are identified in each hemisphere. Both in number and position, these compartments correspond precisely to the bands revealed by using another antibody, mabQ113 (anti-zebrin I). In both fish and rat the compartmentation revealed by zebrin II immunocytochemistry is related to the organization of cerebellar afferent and efferent projections and may provide clues as to the fundamental architecture of the vertebrate cerebellum.

Animals↗
PubMed1990

Organization and postnatal development of zebrin II antigenic compartmentation in the cerebellar vermis of the grey opossum, Monodelphis domestica.

The mammalian cerebellar cortex consists of a number of parasagittal Purkinje cell compartments that can be demonstrated cytochemically. The afferent inputs to the cerebellum are also compartmentalized, and a complex but reproducible relationship exists between the afferents and the intrinsic maps. Developmental studies in the rat have shown that many of the main features of compartmentation are already established at birth, and are therefore not easily manipulated experimentally. The compartmentation antigen zebrin II is expressed selectively by Purkinje cell subsets in a range of species, including fish and primates. In this study, zebrin II immunoreactivity has been studied in the grey opossum, Monodelphis domestica, in order to develop a marsupial model of compartment formation in which the early developmental events are more readily accessible. A monoclonal antibody to zebrin II from the weakly electric fish Apteronotus recognizes a 36 kD polypeptide in homogenates of Monodelphis cerebellum that appears to be identical to the antigen in the rat. Immunocytochemistry reveals that zebrin II in adult Monodelphis is confined exclusively to the cerebellum, where it is expressed by a subset of Purkinje cells. All regions of the cell, except the nucleus, are stained. The zebrin II+ Purkinje cells are arranged in a set of parasagittal compartments interposed by similar zebrin II- compartments. In each hemicerebellum there is one zebrin II+ band abutting the midline (P1+), and two others laterally in the vermis (P2+, P3+). A fourth zebrin II+ compartment straddles the paravermian region (P4+). Three other compartments have been identified in the hemisphere (P5+, P6+, P7+). This arrangement is very similar to that found in the rat. During postnatal development, zebrin II is first expressed between P14 and P21 in Purkinje cells of the posterior lobe vermis, and spreads throughout the cerebellar cortex by P28. As in rat, there is a stage at which all Purkinje cells are zebrin II+, including those destined to be zebrin II- in the adult. The mature pattern of expression emerges after P35 as immunoreactivity gradually disappears from the cells destined to become zebrin II-. The adult appearance is attained only after P56. The developmental timetable is therefore similar to that in rat, but is rather more protracted. Monodelphis should prove to be a valuable experimental model in which to study the early events leading to the formation of cerebellar compartments.

Animals↗
PubMed1990

Parasagittal organization of the rat cerebellar cortex: direct comparison of Purkinje cell compartments and the organization of the spinocerebellar projection.

Retrograde and anterograde transport of tracers, electrophysiological recording, somatotopic mapping, and histochemical and immunological techniques have all revealed a parasagittal parcellation of the cerebellar cortex, including its efferent and many of its afferent connections. In order to establish whether the different compartments share a common organizational plan, a systematic comparative analysis of the patterns of parasagittal zonation in the cerebellar cortex of the rat has been undertaken, by using the parasagittal compartmentation of zebrin I+ and zebrin I- Purkinje cells as revealed by monoclonal antibody Q113 as a reference frame. The distribution of mossy fiber terminals originating from the lower thoracic-higher lumbar spinal cord was compared to the distribution of zebrin I bands. Three-dimensional reconstructions from alternate frontal sections processed either for the anterograde transport of tracer or for zebrin I immunoreactivity reveal that the limits of the spinocerebellar terminal fields in the granular layer correlate well with the boundaries of some, but not all, zebrin I compartments in the molecular layer above. This leads to a subdivision of the zebrin I compartments into spinal receiving and spinal nonreceiving portions. In lobules II and VIII, the spinocerebellar terminal fields assume different positions relative to the zebrin I compartments in the ventral compared to the dorsal faces. Thus, each longitudinal compartment may be further divided transversely into subzones, each receiving a specific combination of mossy fiber afferents. The further subdivision of zebrin I compartments by mossy fiber terminal fields increases the resolution of the topography to such a point that anatomical compartment widths become compatible with the width of the microzones and the patches identified by electrophysiological methods.

Animals↗
PubMed1990

Maturation of the corpus callosum of the rat: I. Influence of thyroid hormones on the topography of callosal projections.

The normal adult rat corpus callosum contains numerous axonal profiles that are immunoreactive for the high molecular weight subunit of the neurofilament triplet (NF-H). NF-H immunoreactivity develops gradually during the first 2 postnatal weeks. The expression of NF-H immunoreactivity is almost completely suppressed in rats rendered hypothyroid by neonatal treatment with propylthiouracil. To ensure that the cytoskeletal deficit was due to a shortage of thyroid hormones rather than to unspecific, toxic effects of propylthiouracil, hypothyroid animals kept on the propylthiouracil diet were given restorative thyroxine injections daily. Such animals express NF-H at normal levels. This suggests that the callosal axons may be arrested at an immature stage of development. The immaturity of the hypothyroid corpus callosum can also be revealed by a comparison of the myelin content in the corpus callosum between normal rats, hypothyroid rats, and hypothyroid rats under thyroxine therapy. Hypothyroid rats are severely deficient in myelin, and again this deficit can be corrected by postnatal thyroxine treatment. During normal callosal development, there is a progressive spatial restriction of the transcallosal projection that creates in the adult patches of callosally projecting cortex interposed by acallosal regions. Given the structural immaturity of the hypothyroid callosal axons, it was interesting to investigate the state of development of their topography. For this purpose, multiple injections of wheat germ agglutinin-horseradish peroxidase were made into the occipital and parietal cortices of adult hypothyroid animals. In normal rats, the majority of visual callosally projecting cells are located in three groups--in area 18b, at the boundary of area 17 and 18a, and in the lateral portion of area 18a. Within these areas projecting cells are concentrated in layers II-III, Va, and Vc-VIa. The callosal axon terminals are concentrated in these same regions, with a laminar distribution as far as the somata plus layer I. In the midportion of areas 17 and 18a, fewer callosal cells are found, and they occupy mainly layers Vc-VIa, as in the case for terminals in these same areas. In the parietal cortex, callosal cells and terminals are disposed in vertical arrays alternating with almost empty zones. Most are concentrated in layers III and V. The topography of the callosal axon terminal fields is unaffected by hypothyroidism. However, there is a dramatic redistribution of the callosally projecting cell somata.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Maturation of the corpus callosum of the rat: II. Influence of thyroid hormones on the number and maturation of axons.

Quantitative electron microscopy has been used to study the number of callosal axons in the corpus callosum of normal and hypothyroid rats during postnatal development. At birth, the normal corpus callosum contains 4.4 x 10(6) axons. This number increases to 11.4 x 10(6) by 5 days of age (P5) and then, in contrast to cats and primates, remains constant until at least P60, the oldest age examined. The number of axons in the corpus callosum of hypothyroid animals is not significantly different from the values observed in normal rats at all ages studied, although the callosal axons of hypothyroid rats remain structurally immature. As extensive elimination of callosal axons has been shown to occur in normal rats past P5, we conclude that new callosal processes grow through the corpus callosum past this age that compensate numerically for the loss. Moreover, as the number of callosally projecting neurons seems to be higher in hypothyroid rats than in normal controls, it seems that the constant axon number derives from more parent neurons, and thus that there are more axon collaterals per callosal neuron in a normal animal than in a hypothyroid one. Taken together, these data indicate that although hypothyroidism does not alter the total number of callosally projecting axons, it interferes with the normal processes that define or sculpt the projection fields, thereby leading to a numerically normal projection with abnormal topography.

Animals↗
PubMed1990

The compartmentalization of the monkey and rat cerebellar cortex: zebrin I and cytochrome oxidase.

The cerebellar cortex of mammals is composed of parasagittal zones that encompass the afferent inputs, the efferent corticonuclear and corticovestibular projections, and a number of intrinsic molecular markers. One such marker is the polypeptide antigen zebrin I that is recognized by monoclonal antibody (mab) Q113. In rodents, zebrin I immunocytochemistry reveals an array of parasagittal Purkinje cell compartments. In the present study, zebrin I has been used to reveal the molecular heterogeneity of the cerebellar cortex in the squirrel monkey (Saimiri sciureus). As in rodents, zebrin I is Purkinje cell specific in the primate cerebellum and not all Purkinje cells are immunoreactive. Immunocytochemistry on frontal or horizontal sections reveals a system of bands of zebrin I+ cells extending through the vermis of both anterior and posterior lobes. A midline (P1+) band and two more lateral bands (P2+ and P3+) are found in all lobules. The situation in the paravermis and hemispheres is similar, with alternating zebrin I+ and zebrin I- compartments, but the complex lobulation obscures the precise band pattern: it seems probable that 4 additional bands are present in the hemispheres, as in rodents. Comparison of rat and monkey cerebellums suggests that the cortex has expanded in primates by the growth of the same individual bands found in rats rather than by the addition of supplementary compartments. The zebrin I compartmentalization revealed by using mab Q113 is reproducible from individual and thus provides a stable frame of reference that has been used to compare the different chemoarchitectonic patterns found in the cerebellar cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Synaptophysin expression during synaptogenesis in the rat cerebellar cortex.

In order to study the mechanisms of synaptogenesis in the rat cerebellar cortex, a library of monoclonal antibodies has been generated against proteins of the isolated synapse. One recognizes a glycosylated 38 kDa protein that is concentrated in the synaptic vesicle fraction and resembles synaptophysin biochemically in its molecular weight, charge, and pattern of glycosylation. In the adult cerebellar cortex, the antisynaptophysin(mabQ155) immunoreactivity is codistributed with synapses. Immunoreactivity is strongest in the molecular layer where punctate deposits of reaction product outline the Purkinje cell dendrites. Discrete small profiles, consistent with the distribution of basket cell axon terminals, surround the Purkinje cells, and in the granular layer the synaptic glomeruli are intensely stained. There is no immunoreactivity in the white matter axon tracts. Electron microscope immunocytochemistry confirms the synaptic location of the antigen and suggests that the reaction product is associated with synaptic vesicles. Both round and flat vesicle populations are immunoreactive. Antisynaptophysin(mabQ155) has been used to follow synaptogenesis in the developing rat cerebellum. In the newborn rat (P0), despite the paucity of synapses, there is some specific immunoreactivity, especially in the subcortical white matter. Electron microscopy shows that the antigenicity is associated with vesicles within growth cones, filopodia, and immature axon profiles. During development, antisynaptophysin immunoreactivity increases progressively, along with the maturing cell populations, for both the granule cell-Purkinje cell and the mossy fiber-granule cell synapses. Quantitative biochemical analysis confirms the cytochemical results. These data suggest that neuronal growth cones express a synapse-specific antigen before complete morphological synapses are present.

Aging↗
PubMed1989

Purkinje cell axon collateral distributions reflect the chemical compartmentation of the rat cerebellar cortex.

Monoclonal antibody mabQ113 has been used to study the distribution of Purkinje cell axon collaterals in the rat cerebellar cortex. MabQ113 recognizes a polypeptide antigen, zebrin I, that is confined to a subset of Purkinje cells. Antigenic Purkinje cells are arranged in parasagittal compartments running throughout the cortex. No other cerebellar cells are immunoreactive. Immunoreactive axon collaterals are confined principally to the infraganglionic plexus with only a few extending into the molecular layer. Three probable target cells for the axon collaterals have been identified: Golgi cells, Lugaro cells, and other Purkinje cells. About 90% of immunoreactive axon collaterals in the anterior lobe are located beneath the mabQ113+ Purkinje cell compartment in which they originate but some do invade the neighboring mabQ113- territory. In the anterior lobe vermis, the distribution of invading mabQ113+ collaterals is not symmetrical, such that the probability of an invading collateral from the P2+ compartment is greater at the medial boundary into P1- than at the lateral into P2-. The distribution of immunoreactive collaterals is consistent with their playing a role in synchronizing the firing of Purkinje cells within the same compartment.

Animals↗
PubMed1988

Development of parasagittal zonation in the rat cerebellar cortex: MabQ113 antigenic bands are created postnatally by the suppression of antigen expression in a subset of Purkinje cells.

Monoclonal antibody mabQ113 recognizes a polypeptide antigen that, in the adult cerebellum, is confined to a subset of Purkinje cells that are clustered together to form parasagittal bands interposed by similar nonimmunoreactive bands. The Purkinje cell compartments are congruent with bands of climbing fibers projecting from subregions of the inferior olivary complex (IOC). The array of mabQ113 parasagittal bands appears late in the development of the cortex. Weak mabQ113 immunoreactivity is first seen at postnatal day 6 (P6) in the Purkinje cells of the posterior lobe of the vermis. From the earliest stages there are signs of differential expression of the mabQ113 antigen in clusters of Purkinje cells: four mabQ113+ clusters are clearly present in the posterior lobe of the vermis at P6-P7. Their relation to the adult band display remains uncertain. During the next few days immunoreactivity spreads rostrally throughout the rest of the vermis and laterally to include the Purkinje cells in the hemispheres, until by P12 all the Purkinje cells in the cerebellum are mabQ113+. Nevertheless, signs of the adult band display are seen already in the vermis where the cells destined to become the vermal mabQ113+ bands (P1+, P2+ and P3+) stain more intensely than their neighbours. Following the stage of global mab113 epitope expression, bands are created by the selective suppression of immunoreactivity by Purkinje cells in the P- regions. By P15 the mabQ113+ and mabQ113- bands are clearly differentiated in the vermis and selective staining has begun to appear in the hemispheres also. The band pattern matures gradually during the third and fourth postnatal weeks until the adult appearance is attained by P30. The cerebellar afferent projections were lesioned to explore the interplay of cerebellar input and mabQ113 expression. The olivocerebellar projection was lesioned bilaterally by using 3-acetylpyridine in the adult and unilaterally in the newborn by electrolytic lesion and unilateral inferior cerebellar pedunculectomy. Mossy fibers from the dorsal and ventral spinocerebellar tracts were lesioned surgically both in adults and in newborn and trigeminal projections to the cerebellum were removed in the newborn by unilateral ablation of the spinal trigeminal nucleus. The consequences of total blockage of vibrissal and hindlimb inputs were also explored in both adults and neonates. None of these treatments led to a modification in the pattern of mabQ113 epitope expression.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1988

Zonation in the rat cerebellar cortex: patches of high acetylcholinesterase activity in the granular layer are congruent with Purkinje cell compartments.

The rat cerebellar cortex is built from parasagittally arranged modules with topographically ordered afferent and efferent projections. The intrinsic organization of the cerebellum is revealed by immunocytochemical staining with monoclonal antibody, mabQ113. In the cerebellum, mabQ113 recognizes a polypeptide epitope that is restricted to a subset of Purkinje cells. Antigenic Purkinje cells are clustered to form a complex pattern of parasagittal compartments. Several biochemical markers reveal a superficially similar organization of the cortex, and so it is important to determine how many independent maps are present. This report compares the mabQ113 antigen display to the patchy distribution of acetylcholinesterase (AChE). In the granular layer and the white matter of the adult cerebellar cortex there is a patchy AChE staining that includes both the hemispheres and the vermis. The staining is often not sharply resolved cytologically, but seems to be associated primarily with the synaptic glomeruli. The boundaries of these granular layer patches in the vermis correspond to the mabQ113+/mabQ113- boundaries of the overlying Purkinje cell compartments. Thus, AChE and mabQ113 antigen share a common compartmentation both in the vermis, and in the hemispheres. Both mabQ113 and AChE distributions develop postnatally in the cerebellar cortex. At birth (PO) there is neither AChE activity nor mabQ113 immunoreactivity. Both staining patterns emerge during the second postnatal week. In the vermis at P10, there is AChE activity in the granular layer and white matter, and the distribution is already patchy despite the absence of synaptic glomeruli. At the same age the mabQ113 immunoreactivity is found in all Purkinje cells rather than a subset, and the band pattern has yet to mature. There is also transient AChE staining of Purkinje cell somata and dendrites. The AChE patches clarify between P10 and P20 along with the appearance of the synaptic glomeruli and the development of differential mabQ113 staining, but there is no reason to believe that the two are causally linked. In contrast to the cerebellar cortex, AChE staining in the cerebellar nuclei matures very early and at P0 the activity is already high. Zones of high and low AChE activity are seen in all the cerebellar nuclei and may be related to the distribution of the terminal fields of the different Purkinje cell populations.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholinesterase↗
PubMed1988

Expression of monoclonal antibody Q113 immunoreactivity in the rat cerebral cortex: unique differential sublayering of layer I: staining of radial glia.

Monoclonal antibody mabQ113 recognizes a 120-kilodalton polypeptide which, in the cerebellar cortex, is confined exclusively to a subset of Purkinje cells which are organized in parasagittal bands (Hawkes et al.: Brain Research 333:359-365, 1985). In all other areas of the adult rat brain examined the localization of the mabQ113 epitope was marked by regional neuronal and glial co-expression (Plioplys and Hawkes: Brain Research 375:1-12, 1986). Similar neuronal-glial co-expression was characteristic of the adult rat cerebral cortex. Intriguingly, mabQ113 revealed a unique differential sublamination of layer I. In the neocortex, layer I was split into two sublayers, with the more superficial sublayer weakly stained and the deeper sublayer stained more intensely, whereas in the pyriform cortex, layer I was split into three. These sublaminations do not correspond to previously described subdivisions of layer I. In the developing cortex, the mabQ113 epitope is found in radial glial fibers. Stained radial fibers are first seen beginning at E17, reach a maximum at P4 and finally disappear between P12 and P14. The laminar distribution of mabQ113-immunoreactivity emerges earlier in the pyriform cortex than the neocortex: the sublamination of layer I is seen at P4 in the pyriform cortex but not until P8 in the neocortex. The significance of these observations is discussed.

Aging↗
PubMed1987

Parasagittal organization of the rat cerebellar cortex: direct correlation between antigenic Purkinje cell bands revealed by mabQ113 and the organization of the olivocerebellar projection.

The Purkinje cells of the cerebellar cortex and the cortical afferent and efferent projections are organized into parallel parasagittal zones. The parasagittal organization is clearly revealed by immunocytochemistry with a monoclonal antibody, mabQ113. The mabQ113 antigen is confined to a subset of Purkinje cells that are clustered together to form an elaborate, highly reproducible pattern of bands and patches, interspersed with similar mabQ113- regions. The mabQ113+ territories have been classified into seven parasagittal bands (P1+-P7+) in each hemicerebellum. The degree of correspondence between the compartments revealed by the anterograde labeling of the olivocerebellar projection and by mabQ113 immunocytochemistry has been explored in the adult rat. Horseradish peroxide-wheat germ agglutinin conjugate was injected as an anterograde tracer into the inferior olivary complex. When the injection site did not encompass all the olive, an incomplete, patchy labeling of the molecular layer was seen in the cerebellar cortex. Labeled zones of the molecular layer were interrupted by unlabeled regions to give a pattern of parasagittal cortical bands. The positions of these bands were compared with the distribution of the mabQ113+ antigenic bands as seen on the two adjacent sections. Labeled climbing fibers were found to terminate on both mabQ113+ and mabQ113- Purkinje cell zones. The mabQ113+/mabQ113- boundaries and the bands of climbing fibers seen by using the anterograde tracer typically coincide. The one consistent exception is the midline band of mabQ113+ Purkinje cells, P1+. The normal olivocerebellar projection is exclusively contralateral and the climbing fiber projection to the paramedian vermis splits P1+ down the middle, implying that it consists of two adjacent mabQ113+ bands not separated by mabQ113-territory. It is likely that the climbing fiber projection to the cerebellar cortex and the distribution of the two Purkinje cell phenotypes share a common compartmental organization.

Afferent Pathways↗
PubMed1987

Thyroid hormone modulates the expression of a neurofilament antigen in the cerebellar cortex: premature induction and overexpression by basket cells in hyperthyroidism and a critical period for the correction of hypothyroidism.

Neurofilament expression by basket cells of the cerebellar cortex is suppressed in hypothyroidism. By using a monoclonal antibody (mabN210) that selectively recognizes an epitope associated with the 210-kDa neurofilament subunit, we have explored the relationship between thyroid hormone levels and basket cell maturation. In animals rendered hypothyroid by inclusion of propylthiouracil in the maternal drinking water from embryo age E17, there is a complete absence of mabN210 immunoreactivity in the basket cell axons, while the other immunoreactive axons in the cerebellar cortex, primarily Purkinje cell axons and mossy fibers, are apparently unaffected. This deficit can be corrected by treatment with thyroid hormone but there seems to be a critical period for full recovery, for animals treated from birth recover normally whereas there is a gradual diminution in the efficacy of treatment the later it begins. Thyroid hormone therapy begun after postnatal day 30 (P30) leads only to very minor recovery. By contrast, animals on a hyperthyroid regime show premature mabN210-antigen induction in the basket cells and supranormal levels of expression at P25, despite the severe reduction in the number of basket cell somata. This suggests either abnormal compensatory sprouting of axon collaterals by the remaining basket cells or the occurrence, during normal cerebellar corticogenesis, of competition between basket cell axons for a limited number of Purkinje cell targets followed by the elimination of the excess collaterals.

Animals↗