摘要:

AbstractDuring certain sensitive periods early in postnatal life, the anatomical and physiological development of the central visual pathways of cats and monkeys can be affected by the nature of an animal's early visual experience. In the last few years, studies have been started on some of the molecular and biochemical events that underlie the many functional changes induced by early selected visual deprivation in the visual cortex of kittens. In this respect, the monoclonal antibody Cat‐301 provides a potentially powerful tool, because it recognizes in the cat dorsal lateral geniculate nucleus (dLGN) a proteoglycan associated with the surface of a particular class of cells, namely Y cells. In the dLGN, the Cat‐301 proteoglycan appears late in postnatal development, and its expression has been shown to be experience dependent in both the dLGN and visual cortex (M. Sur, D. Frost, and S. Hockfield, 1988, J. Neurosci.8:874–882; A. Guimaraes, S. Zaremba, and S. Hockfield, 1990, J. Neurosci. 10:3014–3024).We have explored further the experience‐dependent nature of Cat‐301 expression in the dLGN with a view to establishing a biochemical correlate of the many functional changes induced by early monocular deprivation and its reversal in the kitten visual system. In addition to demonstrating differences in Cat‐301 expression between deprived and nondeprived laminae of the dLGNs of kittens monocularly deprived to only 4 or 5 weeks of age, the magnitude of the laminar difference was found to increase as the period of deprivation was extended. Moreover, monocularly deprived kittens that subsequently received long periods of reverse lid suture exhibited a reversal of the pattern of immunoreactivity, so that the greatest immunoreactivity occurred in laminae innervated by the initially deprived eye. However, possibly the most surprising and important finding was the extremely low levels of immunoreactivity observed in both A laminae of monocularly deprived animals that had received relatively short periods of reverse lid suture. These data suggest that Y cell development can be drastically altered depending on the time of initiation of the period of reverse lid suture and its duration. © 1995 W

ISSN:0092-7317    

DOI:10.1002/cne.903590402

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractCone photoreceptors in the zebrafish retina are arranged in a crystalline lattice, with each spectral subtype at a specific position in the array: rod photoreceptors are inserted around the cones. Patterning events and developmental mechanisms that lead to the formation of the cone mosaic are not known. To begin investigating this issue, we examined the initial stages of opsin expression in zebrafish embryos by in situ hybridization with goldfish opsin cRNA probes to determine how and when the cone mosaic pattern arises. We found both differences and similarities in the spatiotemporal patterns of rod and cone development, which suggest the following: (1) Expression of opsin message (including rod opsin, blue and red cone opsins) was initiated at 50–52 hours postfertilization by a few photoreceptors which were consistently found in a ventral patch of retina located nasal to the choroid fissure. (2) The cone mosaic pattern was generated by a crystallization‐like process initiated in the precocial ventral patch and secondarily in nasal retina, which then swept like a wave into dorsotemporal retina. (3) The pattern of differentiation of rods in the ventronasal patch differed substantially from that in the remainder of the retina, suggesting that these precocial rods might differ from typical rods. (4) Developmental maturation of rods in zebrafish, as reflected by expression of opsin, may be accelerated compared to cones, which are thought to become postmitotic before rods. These data are consistent with a model in which lateral inductive interactions among differentiating photoreceptors lead to patterning of the array. © 1995 Wiley‐Lis

ISSN:0092-7317    

DOI:10.1002/cne.903590403

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractThe visual wulst is the telencephalic target of the thalamofugal visual pathway of birds, and thus the avian equivalent of the striate cortex of mammals. The anterograde tracerPhaseolus vulgarisleucoagglutinin was used to follow the intratelencephalic connections of the major constituents of the visual wulst in pigeons. In particular, efferent pathways from the granular layer (Intercalated nucleus of the hyperstriatum accessorium, IHA), supragranular layer (hyperstriatum accessorium, HA), and infragranular layers (hyperstriatum intercalatus superior and/or hyperstriatum dorsale, HIS/HD) were investigated. These efferent projections were confirmed by injections of the retrograde tracer cholera toxin subunit B into their terminal fields.When a deposit of the anterograde tracer was centered in IHA, which receives the visual thalamic input, efferent fibers were seen to extend mainly dorsomedially to HA. When a deposit of the anterograde tracer was centered in HA, efferent fibers were seen to extend mainly in three directions: (1) medially to the tractus septomesencephalicus, which sends projections to extratelencephalic visual nuclei; (2) ventrolaterally to the lateral portion of the neostriatum frontale, where there were also labeled cells after the retrograde tracer was injected in HA; and (3) ventromedially to the paleosfriatal complex, which is the avian equivalent of the mammalian basal ganglia. Furthermore, relatively minor terminal fields were seen in (4) the neostriatum caudale, (5) neostriaturn intermedium, (6) archistriatum intermedium, and (7) hyperstriatum laterale. Finally, HIS/HD have projections predominantly to HA and the dorsocaudal telencephaion (area corticoidea dorsolateralis and area parahippocampalis), as well as relatively minor projections to the areas which also receive projections from HA. No anterogradely labeled fibers were seen in the tractus septomesencephalicus following the tracer injections in HIS/HD.These results indicate that the visual information from the granular layer is distributed via the supragranular layer HA to multiple areas within the telencephalon, such as the neostriatum frontale and paleostriatal complex. In addition, HA is the source of an extratelencephalic projection via the tractus septomesencephalicus. Thus, the avian supragranular layer HA contains neurons which are the source of both intratelencephalic and extratelencephalic projections, whereas neurons of the mammalian cortex are segregated into two distinct layers, supragranular and infragranular layers, based on the targets of their projections. The findings are further discussed and compared to the mammalian striate cortex. © 1995 Wiley‐Liss, I

ISSN:0092-7317    

DOI:10.1002/cne.903590404

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractExperimental lesions have been widely used to induce neuronal degeneration and to test the ability of trophic molecules to prevent lesion‐induced alterations, but these studies have not demonstrated unequivocally that afflicted neurons die as a result of these manipulations. The documentation of neuronal death in the above‐described models and the time when it occurs after injury are crucial for the interpretation of trophic effects. In the present study, we combined multiple approaches to investigate the nature of retrograde neuronal changes in holinargic neurons of the medial septal nucleus (MSN) after complete, unilateral transection of the fimbria‐fornix (F‐F). Projection neurons of the MSN were prelabeled with the fluorescent tracer Fluoro‐gold (FG) 1 week prior to lesion. By counting both FG‐labeled and choline acetyltransferase (ChAT)‐immunoreactive neurons in the MSN at multiple time points postaxotomy, we differentiated the phenotypic response to injury from the degenerative process and established a critical time between the third and fourth weeks postaxotomy, during which ∼ 50% of fluorescent perikarya disappear. Working in the previous time window, we identified dying cells by electron microscopy (EM) and terminal transferase‐mediated (TdT) deoxyuridine triphosphate (d‐UTP)‐biotin nick end labeling (TUNEL) and showed that MSN neurons die via apoptosis, beginning at 16 days postaxotomy. An additional group of animals was allowed to survive for 1 month (i.e., 10 days after cell death has been completed); during this period, animals were treated with intraventricular nerve growth factor (NGF). Quantitative analysis of surviving cholinergic perikarya showed that NGF prevented retrograde degeneration of the majority of neurons. In concert, the results of the present study establish that NGF does not merely protect the phenotype but also prevents cell death in lesioned central cholinergic neurons.

ISSN:0092-7317    

DOI:10.1002/cne.903590405

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractTo help clarify the distinction between the nerve growth factor (NGF)‐dependent collateral sprouting of sympathetic nerves and their NGF‐independent regeneration after crush, we used 6‐hydoxydopamine (OHDA) to destroy the sympathetic terminals in adult rats; this leaves the axons damage‐free. Would recovery occur by regeneration and/or collateral sprouting? A single 6‐OHDA injection abolished the sympathetic pilomotor field revealed by electrical stimulation of a cutaneous nerve. Recovery began within 2 days, and by 20 days the field was reestablished. If the field was “isolated” by adjacent denervations at the time of 6‐OHDA treatment, the recovering pilomotor field expanded extensively into the surrounding territory. In the presence of anti‐NGF, however, the pilomotor field expansion ceased at about 60% of its former size; if anti‐NGF treatment was discontinued, expansion recommenced and extended into the surrounding skin. We suggest that the latter, NGF‐dependent, growth phase corresponds to collateral sprouting, and the initial NGF‐independent one to regeneration. After simple nervecrush, however, such regeneration can triple the normal sympathetic field size. This difference between crush‐ and 6‐OHDA‐induced regeneration might relate to the “cell body reaction” (CBR); the CBR is reduced with increasing distance of the lesion and is undetectable after a 6‐OHDA lesion. Since the CBR and the vigor of regeneration are both increased by repeated axonal injury, we tested the effects ofmultiple6‐OHDA treatments; this significantly increased the initial NGF‐independent expansion. We hyprthesize that regeneration is regulated largely by mechanisms associated with the CBR, and that neurotrophin‐dependent collateral sprouting occurs indep

ISSN:0092-7317    

DOI:10.1002/cne.903590406

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractThe complementary pattern of immunohistochemical staining for the calcium‐binding proteins parvalbumin (PV) and calbindin D‐28k (CB) was used to delineate four major subdivisions of the rabbit medial geniculate body (MGB). PV immunoreactivity predominates in the ventral and medial divisions, whereas CB‐immunoreactiv cells characterize the dorsal and internal divisions. The ventral nucleus is strongly PV+ due to dense neuropil labeling and moderately labeled somata. The medial nucleus contains both medium‐sized and large PV+ somata, as well as thick PV+ axons and terminals. The wedge‐shaped internal nucleus, composed of densely labeled CB+ cells, separates the dorsal and ventral nuclei rostrally, and expands caudally to encapsulate the posterior MGV. Large multipolar CB+ neurons with radiate dendrites characterize the dorsal nucleus. The differential expression of PV and CB also distinguishes the deep dorsal and superficial dorsal subnuclei in the dorsal division and a ventrolateral component in the ventral division. A comparison with studies of MGB connectivity in a variety of species suggests that PV immunoreactivity is highest in subdivisions that receive a substantial input from the central nucleus of the inferior colliculus and that project to primary auditory cortex. In contrast, CB immunoreactivity characterizes nuclei that receive input primarily from other sources, such as the paracentral nuclei of the inferior colliculus, the lateral tegmentum, and the spinal cord, and that project to secondary auditory areas. The ability of calcium‐binding protein immunohistochemistry to delineate neuronal compartments across indistinct cytoarchitectonic borders makes it a powerful tool for guiding future connectional and physiological studies of the MGB. © 1995 Wil

ISSN:0092-7317    

DOI:10.1002/cne.903590407

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractThe perireticular nucleus is a recently described thin sheet of small cells among the fibres of the internal capsule, lying lateral to the thalamic reticular nucleus and medial to the globus pallidus (Clemence and Mitrofanis [1992]. J. Comp. Neurol.322:167–180). During development, the perireticular nucleus is relatively large, lying in the path of the growing corticofugal and thalamocortical axons and filling the area of the internal capsule lateral to the thalamic reticular nucleus. After these axons have formed their connections, the perireticular nucleus rapidly decreases in size, leaving only a few cells in the adult (Mitrofanis [1992] J. Comp. Neurol.320:161–181).In this study, we aiwed to investigate the connections between the developing cortex and thalamus by making injections of tracer into the cortical plate. Injections of Horse Radish Peroxidase (HRP), Wheat Germ Agglutinin bound to HRP (WGA‐HRP) and l'dioctadecyl 3, 3, 3′, 3 tetramethycarbocyanine perchlorate (DiI) were made in vivo between embryonic day (E)18 and adult and DiI was placed in the fixed brains of rats aged between E16 and postnatal day (P)1.Between E17 and P10, the retrograde perikaryal labelling resulting from these injections revealed a transient projection from the perireticular nucleus to the ipsilateral cortical plate. No cells were labelled in the thalamic reticular nucleus.This suggests that the perireticular nucleus must be regarded as a group of cells distinct from the thalamic reticular nucleus and having a separate role in development. Comparisons between the perireticular cells and the cells of the cortical subplate suggest that both may be playing comparable roles in early development, possibly guiding fibres towards their end stations or serving to rearrange the complex mapped projections linking thalamus and cortex. © 1995 Wiley

ISSN:0092-7317    

DOI:10.1002/cne.903590408

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractThe present study used autoradiography to determine the location of the projections of presumptive peripheral afferent neurons into the central nervous system ofAplysia. Selected peripheral tissues (with an empliasis on structures involved in feeding behavior) were exposed to radioactive amino acids, and the distribution of macromolecules transported into the nervous system via afferent fibers was determined by autoradiography. Different regions of the body exhibited different patterns of projections, and within the neuropil of the cerebral ganglion, there was a loose topographical prganization of projections from the head. For some regions of the body, the projection was largely limited to the ganglion from which the nerve enters; for other regions, the projection was very widespread. In some cases (e.g., rhinophore to eye), there was evidence of projections from one peripheral structure to another. Experiments with all peripheral tissues that were studied resulted in extensive labeling of central ganglia, indicating that afferents with peripheral cell bodies may provide a major source of sensory input to the central nervous system and suggesting that many or all of the numerous ultrafine axons visualized via electron microscopy in the nerves ofAplysiamay originate from first‐ or second‐order sensory afferents whose cell bodies are located in the periphery. © 1995 Wiley‐Lis

ISSN:0092-7317    

DOI:10.1002/cne.903590409

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractCell death in theDrosophilaembryonic central nervous system (CNS) proceeds by apoptosis, which is revealed ultrastructurally by nuclear condensation, shrinkage of cytoplasmic volume, and preservation of intracellular organelles. Apoptotic cells do not accumulate in the CNS but are continuously removed and engulfed by phagocytic haemocytes. To determine whether embryonic glia can function as phagocytes, we studied serial electron microscopic sections of theDrosophilaCNS. Apoptotic cells in the nervous system are engulfed by a variety of glia including midline glia interface (or longitudinal tract) glia, and nerve root glia. However, the majority of apoptotic cells in the CNS are engulfed by subperineurial glia in a fashion similar to the microglia of the vertebrate CNS. A close proximity between macrophages and subperineurial glia suggests that glia may transfer apoptotic profiles to the macrophages. Embryos affected by the maternal‐effect mutationBicaudal‐Dhave no macrophages. In the absence of macrophages, most apoptotic cells are retained at the outer surfaces of the CNS, and subperineurial glia contain an abundance of apoptotic cells. Some apoptotic cells are expelled from the CNS, which suggests that the removal of apoptotic cells can occur in the absence of macrophages. The number of subperineurial glia is unaffected by changes in the rate of neuronal apoptosis. © 1995 Wiley‐Lis

ISSN:0092-7317    

DOI:10.1002/cne.903590410

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY

摘要:

AbstractWe examined the response to axon injury in the facial motoneurons and dorsal root ganglion (DRG) neurons of C57BL/Ola (Wld) mice, compared with the responses of C57BL/6J mice. The peripheral nerves of Ola mutants undergo remarkably slowed and muted Wallerian degeneration after injury. The increase in GAP‐43 mRNA levels in facial motoneurons and DRG neurons was similar in both strains of mice, as was the initial decrease in medium‐weight neurofilament (NFM) mRNA in facial motoneurons, and the increase in JUN immunoreactivity in both types of neurons. However, the subsequent recovery to normal low levels of JUN and GAP‐43 mRNA expression and high levels of NFM mRNA was delayed in Ola motoneurons. We ascribe this delay to the slow regeneration and target reinnervation of facial axons in the Ola mice.These results show that absence of rapid Wallerian degeneration does not affect the initial cell body response to axonal injury. They also provide further evidence that restoration of normal levels of expression of GAP‐43 and NFM mRNAs is dependent on target reinnervation and/or trophic factors provided by the distal nerve, Impaired regeneration in the Ola mouse does not seem to be a consequence of a defective cell body response to injury, and our results illustrate the general principle that, even if there is a vigorous cell body response to injury, normal axonal regeneration requires the additional provision of a favorable environment for growth. © 1995 Wiley

ISSN:0092-7317    

DOI:10.1002/cne.903590411

出版商:Wiley‐Liss, Inc.    

年代:1995

数据来源: WILEY