Transport experiences of people with disabilities during learnerships

Transport is a known national barrier for people with disabilities in South Africa. It is similarly identified as a barrier in learnerships and economic opportunity programmes. This article discusses the extent to which transport is a barrier during learnerships for students with disabilities. The Department of Transport administered an online evaluation questionnaire to a random sample of students with disabilities. Results were coded in terms of 'barriers to access' and 'barriers to participation'. The data were organised into themes. The collated evidence is discussed in this article. The findings demonstrated that transport barriers were present in different modes of transport and different parts of the travel chain. However, the findings also demonstrated the negative impact of transport on the learnership experience and economic opportunities. The findings indicated that inaccessible transport is an integral cause of learnership incompletion for students with disabilities, where the universal accessibility of both transport and the built environment are a prerequisite need. Most students with disabilities reported that transport was not a barrier to learnership participation or that problems with transport could be resolved. Nevertheless, it was one of the identified barriers that negatively affected learnership participation experiences. It was a significant barrier to learnership completion for students with the most severe experience of disability. The sample consisted of only 32 students and a high number of unspecified responses. Evidence from other studies indicates that transport for all persons with disabilities remains a barrier warranting further examination, because public transport has remained inaccessible for over 23 years. Further research is required to verify this study and to investigate learnership cost­benefit for all students

A new method for quantifying mitochondrial axonal transport

Axonal transport of mitochondria is critical for neuronal survival and function. Automatically quantifying and analyzing mitochondrial movement in a large quantity remain challenging. Here, we report an efficient method for imaging and quantifying axonal mitochondrial transport using microfluidic-chamber-cultured neurons together with a newly developed analysis package named "MitoQuant". This tool-kit consists of an automated program for tracking mitochondrial movement inside live neuronal axons and a transient-velocity analysis program for analyzing dynamic movement patterns of mitochondria. Using this method, we examined axonal mitochondrial movement both in cultured mammalian neurons and in motor neuron axons of Drosophila in vivo. In 3 different paradigms (temperature changes, drug treatment and genetic manipulation) that affect mitochondria, we have shown that this new method is highly efficient and sensitive for detecting changes in mitochondrial movement. The method significantly enhanced our ability to quantitatively analyze axonal mitochondrial movement and allowed us to detect dynamic changes in axonal mitochondrial transport that were not detected by traditional kymographic analyses.

Changes in expression of motor protein for axonal transport in nerve tissues of carbon disulfide-intoxicated rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the changes in microtubule motor protein expression in the spinal cord and sciatic nerve of rats exposed to carbon disulfide, and to investigate the possible molecular mechanism of changes in axonal transport in carbon disulfide-induced peripheral neuropathy.</p><p><b>METHODS</b>Healthy adult male Wistar rats were randomly divided into one control group and three experimental groups (10 rats per group). The rats in experimental groups were intoxicated by gavage of carbon disulfide at a dose of 200, 400, or 600 mg/kg 6 times a week for 6 consecutive weeks, while the rats in control group were given the same volume of corn oil by gavage. Animals were sacrificed after exposure, with nerve tissue separated. The levels of dynein, dynactin, and kinesin in the spinal cord and sciatic nerve were determined by Western blot.</p><p><b>RESULTS</b>The content of dynein, dynactin, and kinesin in the sciatic nerve decreased significantly under exposure to carbon disulfide. The levels of dynein in the sciatic nerve were reduced by 23.47% and 33.34% at exposure doses of 400 and 600 mg/kg, respectively. The levels of dynactin in the sciatic nerve of the three experimental groups were reduced by 19.91%, 24.23%, and 41.30%, respectively. The level of kinesin was reduced by 25.98%under exposure to 600 mg/kg carbon disulfide. All the differences were statistically significant (P < 0.01). As compared with the control group, the 600 mg/kg group experienced a 28.24% decrease in level of dynactin in the spinal cord (P < 0.01), but no significant change was observed in the level of dynein or kinesin.</p><p><b>CONCLUSION</b>Carbon disulfide has an impact on microtubule motor protein expression in nerve tissues, which might be involved in the development of carbon disulfide-induced peripheral neuropathy.</p>

Neuroprotection in glaucoma: present and future / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To review the updated research on neuroprotection in glaucoma, and summarize the potential agents investigated so far.</p><p><b>DATA SOURCES</b>The data in this review were collected from PubMed and Google Scholar databases published in English up to September 2012, with keywords including glaucoma, neuroprotection, and retinal ganglion cells, both alone and in combination. Publications from the past ten years were selected, but important older articles were not excluded.</p><p><b>STUDY SELECTION</b>Articles about neuroprotection in glaucoma were selected and reviewed, and those that are cited in articles identified by this search strategy and judged relevant to this review were also included.</p><p><b>RESULTS</b>Although lowering the intraocular pressure is the only therapy approved as being effective in the treatment of glaucoma, increasing numbers of studies have discovered various mechanisms of retinal ganglion cells death in the glaucoma and relevant neuroprotective strategies. These strategies target neurotrophic factor deprivation, excitotoxic damage, oxidative stress, mitochondrial dysfunction, inflammation, activation of intrinsic and extrinsic apoptotic signals, ischemia, and protein misfolding. Exploring the mechanism of axonal transport failure, synaptic dysfunction, the glial system in glaucoma, and stem cell used in glaucoma constitute promising research areas of the future.</p><p><b>CONCLUSIONS</b>Neuroprotective strategies continue to be refined, and future deep investment in researching the pathogenesis of glaucoma may provide novel and practical neuroprotection tactics. Establishing a system to assess the effects of neuroprotection treatments may further facilitate this research.</p>

Differential gene expression pattern in brains of acrylamide-administered mice / 대한수의학회지

The present study was performed to evaluate the relationship between the neurotoxicity of acrylamide and the differential gene expression pattern in mice. Both locomotor test and rota-rod test showed that the group treated with higher than 30 mg/kg/day of acrylamide caused impaired motor activity in mice. Based on cDNA microarray analysis of mouse brain, myelin basic protein gene, kinesin family member 5B gene, and fibroblast growth factor (FGF) 1 and its receptor genes were down-regulated by acrylamide. The genes are known to be essential for neurofilament synthesis, axonal transport, and neuro-protection, respectively. Interestingly, both FGF 1 and its receptor genes were down-regulated. Genes involved in nucleic acid binding such as AU RNA binding protein/enoyl-coA hydratase, translation initiation factor (TIF) 2 alpha kinase 4, activating transcription factor 2, and U2AF 1 related sequence 1 genes were down-regulated. More interesting finding was that genes of both catalytic and regulatory subunit of protein phosphatases which are important for signal transduction pathways were down-regulated. Here, we propose that acrylamide induces neurotoxicity by regulation of genes associated with neurofilament synthesis, axonal transport, neuro-protection, and signal transduction pathways.

Expression of tau-related protein in spinal cord of patients with Alzheimer's disease / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the expression of tau-related protein in spinal cord of Chinese patients with Alzheimer's disease.</p><p><b>METHODS</b>Gallays-Braak stain and immunohistochemical study for tau protein (AT8) were carried out in the spinal cord tissue (T2, T8, T10, L2 and S2 segments) of 3 Chinese patients with Alzheimer's disease. Seven age-matched cases without evidence of dementia or neurologic disease were used as controls.</p><p><b>RESULTS</b>Neurofibrillary tangles were identified in the neurons of anterior horn in 2 Alzheimer's disease cases but none was observed in the controls. Tau-positive axons and astroglia were detected in all Alzheimer's disease cases. Tau immunoreactivity in spinal cord of the patients correlated with that in brain tissue.</p><p><b>CONCLUSION</b>The expression of tau-related protein is demonstrated in the spinal cord of Alzheimer's disease patients suggesting that axonal transport defect may play a role in the pathogenesis of Alzheimer's disease.</p>

Slow axoplasmic transport under scrutiny

The origin of axoplasmic proteins is central for the biology of axons. For over fifty years axons have been considered unable to synthesize proteins and that cell bodies supply them with proteins by a slow transport mechanism. To allow for prolonged transport times, proteins were assumed to be stable, i.e., not degraded in axons. These are now textbook notions that configure the slow transport model (STM). The aim of this article is to cast doubts on the validity of STM, as a step toward gaining more understanding about the supply of axoplasmic proteins. First, the stability of axonal proteins claimed by STM has been disproved by experimental evidence. Moreover, the evidence for protein synthesis in axons indicates that the repertoire is extensive and the amount sizeable, which disproves the notion that axons are unable to synthesize proteins and that cell bodies supply most axonal proteins. In turn, axoplasmic protein synthesis gives rise to the metabolic model (MM). We point out a few inconsistencies in STM that MM redresses. Although both models address the supply of proteins to axons, so far they have had no crosstalk. Since proteins underlie every conceivable cellular function, it is necessary to re-evaluate in-depth the origin of axonal proteins. We hope this will shape a novel understanding of the biology of axons, with impact on development and maintenance of axons, nerve repair, axonopathies and plasticity, to mention a few fields.

Immunochemical changes of calbindin, calretinin and SMI32 in ischemic retinas induced by increase of intraocular pressure and by middle cerebral artery occlusion / 대한해부학회지

The reaction of neuroactive substances to ischemic conditions in the rat retina evoked by different methods was immunochemically evaluated in adult Sprague-Dawley rats. Ocular ischemic conditions were unilaterally produced by elevating intraocular pressure (EIOP) or by middle cerebral artery occlusion (MCAO). Two EF-hand calcium binding proteins, calbindin D28K (CB) and calretinin (CR), in the normal retina showed similar immunolocalization, such as the amacrine and displaced amacrine cells, the ganglion cells, and their processes, particularly CB in horizontal cells. CB immunoreactive neurons in the ganglion cell layer in both types of ischemic retinas were more reduced in number than CR neurons compared to those in a normal retina. The CB protein level in both ischemic retinas was reduced to 60-80% of normal. The CR protein level in MCAO retinas was reduced to about 80% of normal but increased gradually to the normal value, whereas that in the EIOP showed a gradual reduction and a slight recovery. SMI32 immunoreactivity, which detects a dephosphorylated epitope of neurofilaments-M and -H, appeared in the axon bundles of ganglion cells in the innermost nerve fiber layer of normal retinas. The reactivity in the nerve fiber bundles appeared to only increase slightly in EIOP retinas, whereas a moderate increase occurred in MCAO retinas. The SMI32 protein level in MCAO retinas showed a gradual increasing tendency, whereas that in the EIOP showed a slight fluctuation. Interestingly, the MCAO retinas showed additional SMI32 immunoreactivity in the cell soma of presumed ganglion cells, whereas that of EIOP appeared in the Muller proximal radial fibers. Glial fibrillary acidic protein (GFAP) immunoreactivity appeared in the astrocytes located in the nerve fiber layer of normal retinas. Additional GFAP immunoreactivity appeared in the Muller glial fibers deep in EIOP retinas and at the proximal end in MCAO retinas. These findings suggest that the neurons in the ganglion cell layer undergo degenerative changes in response to ischemia, although EIOP retinas represented a remarkable Muller glial reaction, whereas MCAO retinas had only a small-scaled axonal transport disturbance.

Genetics of Hereditary Peripheral Neuropathies

Hereditary peripheral neuropathies can be categorized as hereditary motor and sensory neuropathies (HMSN), hereditary motor neuropathies (HMN), and hereditary sensory neuropathies (HSN). HMSN, HMN, and HSN are further subdivided into several subtypes. Here, we review the most recent findings in the molecular diagnosis and therapeutic strategy for hereditary peripheral neuropathies. The products of genes associated with hereditary peripheral neuropathy phenotypes are important for neuronal structure maintenance, axonal transport, nerve signal transduction, and functions related to the cellular integrity. Identifying the molecular basis of hereditary peripheral neuropathy and studying the relevant genes and their functions is important to understand the pathophysiological mechanisms of these neurodegenerative disorders, as well as the processes involved in the normal development and function of the peripheral nervous system. These advances and the better understanding of the pathogenesis of peripheral neuropathies represent a challenge for the diagnoses and managements of hereditary peripheral neuropathy patients in developing future supportive and curative therapies.

Inmunohistoquímica de los cambios degenerativos del sistema nervioso central en paraparesias esp sticas asociadas al virus linfotrópico humanoTtipol(HTLV-l) / Immunohistochemistry of degenerative changes in the central nervous system in spastic paraparesis associated to human T lymphotropic virus type I (HTLV-I)

Background: Human T lymphotropic virus type I is associated with tropical spastic paraparesis, that is a chronic and progressive disease which damages specially the cortiespinal tracts. The pathogenesis of this degenerative process remains unknown. Aim: To identify histopathological aspects that could suggest a pathogenic hypothesis we studied immunohistochemical features in spinal cords obtained from patients that died due to progressive spastic paraparesis. Patients and Methods: Five males and five females, who died between 1990 and 2000, with a mean age of 52 years and mean disease duration of 8.6, were studied. All had a complete clinical and virological diagnosis. Samples were obtained from the frontal motor cortex and spinal cord (cervical, dorsal and lumbar segments), were fixed in formol (10 percent), included in paraffin, and stained with Haematoxylin and Luxol-fast-blue. Immunohistochemical study was made with anti-neurofilament antibodies 1:100 (M0762, DAKO), anti-APP 1:20 (Rabbit Pre Amyloid protein 51-2700 ZYMED), anti-tau 1:100 (A0024DAKO) and anti-ubiquitine 1:50 (NCL UBIQm Novocastra). Results: All cases had demyelinization and axonal loss in the cortico-spinal tracts; distal and segmental demyelinization of Goll tract; axonal thickening, amyloid precursor protein deposits in the white matter; tau protein aggregation in the spinal cord oligodendrocytes; axonal ubiquitination of sensitive and motor tracts, and subcortical white matter. Neurona! injury was absent. Conclusions: The systematic damage of motor and sensitive tracts of the spinal-cord and the absence of neurona! damage, defines a degenerative process limited to axons. This central axonopathie could be caused by a disturbance of axoplasmic transport.

Pathogenesis of Alzheimer's Dementia

Alzhelmer's disease (AD) is the most common cause of dementia that arises on a neuropathological background of amyloid plaques containing betaamylold (Abeta) derived from amyloid precursor protein (APP) and tau-rich neurofibrillary tangles. To date, the cause and progression of familial or sporadic AD have not been fully elucidated. About 10% of all cases of AD occur as autosomal dominant inherited forms of early-onset AD, which are caused by mutations in the genes encoding APP, presenilin-1 and presenilin-2. Proteolytic processing of APP by beta-gamma-secretase and caspase generates Abetaand carboxyl-terminal fragments of APP (APP-CTFs), which have been implicated in the pathogenesis of AD. The presenilins function as one of the gamma-secretases. Abetawhich is the main component of the amyloid plaques found, is known to exert neurotoxicity by accumulating free radicals, disturbing calcium homeostasis, evoking inflammatory response and activating signaling pathways. The CTFs have been found in AD patients' brain and reported to exhibit much greater neurotoxicity than Abeta. Furthermore CTFs are known to impair calcium homeostasis and learning and memory, triggering a strong inflammatory reaction through MAPKs- and NF-kappaB-dependent astrocytosis and iNOS induction. Recently, it was reported that CTF translocated into the nucleus and in turn, affected transcription of genes including glycogen synthase kinase-3beta which results in the induction of tau-rich neurofibrillary tangles and subsequently cell death. One of the hallmarks of AD, neurofibrillary tangles (NFT), is formed by insoluble intracellular polymers of hyperphosphorylated tau that is believed to cause apoptosis by disrupting cytoskeletal and axonal transport. This review covers the processing of APP, toxic mechanisms of Abetaand CTFs of APP, presenilin and also tau in relation to the pathogenesis of AD.

Axoplasmic Transport of Herpes Simplex Virus Co-Cultured with Ciliary Nerve

PURPOSE: To investigate the replication of HSV within cultured cell and axonal transport of HSV within the axon of the ciliary nerve following the injection of HSV into a cultured ciliary nerve. METHODS: The explant of the ciliary nerve was cultured with a medium containing nerve growth factor for 30 days when the suspension of HSV-1 (Kos strain) was introduced into the culture dish to co-culture with the ciliary nerve. The ciliary nerve was examined with transmission electron microscopy 30 days after culture and 6 days after co-culture with HSV. RESULTS: The ultrastructure of the explant of the ciliary nerve co-cultured with HSV showed that the viral capsid acquired a viral envelope and viral core, and a capsid and inclusion body within the nucleus. The enveloped virus was scattered within the vesicles of the cytoplasm. The virus-like particles were identified at the axonal fibers. CONCLUSIONS: The co-culture of the explant of the ciliary nerve and HSV showed the replicative process of the HSV within the cultured cell. The virus-like particles within the axon showed the evidence axonal transport of the virus under culture conditions.

Ganglion Cell Death in Rat Retinaby Persistent Intraocular Pressure Elevation

Glaucoma is characterized by loss of retinal ganglion cells (RGCs) and their axons. Retrograde axoplasmic transport blockade and excitotoxicity were proposed to be a major cause of RGC apoptosis. We conducted this study to characterize the episcleral vessel cauterization glaucoma model in the rat with respect to decreased retrograde axoplasmic flow and subsequent apoptotic RGC death. After episcleral vessels were cauterized in Sprague-Dawley rats, Fluorogold was injected into their superior colliculi by stereotactic method. Retrograde axoplasmic flow and TUNEL-stained apoptotic dead cells were observed microscopically. Elevated intraocular pressure was maintained for up to 6 weeks during follow-up. Retrograde axoplasmic flow to the rat retina was significantly decreased. Apoptotic RGC was selectively TUNELstained in the retina, especially at the ganglion cell layers. We concluded that elevated intraocular pressure caused apoptotic RGC death through retrograde axoplasmic flow blockage. Further studies will elucidate the neuroprotection strategies in glaucoma patients.

Protection of retinal ganglion cells against glaucomatous neuropathy by neurotrophin-producing, genetically modified neural progenitor cells in a rat model / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To investigate in vivo survival of retinal ganglion cells (RGCs) after partial blockage of optic nerve (ON) axoplasmic flow by sub-retinal space or vitreous cavity injection of brain-derived neural factor (BDNF) produced by genetically modified neural progenitor cells (NPCs).</p><p><b>METHODS</b>Adult Sprague-Dawley (SD) rat RGCs were labeled with granular blue (GB) applied to their main targets in the brain. Seven days later, the left ON was intra-obitally crushed with a 40 g power forceps to partially block ON axoplasmic flow. Animals were randomized to three groups. The left eye of each rat received a sham injection, NPCs injection or an injection of genetically modified neural progenitors producing BDNF (BDNF-NPCs). Seven, 15 and 30 days after ON crush, retinas were examined under a fluorescence microscope. By calculating and comparing the average RGCs densities and RGC apoptosis density, RGC survival was estimated and the neuro-protective effect of transplanted cells was evaluated.</p><p><b>RESULTS</b>Seven, 15 and 30 days after crush, in the intra-vitreous injection group, mean RGC densities had decreased to 1885 +/- 68, 1562 +/- 20, 1380 +/- 7 and 1837 +/- 46, 1561 +/- 58, 1370 +/- 16, respectively with sham injection or neural progenitors injection. However, RGCs density in the groups treated with intra-vitreous injection of BDNF-NPC was 2101 +/- 15, 1809 +/- 19 and 1625 +/- 34. Similar results were found in groups after sub-retinal injection. Higher densities were observed in groups treated with BDNF-NPCs. There were statistically significant differences among groups through nonparametric tests followed by the Mann-Whitely test. RGC apoptosis density in BDNF-NPC at each follow-up time was less than in other groups.</p><p><b>CONCLUSIONS</b>A continuous supply of neurotrophic factors by the injection of genetically modified neural progenitors presents a highly effective approach to counteract optic neuropathy and RGC degeneration after partial ON axoplasmic flow blockage.</p>

Ultrastructure of the Optic Neuritis Induced by Herpes Simplex Virus-1 Injection in Rabbits

PURPOSE: This study was performed to investigate the ultrastructural changes of the optic nerve after intravitreal injection of herpes simplex virus-1. METHODS: Herpes simplex virus was separated from the culture media after observing the cytopathic effect on cultured vero cells. Viruses were then injected on the optic nerve head of 21 rabbit eyes. Eyes were enucleated at 1, 2, 3, 5, 7, 10, and 14 days after injection of herpes simplex virus and examined under the electron microscope. RESULTS: The intranuclear inclusion body was noted in eyes examined at 2 days after injection. The histopathological changes were perivascular infiltration of inflammatory cells, cytoskeletal degeneration of large diameter of myelinated nerve, demyelination of axonal nerve fiber, and the accumulation of mitochondria within axonal nerve fiber. CONCLUSIONS: These results suggest that optic neuritis may be induced by herpes simplex virus. The accumulation of mitochondria may be related to the interruption of the axonal transport through the axonal nerve fibers of optic nerve.

The autonomous axon: a model based on local synthesis of proteins

In the current understanding of axons, axoplasmic synthesis of proteins is negated, and it is asserted that proteins are transported from perikarya to axons. This 'transport model' in which axons are fully dependent of perikarya is seriously flawed. The 'autonomous axon' proposed here negates in turn transport of proteins, and asserts (i) local synthesis of axoplasmic proteins, corner stone of this model, (ii) existence of internal programs in axon and terminals, (iii) external control of programs resulting in local regulation of phenotype of axons and terminals, hence they are autonomous from perikarya; (iv) participation of perikarya through the fast transport in setting up the axonal programs but not in their immediate regulation. The word merotrophism (meros meaning part) denotes post-transcriptional regulation of phenotype of restricted regions of a cell. We surmise that merotrophism is at the base of many plastic phenomena.

Jaime Alvarez and the case against slow axoplasmic transport: some epistemological reflections

The 'slow axoplasmic transport theory' has been the prevailing view over the last forty years in order to explain the metabolic maintenance of neuronal axons and nerve endings. A significant amount of evidence against this theoretic interpretation of the existing experimental data has been presented by J. Alvarez, A. Giuditta and E. Koenig in an exhaustive review. They propose an alternative theoretical interpretation called the 'local synthesis model', integrating recent evidence for axon biology and regeneration. We present some epistemological considerations that reinforce the above criticisms and propositions.

Translocational changes of localization of synapsin in axonal sprouts of regenerating rat sciatic nerves after ligation crush injury

Time-dependent translocational changes of Synapsin I (SyI), a synaptic vesicle-associated phosphoprotein and its involvement in the axonal transport were investigated in the regenerating axonal sprouts. A weak SyI immunoreactivity (IR) was found in the axoplasm of normal axons. Rat sciatic nerves were crush-injured by ligating with 1-0 silk thread at the mid-thigh level and released from the ligation 24 h later. At various times after release, immunocytochemistry was performed. SyI was translocated from the proximal to the distal site of ligation and also involved in the sprouting of regenerating axons. The distribution patterns of SyI IR were changed in the crush-injured nerves. SyI immunoreactive thin processes were strongly appeared in the proximal region from 1 h after release. After 3 h, a very strong IR was expressed. The intense SyI immunoreactive thin processes were elongated distally and were changed the distribution pattern by time-lapse. After 12 h, strong immunoreactive processes were extended to the ligation crush site. At 1 day, a very intense IR was expressed. At 2 days, immunoreactive thin processes extended into the distal region over the ligation crush site and strong IR was observed after 3 days. SyI was accumulated in the proximal region at the early phases after release. These results suggest that SyI may be related to the translocation of vesicles to the elongated membranes by a fast axonal transport in the regenerating sprouts.

The Effects of Nerve Growth Factor on Satellite Cell of the Dorsal Rott Ganglia in Streptozotocin-induced Diabetic Rats / 대한해부학회지

Diabetic neuropathy is an axonal degenerative disease characterized by progressive axonal atrophy and reduced axonal transport. We were interested in the potential neuroprotective effects of nerve growth factor against diabetic neuropathies. To this aim we studied the effect of nerve growth factor on satellite cells, which might play a trophic role toward the related neuron, of the dorsal root ganglion in the streptozotocin-induced diabetic rats by electron in microscope . Diabetes was induced in rats by the streptozotocin. And recombinant human NGF was administrated everyday for 10 consecutive weeks. The results obtained are as follows : 1.In the diabetic induced group, the satellite cells revealed irregular nuclei.The neuron-satellite cell interface was more irregular and plicated than that of control. Large vacuoles and dense bodies were observed and no defects were in the ribosomes and rough endoplasmic reticulum. In the vacuoles, medium electron dense, fiber -like materials were occasionally observed. 2. In the experimental group of diabetic rats treated with NGF for 10 weeks, nucleus was round and the neuron-satellite interface was more regular. Vacuoles and dense bodies were less seen than diabetic rats. In the cytoplasm, many microtubules were observed. In these studies, we considered that streptozotocin induces changes of the satellite cell structure and NGF might improve cellular changes of the satellite cell exposed with streptozotocin.

Developmental strategies underlyng the elaboration of cortical circuits

The mammalian cerebral cortex is organized in layers and columns, which are reflected in the local intrinsic connections and in the projections to and from the cortex. It is well established that the development of the columnar architecture is under the influence of neuronal activity, but little is known about the mechanisms that control the laminar specificity of cortical circuits. Here we review some recent studies which show that diffusible and membrane-associated molecules provide sufficient information to reconstruct layer-specific intrinsic and extrinsic cortical circuits under in vitro conditions.