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  • 1
    Electronic Resource
    Electronic Resource
    Androgen-induced up-regulation of tubulin isoforms in neuroblastoma cells (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Androgens regulate the physiology of motor neurones both during development and in adult life. In particular, androgens increase the rate of axonal regeneration after axotomy, an effect correlated with the up-regulation of tubulin. In order to determine whether this was the result of a direct hormone action on neurones, we examined the effect of testosterone on microtubular proteins in human neuroblastoma SH-SY5Y cells. Treatment of proliferating SH-SY5Y cells with testosterone resulted in an up-regulation of α- and β-tubulin. By contrast, no change in tubulin was observed either in cells differentiated into a neuronal phenotype by retinoic acid or in adrenal SW13 cells. We also show that an up-regulation of the ubiquitous βII-tubulin and of the neurone-specific βIII-tubulin isoforms contributes to the overall increase in tubulin in response to androgen treatment. The increase in tubulin levels following testosterone treatment was abolished by co-incubation with antiandrogens, indicating that this effect is mediated through a classical mechanism of steroid action. The two microtubule-associated proteins, tau and MAP2b, remained unchanged following testosterone exposure. Thus, these results demonstrate that tubulin is a direct neuronal target of androgen regulation and suggest that dysregulation of tubulin expression may contribute to the pathogenesis of some motor neuronopathies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00475.x
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  • 2
    Electronic Resource
    Electronic Resource
    Hydrodynamic voltammetry with channel microband electrodes: potential step transients (1994)
    s.l. : American Chemical Society
    The @journal of physical chemistry 〈Washington, DC〉 98 (1994), S. 1270-1275 
    Details
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/j100055a037
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  • 3
    Electronic Resource
    Electronic Resource
    p35/cdk5 binds and phosphorylates β-catenin and regulates β-catenin/presenilin-1 interaction (2001)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 13 (2001), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The neuronal cyclin-dependent kinase p35/cdk5 comprises a catalytic subunit (cdk5) and an activator subunit (p35). To identify novel p35/cdk5 substrates, we utilized the yeast two-hybrid system to screen for human p35 binding partners. From one such screen, we identified β-catenin as an interacting protein. Confirmation that p35 binds to β-catenin was obtained by using glutathione S-transferase (GST)–β-catenin fusion proteins that interacted with both endogenous and transfected p35, and by showing that β-catenin was present in p35 immunoprecipitates. p35 and β-catenin also displayed overlapping subcellular distribution patterns in cells including neurons. Finally, we demonstrated that p35/cdk5 phosphorylates β-catenin. β-catenin also binds to presenilin-1 and altered β-catenin/presenilin-1 interactions may be mechanistic in Alzheimer's disease (AD). Abnormal p35/cdk5 activity has also been suggested to contribute to AD. We therefore investigated how modulation of p35/cdk5 activity influenced β-catenin/presenilin-1 interactions. Inhibition of p35/cdk5 with roscovitine did not alter the steady state levels of either β-catenin or presenilin-1 but reduced the amount of presenilin-1 bound to β-catenin. Thus, p35/cdk5 binds and phosphorylates β-catenin and regulates its binding to presenilin-1. The findings reported here therefore provide a novel molecular framework to connect p35/cdk5 with β-catenin and presenilin-1 in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1460-9568.2001.01376.x
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  • 4
    Electronic Resource
    Electronic Resource
    Living with motor neurone disease: lives, experiences of services and suggestions for change (2005)
    Oxford, UK : Blackwell Science Ltd
    Health & social care in the community 13 (2005), S. 0 
    Details
    ISSN: 1365-2524
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Palliative care involves the complete, holistic care of people with progressive illness and their families. People living with motor neurone disease (MND) require a range of multidisciplinary palliative care services. However, there are significant gaps in our understanding of these people's lives, experiences of services and their suggestions for service change. The present study addressed the following questions: (1) What are the lived experiences of people living with MND? (2) What are people's experiences of services? and (3) Can improvements to care be identified? A qualitative research design was adopted using semi-structured interviews. The topic guide was developed from existing literature. The study was based in three boroughs in London, UK. People living with MND and professionals were drawn from a database at King's College Hospital, and additionally, through ‘snowball’ sampling. Nine people with MND, five carers/family members and 15 professionals took part in the interviews. These interviews were audio-taped, transcribed and checked for accuracy against the original recordings. Themes within the interviews were coded and grouped. The analysis was facilitated with the NVIVO computer software package. The findings are presented within three substantive groups: (1) the impact of MND on people's lives (the physical impacts of the illness, including increasing disability; social issues, including restrictions on social activities; and adjustments to people's lives, including methods of coping with the illness); (2) experiences of services (accessing service entitlements, information sources, professionals’ attitudes and approaches, and professionals’ knowledge and understanding of MND); and (3) suggestions for service change (better information and communication, including information on service entitlements; improved knowledge amongst professionals about MND; and some suggestions for service restructuring). This study brings a fresh approach to understanding the impacts of MND and the ways in which services can be improved to meet people's needs. The paper concludes with methodological considerations, the implications of the findings for practitioners and policy makers, and suggestions for further research.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2524.2005.00530.x
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  • 5
    Electronic Resource
    Electronic Resource
    The effect of electrical stunning and slaughter on the electroencephalogram of sheep and calves
    Amsterdam : Elsevier
    Meat Science 17 (1986), S. 267-281 
    Details
    ISSN: 0309-1740
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0309-1740(86)90045-8
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  • 6
    Electronic Resource
    Electronic Resource
    Basal ganglia outflow pathways and circling behaviour in the rat (1983)
    Springer
    Journal of neural transmission 58 (1983), S. 1-41 
    Details
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The role of efferents in substantia nigra pars reticulata in the mediation of circling behaviour in the rat has been studied by means of lesions designed to interrupt these pathways or to damage nigral projection areas. The behavioural model used was the circling rodent with a prior 6-hydroxydopamine lesion of the left nigro-striatal pathway in which amphetamine induced ipsiversive rotation and apomorphine induced contraversive rotation. Removal of the left fronto-parietal cortex caused only a transient decrease in drug-induced rotation. An electrolytic lesion of the left, right or both parafascicular thalamic nuclei did not alter circling behaviour. Electrolytic lesioning of the left ventromedial thalamus decreased apomorphineinduced contraversive circling whereas a lesion of the right ventromedial thalamus decreased amphetamine-induced ipsiversive rotation. Bilateral electrolytic lesions of the ventromedial thalamus did not alter drug-induced circling. Unilateral or bilateral electrolytic lesioning of the medial superior colliculus did not alter the rotational response to apomorphine or amphetamine. However, an electrolytic lesion interrupting the dorsal tegmental decussation reduced apomorphine-induced circling but not amphetamine-induced circling. That a critical role for the nigro-thalamic and nigro-tectal pathways is not involved in the mediation of circling behaviour was confirmed by placing knife cuts so as to separate these structures from the substantia nigra; such lesions failed to alter the contraversive rotation induced by the ipsilateral injection of muscimol into substantia nigra pars reticulata. Electrolytic lesions of the ipsilateral nucleus reticularis gigantocellu laris or kainic acid lesions of the ipsilateral nucleus tegmenti pedunculopontinus did not alter drug-induced circling in animals with a prior 6-hydroxydopamine nigral lesion. In contrast, an ipsilateral lesion of the midbrain periaqueductal grey matter and adjacent midbrain reticular formation (the angular complex) decreased apomorphine-induced contraversive rotation in such animals, while bilateral lesions reduced both apomorphine-and amphetamine-induced circling; in each case the postural component of rotation was abolished. Unilateral kainic acid lesions of the angular complex in naive animals caused ipsiversive rotation which was enhanced by apomorphine. Unilateral kainic acid lesions of the angular complex with an ipsilateral 6-hydroxydopamine nigral lesion caused reversal of the previous contraversive rotation to apomorphine, and enhanced amphetamine-induced ipsiversive rotation. A nigro-reticular pathway to the midbrain reticular formation adjacent to the periaqueductal grey matter (the angular complex) appears critical in the mediation of the postural component of drug-induced rotation in animals with a prior unilateral 6-hydroxydopamine lesion of the dopaminergic nigro-striatal system. Nigro-thalamic pathways and pathways from nigra to the superficial and medial superior colliculus do not seem to be involved, although we cannot exclude a role for the deep lateral superior colliculus which, in any case, is anatomically and functionally closely related to the midbrain tegmental reticular formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01249122
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  • 7
    Electronic Resource
    Electronic Resource
    Purkinje cell toxicity ofβ-aminopropionitrile in the rat (1991)
    Springer
    Virchows Archiv 419 (1991), S. 403-408 
    Details
    ISSN: 1432-2307
    Keywords: Amyotrophic lateral sclerosis ; Cerebellum ; β-Aminopropionitrile ; Heat shock proteins ; Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Compounds causing neurolathyrism are putative aetiological agents in neurodegenerative disorders including amyotrophic lateral sclerosis.β-Aminopropionitrile (BAPN) is one such compound. We have administered this lathyrogenic agent at a dose of 1 g/kg by the intraperitoneal route in experiments in adult Sprague-Dawley rats during a period of 10 weeks. The rats developed marked kyphoscoliosis, ataxia with paralysis and muscle wasting of the hind limbs. Vacuolation and loss of Purkinje cells developed, but no anterior horn cell degeneration was noted. Immunohistochemical studies of phosphorylated neurofilaments and the 72 kDa heat shock protein were normal and no intraneuronal ubiquitinated inclusions were seen. High-dose intraperitoneal BAPN in the rat causes Purkinje cell changes, but no other central nervous system abnormalities.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01605074
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  • 8
    Electronic Resource
    Electronic Resource
    Relationships between Lewy bodies and pale bodies in Parkinson's disease (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 525-529 
    Details
    ISSN: 1432-0533
    Keywords: Lewy bodies ; Pale bodies ; Substantia nigra ; Parkinson's disease-Ubiquitin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The prevalance of pale bodies and Lewy bodies was studied in the substantia nigra of 12 patients with typical Parkinson's disease (PD), in 5 patients with diffuse Lewy body disease (DLBD), and in a group of neurologically normal controls. Anti-ubiquitin antibodies labelled pale bodies and Lewy bodies in typical PD and DLBD, and there was a strong positive correlation between numbers of ubiquitin-immunoreactive pale bodies and Lewy bodies. BF10, a monoclonal antibody against a phosphate-dependent epitope of neurofilament 155-kDa polypeptide subunit, immunolabelled 57% of Lewy bodies and 15% of pale bodies in typical PD. Some pale bodies and Lewy bodies were seen in the substantia nigra of 2 of 5 neurologically normal, aged controls, probably representing “incidental PD”. We conclude that there is a close relationship between pale bodies and typical Lewy bodies in the substantia nigra in clinical varicties of PD, and that these inclusions share antigenic determinants. If pale bodies and Lewy bodies reflect separate aspects of the cellular pathology in PD, their formation probably occurs in parallel. Alternatively, these observations may suggest that pale bodies represent a stage in the formation of Lewy bodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00310030
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  • 9
    Electronic Resource
    Electronic Resource
    New aspects of the pathology of neurodegenerative disorders as revealed by ubiquitin antibodies (1989)
    Springer
    Acta neuropathologica 79 (1989), S. 61-72 
    Details
    ISSN: 1432-0533
    Keywords: Lewy bodies ; Pale bodies ; Neurofibrillary tangles ; Pick bodies ; Globose tangles ; Ubiquitin ; Antibodies ; Immunocytochemistry ; Alzheimer's disease ; Parkinson's disease ; Pick's disease ; Progressive supranuclear palsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ubiquitin has previously been identified as a component of neuronal inclusions in neurodegenerative disorders. In this investigation, we examined tissue from cases of Alzheimer's disease (AD), Pick's discase, Parkinson's disease (PD), and progressive supranuclear palsy (PSP) to identify previously unrecognized ubiquitinated structures and to assess the evolution of neuronal inclusions. In AD, approximately 60% of neurofibrillary tangles (NFTs) that were stained with an anti-paired helical filaments (PHF) serum were identified by the ubiquitin antibodies. Extracellular NFTs were not labelled with anti-PHF but were unlabelled or weakly labelled with anti-ubiquitin antibodies. In Pick's disease, most Pick bodies were strongly labelled by the ubiquitin antibodies, and in addition some hippocampal CA1 neurones contained granular or strand-like ubiquitin-immunoreactive (IR) inclusions associated with more typical Pick bodies. Typical Lewy bodies in PD cases showed an unlabelled central core with an outer ring intensely labelled by ubiquitin antibodies. Pale bodies in pigmented substantia nigra neurones appeared as large well-defined, rounded structures without an identifiable core or peripheral zone. Some pale bodies were unlabelled by ubiquitin antibodies, but others showed labelling of variable intensity. Pale bodies which were labelled by ubiquitin antibodies tended also to be labelled by BF10, a monoclonal antibody against phosphorylated neurofilaments. We suggest that pale bodies in PD may represent stages in the formation of Lewy bodies. In addition, we observed numerous spindle-shaped ubiquitin-IR swellings of dendrites of pigmented substantia nigra neurones. In contrast to inclusions of AD and Pick's disease, the PHF-positive fibrillary neuronal inclusions of PSP were either unlabelled or only weakly labelled by ubiquitin antibodies. No ubiquitinated structures were seen in neurones from corresponding areas in aged controls. Identification of ubiquitinated proteins in neurodegenerative disorders may provide insights into molecular events associated with cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00308959
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  • 10
    Electronic Resource
    Electronic Resource
    Enhanced GABA function in the angular complex (lateral periaqueductal grey matter and adjacent reticular formation) alters the postural component of striatal- or nigral-derived circling (1984)
    Springer
    Experimental brain research 56 (1984), S. 1-11 
    Details
    ISSN: 1432-1106
    Keywords: Circling behaviour ; Angular complex ; GABA ; Substantia nigra ; Striatum
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Unilateral injection of muscimol into the angular complex (lateral periaqueductal grey matter and adjacent reticular formation) caused ipsiversive rotation. Focal injection of picrotoxin into the same site produced contraversive rotation. Administration of apomorphine to animals with a unilateral 6OHDA lesion of the left medial forebrain bundle caused contraversive rotation. Focal injection of muscimol into the angular complex reversed the direction of rotation such that apomorphine administration now produced ipsiversive circling. Unilateral injection of muscimol into substantia nigra zona reticulata caused contraversive rotation. Focal injection of picrotoxin into the same site produced ipsiversive rotation. The prior injection of muscimol into the ipsilateral angular complex prevented the contraversive rotation induced by intranigral administration of muscimol such that animals now showed ipsiversive circling. In both 6-OHDA-lesioned animals and animals receiving intranigral muscimol, focal injection of muscimol into the angular complex caused a reversal in the direction of circling through loss of the postural component with no obvious change in locomotor activity. Bilateral electrolytic lesions of the angular complex overall had no effect on amphetamine-induced locomotion. Manipulation of GABA function in the angular complex alters circling behaviour initiated from the striatum or substantia nigra by altering the postural component without affecting the locomotor response of the animals. The data suggest a critical role for the angular complex as an outflow station from basal ganglia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00237436
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