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16. Developmental regulation of N-methyl-D-aspartate- and kainate-type glutamate receptor expression in the rat spinal cord

Author

Stegenga, S. L and Kalb, R. G

Subjects
Life Sciences (General)
Abstract

Spinal motor neurons undergo experience-dependent development during a critical period in early postnatal life. It has been suggested that the repertoire of glutamate receptor subunits differs between young and mature motor neurons and contributes to this activity-dependent development. In the present study we examined the expression patterns of N-methyl-D-aspartate- and kainate-type glutamate receptor subunits during the postnatal maturation of the spinal cord. Young motor neurons express much higher levels of the N-methyl-D-aspartate receptor subunit NR1 than do adult motor neurons. Although there are eight potential splice variants of NR1, only a subgroup is expressed by motor neurons. With respect to NR2 receptor subunits, young motor neurons express NR2A and C, while adult motor neurons express only NR2A. Young motor neurons express kainate receptor subunits GluR5, 6 and KA2 but we are unable to detect these or any other kainate receptor subunits in the adult spinal cord. Other spinal cord regions display a distinct pattern of developmental regulation of N-methyl-D-aspartate and kainate receptor subunit expression in comparison to motor neurons. Our findings indicate a precise spatio-temporal regulation of individual subunit expression in the developing spinal cord. Specific combinations of subunits in developing neurons influence their excitable properties and could participate in the emergence of adult neuronal form and function.

Published
2001
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17. Experience-dependent development of spinal motor neurons

Author

Inglis, F. M, Zuckerman, K. E, Kalb, R. G, and Walton, K. D

Subjects
Life Sciences (General)
Abstract

Locomotor activity in many species undergoes pronounced alterations in early postnatal life, and environmental cues may be responsible for modifying this process. To determine how these events are reflected in the nervous system, we studied rats reared under two different conditions-the presence or absence of gravity-in which the performance of motor operations differed. We found a significant effect of rearing environment on the size and complexity of dendritic architecture of spinal motor neurons, particularly those that are likely to participate in postural control. These results provide evidence that neurons subserving motor function undergo activity-dependent maturation in early postnatal life in a manner analogous to sensory systems.

Published
2000
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26. Loss of RAD-23 Protects Against Models of Motor Neuron Disease by Enhancing Mutant Protein Clearance

Author

Jablonski, A. M., primary, Lamitina, T., additional, Liachko, N. F., additional, Sabatella, M., additional, Lu, J., additional, Zhang, L., additional, Ostrow, L. W., additional, Gupta, P., additional, Wu, C.-Y., additional, Doshi, S., additional, Mojsilovic-Petrovic, J., additional, Lans, H., additional, Wang, J., additional, Kraemer, B., additional, and Kalb, R. G., additional

Published
2015
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30. FOXO3a is broadly neuroprotective in vitro and in vivo against insults implicated in motor neuron diseases

Author

Mojsilovic-Petrovic, J., Nedelsky, N., Boccitto, M., Mano, I., Georgiades, Savvas N., Zhou, W., Liu, Y., Neve, R. L., Taylor, J. P., Driscoll, M., Clardy, J., Merry, D., Kalb, R. G., and Georgiades, Savvas N. [0000-0002-6106-9904]

Subjects
Cell Culture Techniques, nerve degeneration, Cell Count, Rats, Sprague-Dawley, Mice, androgen receptor, Excitatory Amino Acid Agonists, rat, Motor Neurons, Kainic Acid, Cell Death, General Neuroscience, Neurodegeneration, Forkhead Box Protein O3, article, transcription factor DAF 16, Forkhead Transcription Factors, Immunohistochemistry, medicine.anatomical_structure, Neuroprotective Agents, priority journal, Spinal Cord, motor neuron disease, transcription factor FKHRL1, Female, Drosophila, neuroprotection, Signal transduction, Neuron death, excitotoxicity, signal transduction, Signal Transduction, Programmed cell death, in vitro study, animal experiment, Blotting, Western, embryo, Biology, Neuroprotection, Article, Fluorescence, animal tissue, in vivo study, male, In vivo, medicine, Animals, controlled study, Motor Neuron Disease, protein expression, mouse, nonhuman, nerve cell necrosis, animal model, Computational Biology, Motor neuron, medicine.disease, Embryo, Mammalian, nuclear localization signal, Rats, Androgen receptor, Mice, Inbred C57BL, Disease Models, Animal, Tyrosine, Neuroscience
Abstract

Aging is a risk factor for the development of adult-onset neurodegenerative diseases. Although some of the molecular pathways regulating longevity and stress resistance in lower organisms are defined (i.e., those activating the transcriptional regulators DAF-16 and HSF-1 in Caenorhabditis elegans), their relevance to mammals and disease susceptibility are unknown. We studied the signaling controlled by the mammalian homolog of DAF-16, FOXO3a, in model systems of motor neuron disease. Neuron death elicited in vitro by excitotoxic insult or the expression of mutant SOD1, mutant p150glued, or polyQ-expanded androgen receptor was abrogated by expression of nuclear-targeted FOXO3a. We identify a compound [Psammaplysene A (PA)] that increases nuclear localization of FOXO3a in vitro and in vivo and show that PA also protects against these insults in vitro. Administration of PA to invertebrate model systems of neurodegeneration similarly blocked neuron death in a DAF-16/FOXO3a-dependent manner. These results indicate that activation of the DAF-16/FOXO3a pathway, genetically or pharmacologically, confers protection against the known causes of motor neuron diseases. Copyright © 2009 Society for Neuroscience. 29 25 8236 8247 Cited By :52

Published
2009

32. Evidence-based guideline: Assessment and management of psychiatric disorders in individuals with MS: Report of the Guideline Development Subcommittee of the American Academy of Neurology

Author

Minden, S. L., primary, Feinstein, A., additional, Kalb, R. C., additional, Miller, D., additional, Mohr, D. C., additional, Patten, S. B., additional, Bever, C., additional, Schiffer, R. B., additional, Gronseth, G. S., additional, and Narayanaswami, P., additional

Published
2013
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33. Reduced Activity of AMP-Activated Protein Kinase Protects against Genetic Models of Motor Neuron Disease

Author

Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Neve, Rachael L., Lim, M. A., Selak, M. A., Xiang, Z., Krainc, Dimitri, Kraemer, B. C., Watts, J. L., Kalb, R. G., Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences, Neve, Rachael L., Lim, M. A., Selak, M. A., Xiang, Z., Krainc, Dimitri, Kraemer, B. C., Watts, J. L., and Kalb, R. G.

Abstract

A growing body of research indicates that amyotrophic lateral sclerosis (ALS) patients and mouse models of ALS exhibit metabolic dysfunction. A subpopulation of ALS patients possesses higher levels of resting energy expenditure and lower fat-free mass compared to healthy controls. Similarly, two mutant copper zinc superoxide dismutase 1 (mSOD1) mouse models of familial ALS possess a hypermetabolic phenotype. The pathophysiological relevance of the bioenergetic defects observed in ALS remains largely elusive. AMP-activated protein kinase (AMPK) is a key sensor of cellular energy status and thus might be activated in various models of ALS. Here, we report that AMPK activity is increased in spinal cord cultures expressing mSOD1, as well as in spinal cord lysates from mSOD1 mice. Reducing AMPK activity either pharmacologically or genetically prevents mSOD1-induced motor neuron death in vitro. To investigate the role of AMPK in vivo, we used Caenorhabditis elegans models of motor neuron disease. C. elegans engineered to express human mSOD1 (G85R) in neurons develops locomotor dysfunction and severe fecundity defects when compared to transgenic worms expressing human wild-type SOD1. Genetic reduction of aak-2, the ortholog of the AMPK α2 catalytic subunit in nematodes, improved locomotor behavior and fecundity in G85R animals. Similar observations were made with nematodes engineered to express mutant tat-activating regulatory (TAR) DNA-binding protein of 43 kDa molecular weight. Altogether, these data suggest that bioenergetic abnormalities are likely to be pathophysiologically relevant to motor neuron disease.

Published
2012

41. Role of GluR1 in Activity-Dependent Motor System Development

Author

Zhang, L., primary, Schessl, J., additional, Werner, M., additional, Bonnemann, C., additional, Xiong, G., additional, Mojsilovic-Petrovic, J., additional, Zhou, W., additional, Cohen, A., additional, Seeburg, P., additional, Misawa, H., additional, Jayaram, A., additional, Personius, K., additional, Hollmann, M., additional, Sprengel, R., additional, and Kalb, R., additional

Published
2008
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43. A comprehensive strategy for the subtyping of patients with Fanconi anaemia: conclusions from the Spanish Fanconi Anemia Research Network

Author

Antonio Casado, J., primary, Callen, E., additional, Jacome, A., additional, Rio, P., additional, Castella, M., additional, Lobitz, S., additional, Ferro, T., additional, Munoz, A., additional, Sevilla, J., additional, Cantalejo, A., additional, Cela, E., additional, Cervera, J., additional, Sanchez-Calero, J., additional, Badell, I., additional, Estella, J., additional, Dasi, A., additional, Olive, T., additional, Jose Ortega, J., additional, Rodriguez-Villa, A., additional, Tapia, M., additional, Molines, A., additional, Madero, L., additional, Segovia, J. C, additional, Neveling, K., additional, Kalb, R., additional, Schindler, D., additional, Hanenberg, H., additional, Surralles, J., additional, and Bueren, J. A, additional

Published
2007
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44. Disruption of the FA/BRCA pathway in bladder cancer

Author

Neveling, K., primary, Kalb, R., additional, Florl, A.R., additional, Herterich, S., additional, Friedl, R., additional, Hoehn, H., additional, Hader, C., additional, Hartmann, F.H., additional, Nanda, I., additional, Steinlein, C., additional, Schmid, M., additional, Tönnies, H., additional, Hurst, C.D., additional, Knowles, M.A., additional, Hanenberg, H., additional, Schulz, W.A., additional, and Schindler, D., additional

Published
2007
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46. Addendum: The BRCA1-interacting helicase BRIP1 is deficient in Fanconi anemia

Author

Levran, O, primary, Attwooll, C, additional, Henry, R T, additional, Milton, K L, additional, Neveling, K, additional, Rio, P, additional, Batish, S D, additional, Kalb, R, additional, Velleuer, E, additional, Barral, S, additional, Ott, J, additional, Petrini, J, additional, Schindler, D, additional, Hanenberg, H, additional, and Auerbach, A D, additional

Published
2005
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50. Mixtures of tails in clustered automobile collision claims

Author

Kalb, R. (Reinhard), Kofman, P. (Paul), Vorst, A.C.F. (Ton), Kalb, R. (Reinhard), Kofman, P. (Paul), and Vorst, A.C.F. (Ton)

Abstract

Knowledge of the tail shape of claim distributions provides important actuarial information. This paper discusses how two techniques commonly used in assessing the most appropriate underlying distribution can be usefully combined. The maximum likelihood approach is theoretically appealing since it is preferable to many other estimators in the sense of best asymptotic normality. Likelihood based tests are, however, not always capable to discriminate among non-nested classes of distributions. Extremal value theory offers an attractive tool to overcome this problem. It shows that a much larger set of distributions is nested in their tails by the so-called tail parameter. This paper shows that both estimation strategies can be usefully combined when the data generating process is characterized by strong clustering in time and size. We find that the extreme value theory is a useful starting point in detecting the appropriate distribution class. Once that has been achieved, the likelihood-based EM-algorithm is proposed to capture the clustering phenomena. Clustering is particularly pervasive in actuarial data. An empirical application to a four-year data set of Dutch automobile collision claims is therefore used to illustrate the approach.

Published
1996
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