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3. A mutation in the dynein heavy chain gene compensates for energy deficit of mutant SOD1 mice and increases potentially neuroprotective IGF-1

Author

Larmet Yves, Oudart Hugues, Eschbach Judith, Fergani Anissa, Schwalenstocker Birgit, Ludolph Albert C, Loeffler Jean-Philippe, and Dupuis Luc

Subjects
Neurology. Diseases of the nervous system, RC346-429, Geriatrics, RC952-954.6
Abstract

Abstract Background Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motor neurons. ALS patients, as well as animal models such as mice overexpressing mutant SOD1s, are characterized by increased energy expenditure. In mice, this hypermetabolism leads to energy deficit and precipitates motor neuron degeneration. Recent studies have shown that mutations in the gene encoding the dynein heavy chain protein are able to extend lifespan of mutant SOD1 mice. It remains unknown whether the protection offered by these dynein mutations relies on a compensation of energy metabolism defects. Results SOD1(G93A) mice were crossbred with mice harboring the dynein mutant Cramping allele (Cra/+ mice). Dynein mutation increased adipose stores in compound transgenic mice through increasing carbohydrate oxidation and sparing lipids. Metabolic changes that occurred in double transgenic mice were accompanied by the normalization of the expression of key mRNAs in the white adipose tissue and liver. Furthermore, Dynein Cra mutation rescued decreased post-prandial plasma triglycerides and decreased non esterified fatty acids upon fasting. In SOD1(G93A) mice, the dynein Cra mutation led to increased expression of IGF-1 in the liver, increased systemic IGF-1 and, most importantly, to increased spinal IGF-1 levels that are potentially neuroprotective. Conclusions These findings suggest that the protection against SOD1(G93A) offered by the Cramping mutation in the dynein gene is, at least partially, mediated by a reversal in energy deficit and increased IGF-1 availability to motor neurons.

Published
2011
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4. Serotonin 2B receptor slows disease progression and prevents degeneration of spinal cord mononuclear phagocytes in amyotrophic lateral sclerosis

Author

El Oussini, Hajer, Bayer, Hanna, Scekic-Zahirovic, Jelena, Vercruysse, Pauline, Sinniger, Jérôme, Dirrig-Grosch, Sylvie, Dieterlé, Stéphane, Echaniz-Laguna, Andoni, Larmet, Yves, Müller, Kathrin, Weishaupt, Jochen H, Thal, Dietmar R, van Rheenen, Wouter, van Eijk, Kristel, Lawson, Roland, Monassier, Laurent, Maroteaux, Luc, Roumier, Anne, Wong, Philip C, van den Berg, Leonard H, Ludolph, Albert C, Veldink, Jan H, Witting, Anke, Dupuis, Luc, El Oussini, Hajer, Bayer, Hanna, Scekic-Zahirovic, Jelena, Vercruysse, Pauline, Sinniger, Jérôme, Dirrig-Grosch, Sylvie, Dieterlé, Stéphane, Echaniz-Laguna, Andoni, Larmet, Yves, Müller, Kathrin, Weishaupt, Jochen H, Thal, Dietmar R, van Rheenen, Wouter, van Eijk, Kristel, Lawson, Roland, Monassier, Laurent, Maroteaux, Luc, Roumier, Anne, Wong, Philip C, van den Berg, Leonard H, Ludolph, Albert C, Veldink, Jan H, Witting, Anke, and Dupuis, Luc

Published
2016

5. Serotonin 2B receptor slows disease progression and prevents degeneration of spinal cord mononuclear phagocytes in amyotrophic lateral sclerosis

Author

Opleiding Neurologie, Brain, Projectafdeling ALS, Regenerative Medicine and Stem Cells, ZL Neuromusculaire Ziekten Medisch, Neurogenetica, El Oussini, Hajer, Bayer, Hanna, Scekic-Zahirovic, Jelena, Vercruysse, Pauline, Sinniger, Jérôme, Dirrig-Grosch, Sylvie, Dieterlé, Stéphane, Echaniz-Laguna, Andoni, Larmet, Yves, Müller, Kathrin, Weishaupt, Jochen H, Thal, Dietmar R, van Rheenen, Wouter, van Eijk, Kristel, Lawson, Roland, Monassier, Laurent, Maroteaux, Luc, Roumier, Anne, Wong, Philip C, van den Berg, Leonard H, Ludolph, Albert C, Veldink, Jan H, Witting, Anke, Dupuis, Luc, Opleiding Neurologie, Brain, Projectafdeling ALS, Regenerative Medicine and Stem Cells, ZL Neuromusculaire Ziekten Medisch, Neurogenetica, El Oussini, Hajer, Bayer, Hanna, Scekic-Zahirovic, Jelena, Vercruysse, Pauline, Sinniger, Jérôme, Dirrig-Grosch, Sylvie, Dieterlé, Stéphane, Echaniz-Laguna, Andoni, Larmet, Yves, Müller, Kathrin, Weishaupt, Jochen H, Thal, Dietmar R, van Rheenen, Wouter, van Eijk, Kristel, Lawson, Roland, Monassier, Laurent, Maroteaux, Luc, Roumier, Anne, Wong, Philip C, van den Berg, Leonard H, Ludolph, Albert C, Veldink, Jan H, Witting, Anke, and Dupuis, Luc

Published
2016

8. Ionic Currents in Neurones Cultured From Embryonic Cockroach (Periplaneta Americana) Brains

Author

Christensen, Burgess N., Larmet, Yves, Shimahara, Takeshi, Beadle, David, and Pichon, Yves

Abstract

Neurones isolated from embryonic cockroach brains were maintained in culture for up to 8 weeks. A single patch electrode was used to record voltage changes in response to injected current, membrane ionic currents under whole-cell voltageclamp conditions or single-channel currents from isolated membrane patches. The voltage changes in response to injected current that depolarized the cell indicated increases in membrane permeability to calcium and potassium. These observations were confirmed using a voltage clamp. The potassium current observed in the youngest cultures turned on with a delay and was blocked by tetraethylammonium (TEA) and 4-aminopyridine (4-AP). Two kinds of decrease in the outward potassium current were observed. One may be associated with extracellular potassium accumulation, inactivation of the potassium channel or inactivation of a calcium channel. The other appears to be a voltage-dependent inactivation. The magnitude of the calcium permeability appeared to increase as the cultures developed, being most prominent in cultures more than 2 weeks old. Single-channel conductance measured from an analysis of records from six isolated membrane patches ranged from 15 to 110pS. Except for one channel, the probability of the channels being open did not change appreciably with membrane potential. Our results suggest that much of the increase in potassium permeability may be due an increase in intracellular calcium level.

Published
1988
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