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Electrophysiological properties of functionally identified adult mouse motoneurons

100%

Manuel M.

2019

tom 79

nr Suppl.1

A salient feature in Amyotrophic Lateral Sclerosis (ALS) is that the vulnerability of motoneurons depends on the physiological type of their motor unit. The most vulnerable motoneurons, and the first to degenerate, are the motoneurons of the largest motor units that innervate the fast-contracting and fatigable muscle fibers (FF type), followed by the motoneurons of intermediate motor unit size, which innervate the fast-contracting and fatigue-resistant muscle fibers (FR type). Finally, the motoneurons of the smallest motor units, which mainly innervate the slow contracting and fatigue-resistant fibers (S type) are the most resistant and the least affected at the end-stage of disease. However, not much is known about the physiology of motor units in mice, compared to other species (cats and rats in particular). I have spent the last few years studying the intrinsic properties of adult mouse motoneurons while recording simultaneously the force developed by their motor unit. We’ve already demonstrated that the unusual electrical properties of mouse motoneurons have a profound impact on the force recruitment of their motor units. In my talk, I will present recent efforts in characterizing the electrical and mechanical properties of type-identified mouse motoneurons and motor units, and their potential relevance for understanding the pathophysiological mechanisms of ALS.

IA monosynaptic pathway in SODI mouse model of amyothropic lateral sclerosis

45%

Baczyk M. , Martinot C. , Delestree N. , Manuel M. , Zytnicki D.

Acta Neurobiologiae Experimentalis

2015

tom 75

nr Supl.

BACKGROUND AND AIMS: Glutamate excitotoxicity has long been suggested to contribute to the degeneration of motoneurons in Amyotrophic Lateral Sclerosis (ALS). However, it has recently been shown that spinal motoneurons do not display an intrinsic hyperexcitability just prior to their degeneration in SOD1 G93A mice, the standard model of ALS. Furthermore average densities of excitatory (VGLUT1 and VGLUT2) and inhibitory (VGAT) boutons on the dendritic tree and the soma of affected motoneurons were unchanged. However glutamate excitotoxicity can still take place if excitatory pathways are more active. Therefore the aim of this study was to investigate the excitability of the monosynaptic Ia pathway in SOD1 mice. METHODS: Eight SOD1 G93A and six SOD WT control mice were used in this study. Intracellularly penetrated motoneurons were identified as a medial gastrocnemius (MG) or lateral gastrocnemius (LG) motoneurons by their threshold for antidromic activation. Ia monosynaptic EPSPs were recorded from these motoneurons after stimulation of their homonymous nerve. In parallel the afferent Ia volley was recorded from the cord dorsum. Increasing stimulation intensities were used to obtain minimum and maximum Ia Volleys and EPSPs. RESULTS: The average amplitudes of monosynaptic Ia EPSPs in SOD1 motoneurons were significantly smaller when compared to SOD WT controls (1.40 mV and 2.24 mV, respectively). Moreover the EPSP difference was mainly visible for the group of motoneurons characterized by high input resistance (above 3 MΩ). On the other hand, the recruitment curves (normalized amplitude vs. stim intensity) of Ia volleys and EPSPs were unchanged, suggesting no change in excitability of Ia fibers but alterations in Ia monosynaptic synapses. CONCLUSIONS: Results indicate alterations in Ia monosynaptic pathway in presymptomatic SOD1 ALS mouse model. This can stem from several reasons, e.g. increased presynaptic inhibition of Ia terminals or reduced efficacy of post-synaptic receptors.

Structural genomics of the human protein kinase family

17%

Aparicio A. , Brooun A. , Chien E. , Chi E. , Collins B. , Cronin C. N. , Davies A. , Dougan D. , Heien E. , Hilgers M. , Hosfield D. , Hu M. , Kassel D. , Kim S. , Knuth M. W. , Kraus M. , Levin I. , Lim K. , Manuel M. , Mcree D. E. , Mol C. D. , Nowakowski J. , Rogers J. , Roth B. , Sang B. C. , Scheibe D. , Skene R. , Sridhar V. , Swanson R. V. , Thompson D. A. , Witmer D. , Wynands R. , Snell G. , Wilson K. P. , Textor G. , Vaughn D. , Ye S. , Zoa H.

Cellular and Molecular Biology Letters

2003

tom 08

nr 2A