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. 2015 Sep;10(9):1413-5.
doi: 10.4103/1673-5374.165308.

Is hyperexcitability really guilty in amyotrophic lateral sclerosis?

Felix Leroy  1 , Daniel Zytnicki  1
Affiliations

Is hyperexcitability really guilty in amyotrophic lateral sclerosis?

Felix Leroy et al. Neural Regen Res. 2015 Sep.
No abstract available

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Figures

Figure 1
Figure 1
Mechanisms regulating the motoneuron spiking activity and cytosolic calcium concentration. Motoneurons can become hyperexcited following and increase in glutamatergic of cholinergic activation, a decrease in the glutamate clearance by astrocytes or a decrease of the inhibition strength (green). Intrinsically, motoneurons can become hyperexcitable if their passive or active electrical properties (blue) facilitate the emission of action potential in the axon initial segment, for example if the input resistance or the sodium conductance increases. Inversely they can become hypoexcitable if the input resistance decreases or the potassium conductances increase. Calcium can enter through many channels and receptors such as the voltage-operated channels that open during spiking, the ligand-gated channels (AMPA, NMDA) and the second-messenger-activated channels. Finally, various calcium reservoirs (mitochondrial, endoplasmic reticulum) buffer the cytosolic calcium that enters the cell. ER: Endoplasmic reticulum; AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; NMDA: N-methyl-D-aspartate.
See this image and copyright information in PMC

References

    1. Bories C, Amendola J, Lamotte d’Incamps B, Durand J. Early electrophysiological abnormalities in lumbar motoneurons in a transgenic mouse model of amyotrophic lateral sclerosis. Eur J Neurosci. 2007;25:451–459. - PubMed
    1. Calvo-Gallardo E, de Pascual R, Fernandez-Morales JC, Arranz-Tagarro JA, Maroto M, Nanclares C, Gandia L, de Diego AM, Padin JF, Garcia AG. Depressed excitability and ion currents linked to slow exocytotic fusion pore in chromaffin cells of the SOD1(G93A) mouse model of amyotrophic lateral sclerosis. Am J Physiol Cell Physiol. 2015;308:C1–19. - PubMed
    1. Delestree N, Manuel M, Iglesias C, Elbasiouny SM, Heckman CJ, Zytnicki D. Adult spinal motoneurones are not hyperexcitable in a mouse model of inherited amyotrophic lateral sclerosis. J Physiol. 2014;592:1687–703. - PMC - PubMed
    1. Hadzipasic M, Tahvildari B, Nagy M, Bian M, Horwich AL, McCormick DA. Selective degeneration of a physiological subtype of spinal motor neuron in mice with SOD1-linked ALS. Proc Natl Acad Sci U S A. 2014;111:16883–16888. - PMC - PubMed
    1. Ilieva H, Polymenidou M, Cleveland DW. Non-cell autonomous toxicity in neurodegenerative disorders: ALS and beyond. J Cell Biol. 2009;187:761–772. - PMC - PubMed

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