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2019 | 79 | Suppl.1 |

Tytuł artykułu

Modification of monosynaptic Ia EPSP by externally induced electrical fields in SOD1 G93A mouse model of amyotrophic lateral sclerosis

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by a progressive loss of motoneurons with no viable treatment available. A dysregulation of facilitation/inhibition coupling that forces motoneuron hypoexciatability appears to be a key mechanism of the degeneration, and preliminary results suggest that the chemogenetic increase of motoneuron activation ameliorates the disease burden. AIM(S): Here we propose a novel method of manipulating motoneuron synaptic excitation in the SOD1 mouse model of ALS, using the trans-spinal direct current stimulation (tsDCS) technique, which influences both motoneuron intrinsic excitability and synaptic excitation. METHOD(S): Experiments were carried out on presymptomatic SOD1‑G93A mice. Animals were deeply anesthetized with a mix of fentanyl/medetomidine/ midazolam, artificially ventilated, and paralyzed. Intracellular recordings of triceps surae (TS) motoneurons allowed recording of monosynaptic EPSPs from electrically stimulated proprioceptive Ia afferents, which were subsequently conditioned with cathodal tsDCS of 0.1 mA. RESULTS: Cathodal polarization evoked an acute increase of the Ia EPSP amplitude recorded in TS motoneurons (max 200% of control n=10). These alterations were not matched by changes in the Ia afferent activity or motoneuron passive membrane properties, suggesting that the loci of the effects is restricted to the pre- or postsynaptic elements of the Ia synapse. Interestingly, the effects of polarization outlasted its application by at least 15 min. CONCLUSIONS: tsDCS is a potent way of manipulating motoneuron synaptic excitation and may play a role as a therapeutic method for managing ALS. However, the influence of this technique on motoneuron intrinsic excitability and disease progression remains to be elucidated. FINANCIAL SUPPORT: This work was supported by NCN grant no. 2017/26/D/NZ7/00728.

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  • Department of Neurobiology, Poznan University of Physical Education, Poznan, Poland
  • Department of Neurobiology, Poznan University of Physical Education, Poznan, Poland
  • Department of Neurobiology, Poznan University of Physical Education, Poznan, Poland


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