Author, as appears in the article.: Lanuza, Maria A.; Just-Borras, Laia; Hurtado, Erica; Cilleros-Mane, Victor; Tomas, Marta; Garcia, Neus; Tomas, Josep;

Department: Ciències Mèdiques Bàsiques

URV's Author/s: Cilleros Mañé, Víctor / Garcia Sancho, Maria de les Neus / Just Borràs, Laia / Lanuza Escolano, María Angel / Tomás Ferré, José Maria / Tomas Marginet, Marta

Keywords: Trkb Transmitter release Transgenic mouse model Skeletal-muscle Protein-kinase Presynaptic muscarinic autoreceptors Pkc Nmj Neurotrophic factor Neuromuscular Motor-neuron Kinase In-vivo Exercise Bdnf Als Adult-rat Acetylcholine-release trkb pkc nmj kinase exercise bdnf als

Abstract: Brain-derived neurotrophic factor (BDNF) promotes neuron survival in adulthood in the central nervous system. In the peripheral nervous system, BDNF is a contraction-inducible protein that, through its binding to tropomyosin-related kinase B receptor (TrkB), contributes to the retrograde neuroprotective control done by muscles, which is necessary for motor neuron function. BDNF/TrkB triggers downstream presynaptic pathways, involving protein kinase C, essential for synaptic function and maintenance. Undeniably, this reciprocally regulated system exemplifies the tight communication between nerve terminals and myocytes to promote synaptic function and reveals a new view about the complementary and essential role of pre and postsynaptic interplay in keeping the synapse healthy and strong. This signaling at the neuromuscular junction (NMJ) could establish new intervention targets across neuromuscular diseases characterized by deficits in presynaptic activity and muscle contractility and by the interruption of the connection between nervous and muscular tissues, such as amyotrophic lateral sclerosis (ALS). Indeed, exercise and other therapies that modulate kinases are effective at delaying ALS progression, preserving NMJs and maintaining motor function to increase the life quality of patients. Altogether, we review synaptic activity modulation of the BDNF/TrkB/PKC signaling to sustain NMJ function, its and other kinases' disturbances in ALS and physical and molecular mechanisms to delay disease progression.

Thematic Areas: Medicine (miscellaneous) Cell biology Biochemistry, genetics and molecular biology (miscellaneous) Biochemistry, genetics and molecular biology (all)

licence for use: https://creativecommons.org/licenses/by/3.0/es/

ISSN: 20734409

Author's mail: victor.cilleros@urv.cat marta.tomas@urv.cat mariaangel.lanuza@urv.cat laia.just@urv.cat josepmaria.tomas@urv.cat victor.cilleros@urv.cat

Author identifier: 0000-0001-5690-9932 0000-0002-4151-1697 0000-0003-4795-4103 0000-0003-0473-3730 0000-0002-0406-0006 0000-0001-5690-9932

Record's date: 2023-09-23

Papper version: info:eu-repo/semantics/publishedVersion

Link to the original source: https://www.mdpi.com/2073-4409/8/12/1578

Licence document URL: http://repositori.urv.cat/ca/proteccio-de-dades/

Papper original source: Cells. 8 (12):

APA: Lanuza, Maria A.; Just-Borras, Laia; Hurtado, Erica; Cilleros-Mane, Victor; Tomas, Marta; Garcia, Neus; Tomas, Josep; (2019). The Impact of Kinases in Amyotrophic Lateral Sclerosis at the Neuromuscular Synapse: Insights into BDNF/TrkB and PKC Signaling. Cells, 8(12), -. DOI: 10.3390/cells8121578

Article's DOI: 10.3390/cells8121578

Entity: Universitat Rovira i Virgili

Journal publication year: 2019

Publication Type: Journal Publications