Munck García, Estefanía deMuñoz Sáez, EmmaGómez Miguel, BegoñaSolas Alados, Mª TeresaMartínez, AnaArahuetes, Rosa María2023-06-182023-06-182015-051382-668910.1016/j.etap.2015.04.022https://hdl.handle.net/20.500.14352/23212Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive muscle paralysis that reflects the motoneurons’ degeneration. Several studies support the relationship between β-N-methylamino-L-alanine (L-BMAA), a neurotoxic amino acid produced by cyanobacteria and diatoms, and the sporadic occurrence of ALS and other neurodegenerative diseases. Therefore, the study of its neurotoxicity mechanisms has assumed great relevance in recent years. Recently, our research team has proposed a sporadic ALS animal model by L-BMAA administration in rats, which displays many pathophysiological features of human ALS. In this paper, we deepen the characterization of this model corroborating the occurrence of alterations present in ALS patients such as decreased muscle volume, thinning of the motor cortex, enlarged brain's lateral ventricles, and alteration of both bulbar nuclei and neurotransmitters’ levels. Therefore, we conclude that L-BMAA treated rats could be a good model which mimics degenerative features that ALS causes in humans.engjournal articlehttp://dx.doi.org/10.1016/j.etap.2015.04.022restricted access612.8.015576ALSl-BMAARatNeurotransmittersMotor cortexNMRNeurochemistryBiología celular (Biología)Neurociencias (Biológicas)2407 Biología Celular2490 Neurociencias