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Environ Toxicol Pharmacol. 2015 May;39(3):1232-45. doi: 10.1016/j.etap.2015.04.022. Epub 2015 May 11.

Morphometric and neurochemical alterations found in l-BMAA treated rats.

Author information

1
Departamento de Biología Animal II, Universidad Complutense de Madrid, 28040 Madrid, Spain. Electronic address: estefania_nemesis@hotmail.com.
2
Departamento de Bioquímica y Biología Molecular I, Universidad Complutense de Madrid, 28040 Madrid, Spain. Electronic address: emmamunoz@ucm.es.
3
Departamento de Bioquímica y Biología Molecular I, Universidad Complutense de Madrid, 28040 Madrid, Spain. Electronic address: bgomezmi@pdi.ucm.es.
4
Departamento de Biología Celular (Morfología Microscópica), Universidad Complutense de Madrid, 28040 Madrid, Spain. Electronic address: msolas@bio.ucm.es.
5
Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, 28040 Madrid, Spain. Electronic address: ana.martinez@csic.es.
6
Departamento de Biología Animal II, Universidad Complutense de Madrid, 28040 Madrid, Spain. Electronic address: rportero@bio.ucm.es.

Abstract

Amyotrophic 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.

KEYWORDS:

ALS; Motor cortex; NMR; Neurotransmitters; Rat; l-BMAA

PMID:
26002186
DOI:
10.1016/j.etap.2015.04.022
[Indexed for MEDLINE]
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