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β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats
Cyanobacterial β-N-methylamino-l-alanine (BMAA) has been suggested as a causative or contributory factor in the development of several neurodegenerative diseases. However, no BMAA animal model has adequately shown clinical or behavioral symptoms that correspond to those seen in either Alzheimer’s Di...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793103/ https://www.ncbi.nlm.nih.gov/pubmed/29280981 http://dx.doi.org/10.3390/toxins10010016 |
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author | Scott, Laura Louise Downing, Timothy Grant |
author_facet | Scott, Laura Louise Downing, Timothy Grant |
author_sort | Scott, Laura Louise |
collection | PubMed |
description | Cyanobacterial β-N-methylamino-l-alanine (BMAA) has been suggested as a causative or contributory factor in the development of several neurodegenerative diseases. However, no BMAA animal model has adequately shown clinical or behavioral symptoms that correspond to those seen in either Alzheimer’s Disease (AD), Amyotrophic Lateral Sclerosis (ALS) or Parkinson’s Disease (PD). We present here the first data that show that when neonatal rats were exposed to BMAA on postnatal days 3, 4 and 5, but not on gestational day 14 or postnatally on days 7 or 10, several AD and/or PD-related behavioral, locomotor and cognitive deficits developed. Male rats exhibited severe unilateral hindlimb splay while whole body tremors could be observed in exposed female rats. BMAA-exposed rats failed to identify and discriminate a learned odor, an early non-motor symptom of PD, and exhibited decreased locomotor activity, decreased exploration and increased anxiety in the open field test. Alterations were also observed in the rats’ natural passive defense mechanism, and potential memory deficits and changes to the rat’s natural height avoidance behavior could be observed as early as PND 30. Spatial learning, short-term working, reference and long-term memory were also impaired in 90-day-old rats that had been exposed to a single dose of BMAA on PND 3–7. These data suggest that BMAA is a developmental neurotoxin, with specific target areas in the brain and spinal cord. |
format | Online Article Text |
id | pubmed-5793103 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-57931032018-02-06 β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats Scott, Laura Louise Downing, Timothy Grant Toxins (Basel) Article Cyanobacterial β-N-methylamino-l-alanine (BMAA) has been suggested as a causative or contributory factor in the development of several neurodegenerative diseases. However, no BMAA animal model has adequately shown clinical or behavioral symptoms that correspond to those seen in either Alzheimer’s Disease (AD), Amyotrophic Lateral Sclerosis (ALS) or Parkinson’s Disease (PD). We present here the first data that show that when neonatal rats were exposed to BMAA on postnatal days 3, 4 and 5, but not on gestational day 14 or postnatally on days 7 or 10, several AD and/or PD-related behavioral, locomotor and cognitive deficits developed. Male rats exhibited severe unilateral hindlimb splay while whole body tremors could be observed in exposed female rats. BMAA-exposed rats failed to identify and discriminate a learned odor, an early non-motor symptom of PD, and exhibited decreased locomotor activity, decreased exploration and increased anxiety in the open field test. Alterations were also observed in the rats’ natural passive defense mechanism, and potential memory deficits and changes to the rat’s natural height avoidance behavior could be observed as early as PND 30. Spatial learning, short-term working, reference and long-term memory were also impaired in 90-day-old rats that had been exposed to a single dose of BMAA on PND 3–7. These data suggest that BMAA is a developmental neurotoxin, with specific target areas in the brain and spinal cord. MDPI 2017-12-27 /pmc/articles/PMC5793103/ /pubmed/29280981 http://dx.doi.org/10.3390/toxins10010016 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Scott, Laura Louise Downing, Timothy Grant β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title | β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title_full | β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title_fullStr | β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title_full_unstemmed | β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title_short | β-N-Methylamino-l-alanine (BMAA) Toxicity Is Gender and Exposure-Age Dependent in Rats |
title_sort | β-n-methylamino-l-alanine (bmaa) toxicity is gender and exposure-age dependent in rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5793103/ https://www.ncbi.nlm.nih.gov/pubmed/29280981 http://dx.doi.org/10.3390/toxins10010016 |
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