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Lindquist, Nils Gunnar
Publications (4 of 4) Show all publications
Brittebo, E., Karlsson, O., Andersson, M., Berg, A.-L., Roman, E., Lindquist, N. G. & Hanrieder, J. (2012). Neurotoxin-induced fibril formation and protein changes in rodents. Toxicology Letters, 211(Suppl.), S193-193
Open this publication in new window or tab >>Neurotoxin-induced fibril formation and protein changes in rodents
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2012 (English)In: Toxicology Letters, ISSN 0378-4274, E-ISSN 1879-3169, Vol. 211, no Suppl., p. S193-193Article in journal, Meeting abstract (Other academic) Published
National Category
Neurosciences
Identifiers
urn:nbn:se:uu:diva-287605 (URN)10.1016/j.toxlet.2012.03.693 (DOI)
Available from: 2016-04-25 Created: 2016-04-25 Last updated: 2018-01-10Bibliographically approved
Karlsson, O., Berg, C., Brittebo, E. B. & Lindquist, N. G. (2009). Retention of the cyanobacterial neurotoxin beta-N-methylamino-l-alanine in melanin and neuromelanin-containing cells: a possible link between Parkinson-dementia complex and pigmentary retinopathy. Pigment cell & melanoma research, 22(1), 120-130
Open this publication in new window or tab >>Retention of the cyanobacterial neurotoxin beta-N-methylamino-l-alanine in melanin and neuromelanin-containing cells: a possible link between Parkinson-dementia complex and pigmentary retinopathy
2009 (English)In: Pigment cell & melanoma research, ISSN 1755-1471, Vol. 22, no 1, p. 120-130Article in journal (Refereed) Published
Abstract [en]

beta-N-methylamino-l-alanine (BMAA), a neurotoxic amino acid produced by cyanobacteria, has been suggested to be involved in the etiology of a neurodegenerative disease complex which includes Parkinson-dementia complex (PDC). In PDC, neuromelanin-containing neurons in substantia nigra are degenerated. Many PDC patients also have an uncommon pigmentary retinopathy. The aim of this study was to investigate the distribution of (3)H-BMAA in mice and frogs, with emphasis on pigment-containing tissues. Using autoradiography, a distinct retention of (3)H-BMAA was observed in melanin-containing tissues such as the eye and neuromelanin-containing neurons in frog brain. Analysis of the binding of (3)H-BMAA to Sepia melanin in vitro demonstrated two apparent binding sites. In vitro-studies with synthetic melanin revealed a stronger interaction of (3)H-BMAA with melanin during synthesis than the binding to preformed melanin. Long-term exposure to BMAA may lead to bioaccumulation in melanin- and neuromelanin-containing cells causing high intracellular levels, and potentially changed melanin characteristics via incorporation of BMAA into the melanin polymer. Interaction of BMAA with melanin may be a possible link between PDC and pigmentary retinopathy.

Keywords
BMAA, neuromelanin, melanin, frog, Parkinson, ALS/PDC
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:uu:diva-102429 (URN)10.1111/j.1755-148X.2008.00508.x (DOI)000262513500016 ()19154235 (PubMedID)
Available from: 2010-03-31 Created: 2009-05-07 Last updated: 2018-01-13Bibliographically approved
Karlsson, O., Lindquist, N. G., Brittebo, E. B. & Roman, E. (2009). Selective Brain Uptake and Behavioral Effects of the Cyanobacterial Toxin BMAA (β-N-Methylamino-L-alanine) following Neonatal Administration to Rodents. Toxicological Sciences, 109(2), 286-295
Open this publication in new window or tab >>Selective Brain Uptake and Behavioral Effects of the Cyanobacterial Toxin BMAA (β-N-Methylamino-L-alanine) following Neonatal Administration to Rodents
2009 (English)In: Toxicological Sciences, ISSN 1096-6080, E-ISSN 1096-0929, Vol. 109, no 2, p. 286-295Article in journal (Refereed) Published
Abstract [en]

Cyanobacteria are extensively distributed in terrestrial and aquatic environments all over the world. Most cyanobacteria can produce the neurotoxin ss-N-methylamino-L-alanine (BMAA), which has been detected in several water systems and could accumulate in food chains. The aim of the study was to investigate the transfer of BMAA to fetal and neonatal brains and the effects of BMAA on the development of behavioral characteristics during the brain growth spurt (BGS) in rodents Pregnant and neonatal mice were given an injection of (3)H-BMAA on gestational day 14 and postnatal day (PND) 10, respectively, and processed for tape-section autoradiography. The study revealed transplacental transfer of (3)H-BMAA and a significant uptake in fetal mouse. The radioactivity was specifically located in the hippocampus, striatum, brainstem, spinal cord and cerebellum of 10-day-old mice. The effect of repeated BMAA treatment (200 or 600 mg/kg sc) during BGS on rat behavior was also studied. BMAA treatment on PND 9-10 induced acute alterations, such as impaired locomotor ability and hyperactivity, in the behavior of neonatal rats. Furthermore, rats given the high dose of BMAA failed to habituate to the test environment when tested at juvenile age. In conclusion, the results demonstrated that BMAA was transferred to the neonatal brain and induced significant changes in the behavior of neonatal rats following administration during BGS. The observed behavioral changes suggest possible cognitive impairment. Increased information on the long-term effects of BMAA on cognitive function following fetal and neonatal exposure is required for assessment of the risk to children's health.

Keywords
neurotoxin, ALS, PDC, hippocampus, striatum, brain growth spurt, seizure
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:uu:diva-102428 (URN)10.1093/toxsci/kfp062 (DOI)000266357900013 ()19321797 (PubMedID)
Available from: 2010-03-31 Created: 2009-05-07 Last updated: 2018-01-13Bibliographically approved
Ostergren, A., Svensson, A.-L., Lindquist, N. G. & Brittebo, E. B. (2005). Dopamine melanin-loaded PC12 cells: a model for studies on pigmented neurons.. Pigment Cell Res, 18(4), 306-14
Open this publication in new window or tab >>Dopamine melanin-loaded PC12 cells: a model for studies on pigmented neurons.
2005 (English)In: Pigment Cell Res, ISSN 0893-5785, Vol. 18, no 4, p. 306-14Article in journal (Refereed) Published
Keywords
Amyloid beta-Protein/toxicity, Animals, Caspases/metabolism, Cell Survival/drug effects, Enzyme Activation, Heat-Shock Proteins/biosynthesis, Melanins/*metabolism/pharmacology, Microscopy; Electron; Transmission, Molecular Chaperones/biosynthesis, Neurons/drug effects/*metabolism/ultrastructure, PC12 Cells, Peptide Fragments/toxicity, Pigmentation, Rats, Research Support; Non-U.S. Gov't
Identifiers
urn:nbn:se:uu:diva-75601 (URN)16029423 (PubMedID)
Available from: 2006-02-13 Created: 2006-02-13 Last updated: 2011-01-11
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