Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-beta 1-40 peptide in mice

Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-beta 1-40 peptide in mice

Author Amaral, Fabio Agostini Google Scholar
Resk Lemos, Mayra Tolentino Google Scholar
Dong, Karis Ester Google Scholar
Queiroz Prado Bittencourt, Maria Fernanda Google Scholar
Caetano, Ariadiny Lima Google Scholar
Pesquero, Joao Bosco Autor UNIFESP Google Scholar
Viel, Tania Araujo Google Scholar
Buck, Hudson Sousa Google Scholar
Institution Fac Ciencies Med Santa Casa São Paulo
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Abstract Chronic infusion of human amyloid-beta 1-40 (A beta) in the lateral ventricle (LV) of rats is associated with memory impairment and increase of kinin receptors in cortical and hippocampal areas. Deletion of kinin B1 or B2 receptors abolished memory impairment caused by an acute single injection of A beta in the LV. As brain tissue and kinin receptors could unlikely react to acute or chronic administration of a similar quantity of A beta, we evaluated the participation of B1 or B2 receptors in memory impairment after chronic infusion of A beta. Male C57BI/6 J (wt), knock-out B1 (koB1) or B2 (koB2) mice (12 weeks of age) previously trained in a two-way shuttle-box and achieving conditioned avoidance responses (CAR, % of 50 trials) were infused with AB (550 pmol, 0.12 mu L/h, 28 days) or vehicle in the LV using a mini-osmotic pump. They were tested before the surgery (TO), 7 and 35 days after the infusion started (T7; T35). in T0, no difference was observed between CAR of the control (Cwt = 59.7 +/- 6.7%; CkoB1 = 46.7 +/- 4.0%; CkoB2 = 64.4 +/- 5.8%) and A beta (A beta wt = 66.0 +/- 3.0%; A beta koB1 = 66.8 +/- 8.2%; A beta koB2 = 58.7 +/- 5.9%) groups. in T7, A beta koB2 showed a significant decrease in CAR (41.0 +/- 8.6%) compared to the control-koB2 (72.8 +/- 2.2%, P <0.05). in T35, a significant decrease (P <0.05) was observed in A beta wt (40.7 +/- 3.3%) and A beta koB2 (41.2 +/- 10.7%) but not in the A beta koB1 (64.0 +/- 14.0%) compared to their control groups. No changes were observed in the controls at T35. We suggest that in chronic infusion of BA, B1 receptors could playan important role in the neurodegenerative process. Conversely, the premature memory impairment of koB2 suggests that it may be a protective factor. (C) 2009 Elsevier B.V. All rights reserved.
Keywords Bradykinin
Alzheimer
Neurodegeneration
B1 receptor
B2 receptor
Neuroinflammation
Language English
Date 2010-04-01
Published in Neuropeptides. Edinburgh: Churchill Livingstone, v. 44, n. 2, p. 93-97, 2010.
ISSN 0143-4179 (Sherpa/Romeo, impact factor)
Publisher Churchill Livingstone
Extent 93-97
Origin http://dx.doi.org/10.1016/j.npep.2009.10.006
Access rights Closed access
Type Article
Web of Science ID WOS:000276001700005
URI http://repositorio.unifesp.br/handle/11600/32424

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