Participation of kinin receptors on memory impairment after chronic infusion of human amyloid-β 1-40 peptide in mice
Abstract
Chronic infusion of human amyloid-beta 1-40 (Abeta) 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 Abeta in the LV. As brain tissue and kinin receptors could unlikely react to acute or chronic administration of a similar quantity of Abeta, we evaluated the participation of B1 or B2 receptors in memory impairment after chronic infusion of Abeta. Male C57Bl/6J (wt), knock-out B1 (koB1) or B2 (koB2) mice (12weeks of age) previously trained in a two-way shuttle-box and achieving conditioned avoidance responses (CAR, % of 50 trials) were infused with AB (550pmol, 0.12microL/h, 28days) or vehicle in the LV using a mini-osmotic pump. They were tested before the surgery (T0), 7 and 35days 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 Abeta (Abetawt=66.0+/-3.0%; AbetakoB1=66.8+/-8.2%; AbetakoB2=58.7+/-5.9%) groups. In T7, AbetakoB2 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 Abetawt (40.7+/-3.3%) and AbetakoB2 (41.2+/-10.7%) but not in the AbetakoB1 (64.0+/-14.0%) compared to their control groups. No changes were observed in the controls at T35. We suggest that in c…
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The notion that Aβ aggregates are not sufficient to induce memory dysfunction in mice does not contradict studies showing that synthetic Aβ or Aβ aggregates injected into rodent brain may mediate memory formation.
“The notion that Aβ aggregates are not sufficient to induce memory dysfunction in mice does not contradict the results of the studies that show that synthetic Aβ or Aβ aggregates injected into rodent brain may mediate memory formation e.g. [28,57].”
From Normal cognition in transgenic BRI2-Aβ mice (2013) · cites this paper as [28]
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Normal cognition in transgenic BRI2-Aβ mice
Kim, J., Chakrabarty, P., Hanna, A., March, A., Dickson, D. W., Borchelt, D. R., Golde, T., & Janus, C. (2013) · Molecular Neurodegeneration · doi:10.1186/1750-1326-8-15 · Cited by 83 · see citing works
- Authors
- Amaral, F. A., Lemos, M. T. R., Dong, K. E., Bittencourt, M. F. Q. P., Caetano, A. L., Pesquero, J. B., Viel, T. A., & Buck, H. S.
- Affiliations
- Faculdade de Ciências Médicas da Santa Casa de São Paulo (BR)
- Universidade Federal de São Paulo (BR)
- Venue
- Neuropeptides
- Publisher
- Elsevier BV
- Published
- 2010-04
- Volume
- 44
- Issue
- 2
- Pages
- 93-97
- ISSN
- 0143-4179 (ISSN-L)
- OpenAlex
- W2039709943
- Cited by
- 30
- References
- 0
- Citations by year
- 2025: 3 · 2024: 1 · 2020: 2 · 2019: 5 · 2017: 1 · 2016: 4 · 2015: 5 · 2014: 1 · 2013: 4 · 2012: 1
- FWCI
- 0.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropeptides (publishedVersion)
- PubMed (publishedVersion)
- Scientific Electronic Library Online (São Paulo Research Foundation, Latin American and Caribbean Center on Health Sciences Information, Conselho Nacional de Desenvolvimento Científico e Tecnológico) (publishedVersion)
- UNIFESP Institutional Repository (Universidade Federal de São Paulo) (submittedVersion)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Genetics › Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Keywords
- Aβ40, kinin B1 receptor, kinin B2 receptor, memory impairment, conditioned avoidance response, receptor knockout mice, neurodegeneration, Alzheimer's disease, lateral ventricle, hippocampus, cortex, kallikrein-kinin system, neuroprotection, neuroinflammation
- MeSH terms
- Analysis of Variance, Animals, Avoidance Learning, Brain, Male, Memory, Memory Disorders, Motor Activity, Neurons, Peptide Fragments, Amyloid beta-Peptides, Mice, Knockout, Receptor, Bradykinin B2, Receptor, Bradykinin B1, Mice
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