IL-33 Acts to Express Schaffer Collateral/CA1 LTP and Regulate Learning and Memory by Targeting MyD88.
Neural Plast
; 2017: 2531453, 2017.
Article
em En
| MEDLINE
| ID: mdl-29147584
ABSTRACT
Interleukin-33 (IL-33) is recognized to transmit a signal through a heterodimeric receptor complex ST2/interleukin-1 receptor accessory protein (IL-1RAcP) bearing activation of myeloid differentiation factor 88 (MyD88). High-frequency stimulation to the Schaffer collateral induced long-term potentiation (LTP) in the CA1 region of hippocampal slices from wild-type control mice. Schaffer collateral/CA1 LTP in IL-33-deficient mice was significantly suppressed, which was neutralized by application with IL-33. Similar suppression of the LTP was found with MyD88-deficient mice but not with ST2-deficient mice. In the water maze test, the acquisition latency in IL-33-deficient and MyD88-deficient mice was significantly prolonged as compared with that in wild-type control mice. Moreover, the retention latency in MyD88-deficient mice was markedly prolonged. In contrast, the acquisition and retention latencies in ST2-deficient mice were not affected. Taken together, these results show that IL-33 acts to express Schaffer collateral/CA1 LTP relevant to spatial learning and memory in a MyD88-dependent manner and that the LTP might be expressed through an IL-1R1/IL-1RAcP-MyD88 pathway in the absence of ST2.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Potenciação de Longa Duração
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Fator 88 de Diferenciação Mieloide
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Região CA1 Hipocampal
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Aprendizagem Espacial
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Memória Espacial
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Interleucina-33
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Hipocampo
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article