IL-33 Acts to Express Schaffer CollateralCA1 LTP and Regulate Learning and Memory by Targeting MyD88

Abstract EN

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.