Learning about memory.
Learning about memory.
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学习记忆。
DOI:
10.1037/001590
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发表时间:
1998
期刊:
影响因子:
--
通讯作者:
B. Basden
中科院分区:
文献类型:
--
作者:
B. Basden
Although the role of CCR5 in immunity and in HIV infection has been studied widely, its role in neuronal plasticity, learning and memory is not understood. Here, we report that decreasing the function of CCR5 increases MAPK/CREB signaling, long-term potentiation (LTP), and hippocampus-dependent memory in mice, while neuronal CCR5 overexpression caused memory deficits. Decreasing CCR5 function in mouse barrel cortex also resulted in enhanced spike timing dependent plasticity and consequently, dramatically accelerated experience-dependent plasticity. These results suggest that CCR5 is a powerful suppressor for plasticity and memory, and CCR5 over-activation by viral proteins may contribute to HIV-associated cognitive deficits. Consistent with this hypothesis, the HIV V3 peptide caused LTP, signaling and memory deficits that were prevented by Ccr5 knockout or knockdown. Overall, our results demonstrate that CCR5 plays an important role in neuroplasticity, learning and memory, and indicate that CCR5 has a role in the cognitive deficits caused by HIV. were identical to those for the LTP experiments. Once the recordings were established the perfusion solution was switched to magnesium-free ACSF and an NMDA-receptor mediated response was isolated by the addition of 20 m M CNQX to the bath solution. Single extracellular stimuli were delivered at 0.1 Hz. After a stable baseline had been established, stimulation was halted and 10 m M MK-801 was washed onto the slice for 10 min.
影响因子:
56.9
作者:
McClearn, GE;Johansson, B;Plomin, R
通讯作者:
Plomin, R