Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases

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• 作者：PingAn Yuan Xiang^a ; Oliwia Janc^b ; Katarzyna M. Grochowska^a ; Michael R. Kreutz^a ; ^c ; ^d ; ^{kreutz@lin-magdeburg.de" class="auth_mail" title="E-mail the corresponding author} ; Klaus G. Reymann^b ; ^d ; ^{reymann@lin-magdeburg.de" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Amyloid beta oligomers (AβO) ; LTP ; Alzheimer disease ; D1/D5 dopamine receptors ; Src kinases
• 刊名：Neurobiology of Aging
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：40
• 期：Complete
• 页码：98-102
• 全文大小：1237 K

文摘

Soluble forms of oligomeric amyloid beta (AβO) are involved in the loss of synaptic plasticity and memory, especially in early phases of Alzheimer's disease. Stimulation of dopamine D1/D5 receptors (D1R/D5R) is known to increase surface expression of synaptic α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate subtype glutamate and N-methyl-D-aspartate subtype glutamate receptors and facilitates the induction of the late phase of long-term potentiation (LTP), probably via a related mechanism. In this study, we show that the D1/D5R agonist SKF38393 protects LTP of hippocampal CA1 synapses from the deleterious action of oligomeric amyloid beta. Unexpectedly, the D1R/D5R–mediated recovery of LTP is independent of protein kinase A or phospholipase C pathways. Instead, we found that the inhibition of Src-family tyrosine kinases completely abolished the protective effects of D1R/D5R stimulation in a cellular model of learning and memory.