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

PingAn Yuan Xiang; Oliwia Janc; Katarzyna M Grochowska; Michael R  Kreutz; Klaus G Reymann

doi:10.1016/j.neurobiolaging.2016.01.008

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

Standard

Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases. / Xiang, PingAn Yuan; Janc, Oliwia; Grochowska, Katarzyna M; Kreutz, Michael R ; Reymann, Klaus G.

In: NEUROBIOL AGING, Vol. 40, 04.2016, p. 98-102.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Xiang, PY, Janc, O, Grochowska, KM, Kreutz, MR & Reymann, KG 2016, 'Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases', NEUROBIOL AGING, vol. 40, pp. 98-102. https://doi.org/10.1016/j.neurobiolaging.2016.01.008

APA

Xiang, P. Y., Janc, O., Grochowska, K. M., Kreutz, M. R., & Reymann, K. G. (2016). Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases. NEUROBIOL AGING, 40, 98-102. https://doi.org/10.1016/j.neurobiolaging.2016.01.008

Vancouver

Xiang PY, Janc O, Grochowska KM, Kreutz MR, Reymann KG. Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases. NEUROBIOL AGING. 2016 Apr;40:98-102. https://doi.org/10.1016/j.neurobiolaging.2016.01.008

Bibtex

@article{e3937baeacff43a0a6d9d896c842fe27,

title = "Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases",

abstract = "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.",

keywords = "Journal Article, Research Support, Non-U.S. Gov't",

author = "Xiang, {PingAn Yuan} and Oliwia Janc and Grochowska, {Katarzyna M} and Kreutz, {Michael R} and Reymann, {Klaus G}",

year = "2016",

month = apr,

doi = "10.1016/j.neurobiolaging.2016.01.008",

language = "English",

volume = "40",

pages = "98--102",

journal = "NEUROBIOL AGING",

issn = "0197-4580",

publisher = "Elsevier Inc.",

}

RIS

TY - JOUR

T1 - Dopamine agonists rescue Aβ-induced LTP impairment by Src-family tyrosine kinases

AU - Xiang, PingAn Yuan

AU - Janc, Oliwia

AU - Grochowska, Katarzyna M

AU - Kreutz, Michael R

AU - Reymann, Klaus G

PY - 2016/4

Y1 - 2016/4

N2 - 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.

AB - 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.

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1016/j.neurobiolaging.2016.01.008

DO - 10.1016/j.neurobiolaging.2016.01.008

M3 - SCORING: Journal article

C2 - 26973108

VL - 40

SP - 98

EP - 102

JO - NEUROBIOL AGING

JF - NEUROBIOL AGING

SN - 0197-4580

ER -