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

Dopamine agonists rescue Aβ–induced LTP impairment by Src-family tyrosine kinases 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Neurobiology of Aging Elsevier

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

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Publisher
Elsevier
Copyright
Copyright © 2016 Elsevier Inc.
ISSN
0197-4580
D.O.I.
10.1016/j.neurobiolaging.2016.01.008
Publisher site
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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.

Journal

Neurobiology of AgingElsevier

Published: Apr 1, 2016

References

  • Dopaminergic modulation of NMDA-induced whole cell currents in neostriatal neurons in slices: contribution of calcium conductances
    Cepeda, C.; Colwell, C.S.; Itri, J.N.; Chandler, S.H.; Levine, M.S.
  • Characterization of metabotropic glutamate receptor-mediated facilitation of N-methyl-D-aspartate depolarization of neocortical neurones
    Rahman, S.; Neuman, R.S.
  • The late maintenance of hippocampal LTP: requirements, phases, 'synaptic tagging', 'late-associativity' and implications
    Reymann, K.G.; Frey, J.U.
  • Metaplasticity gated through differential regulation of GluN2A versus GluN2B receptors by Src family kinases
    Yang, K.; Trepanier, C.; Sidhu, B.; Xie, Y.F.; Li, H.; Lei, G.; Salter, M.W.; Orser, B.A.; Nakazawa, T.; Yamamoto, T.; Jackson, M.F.; Macdonald, J.F.
  • The upregulation of NR2A-containing N-methyl-D-aspartate receptor function by tyrosine phosphorylation of postsynaptic density 95 via facilitating Src/proline-rich tyrosine kinase 2 activation
    Zhao, C.; Du, C.P.; Peng, Y.; Xu, Z.; Sun, C.C.; Liu, Y.; Hou, X.Y.

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