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MPTP modulates hippocampal synaptic transmission and activity‐dependent synaptic plasticity via dopamine receptors
Author(s) -
Zhu GuoQi,
Huang YuYing,
Chen Ying,
Zhuang YingHan,
Behnisch Thomas
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2012.07815.x
Subject(s) - long term potentiation , synaptic plasticity , neuroscience , ampa receptor , neural facilitation , nmda receptor , excitatory postsynaptic potential , neurotransmission , chemistry , dopamine , synaptic fatigue , biology , receptor , inhibitory postsynaptic potential , biochemistry
J. Neurochem. (2012) 122 , 582–593. Abstract Parkinson’s disease (PD)‐like symptoms and cognitive deficits are inducible by 1‐methyl‐4‐phenyl‐1, 2, 3, 6‐tetrahydropyridine (MPTP). Since cognitive abilities, including memory formations rely also on hippocampus, we set out to clarify the effects of MPTP on hippocampal physiology. We show that bath‐application of MPTP (25 μM) to acute hippocampal slices enhanced AMPA receptor‐mediated field excitatory postsynaptic potentials (AMPAr‐fEPSPs) transiently, whereas N‐methyl‐D‐aspartate (NMDA) receptor‐mediated fEPSPs (NMDAr‐fEPSPs) were facilitated persistently. The MPTP‐mediated transient AMPAr‐fEPSP facilitation was antagonized by the dopamine D2‐like receptor antagonists, eticlopride (1 μM) and sulpiride (1 and 40 μM). In contrast, the persistent enhancement of NMDAr‐fEPSPs was prevented by the dopamine D1‐like receptor antagonist SCH23390 (10 μM). In addition, we show that MPTP decreased paired‐pulse facilitation of fEPSPs and mEPSCs frequency. Regarding activity‐dependent synaptic plasticity, 25 μM MPTP transformed short‐term potentiation (STP) into a long‐term potentiation (LTP) and caused a slow onset potentiation of a non‐tetanized synaptic input after induction of LTP in a second synaptic input. This heterosynaptic slow onset potentiation required activation of dopamine D1‐like and NMDA‐receptors. We conclude that acute MPTP application affects basal synaptic transmission by modulation of presynaptic vesicle release and facilitates NMDAr‐fEPSPs as well as activity‐dependent homo‐ and heterosynaptic plasticity under participation of dopamine receptors.