Activation of the D1 receptors inhibits the long-term potentiation in vivo induced by acute morphine administration through a D1–GluN2A interaction in the nucleus accumbens

Zheng, Qiaohua; Liu, Zhiqiang; Wei, Chunling; Han, Jing; Liu, Yihui; Zhang, Xia; Ren, Wei

doi:10.1097/wnr.0000000000000245

Cited by 7 publications

(3 citation statements)

References 23 publications

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“…The field excitatory postsynaptic potentials (fEPSPs) from CA3‐CA1 synapses were recorded using previously described procedures , and in Supporting Information Materials and Methods 1. Briefly, test fEPSPs were evoked with single‐pulse stimulations at 0.33 Hz.…”

Section: Methodsmentioning

confidence: 99%

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

Wang

et al. 2017

Molecular Nutrition Food Res

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ScopeA high salt (HS) diet is detrimental to cognitive function, in addition to having a role in cardiovascular disorders. However, the method by which an HS diet impairs cognitive functions such as learning and memory remains open.Methods and resultsIn this study, we found that mice on a 7 week HS diet demonstrated disturbed short‐term memory in an object‐place recognition task, and both 4 week and 7 week HS treatments impaired long‐term memory, as evidenced in a fear conditioning test. Mechanistically, the HS diet inhibited memory‐related long‐term potentiation (LTP) in the hippocampus, while also increasing the levels of reactive oxygen species (ROS) in hippocampal cells and downregulating the expression of synapsin I, synaptophysin, and brain‐derived neurotrophic factor in specific encephalic region.ConclusionThis suggests that oxidative stress or synaptic protein/neurotrophin deregulation was involved in the HS diet‐induced memory impairment. Thus, the present study provides novel insights into the mechanisms of memory impairment caused by excessive dietary salt, and underlined the importance of controlling to salt absorb quantity.

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Section: Methodsmentioning

confidence: 99%

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

Wang

et al. 2017

Molecular Nutrition Food Res

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“…D1Rs and NMDARs interact in the NAc to promote methamphetamine reinstatement (Taepavarapruk et al 2015), as well as activation of downstream signaling in the NAc in response to reward-predictive cues (Kirschmann et al 2014). However, studies using the peptide to disrupt direct D1R-NMDAR interactions have produced mixed results, since D1R activation enhances NMDAR-dependent LTP in hippocampal cultures (Nai et al 2009), while D1Rs inhibit NMDAR function (Lee et al 2002) and NMDAR-dependent LTP at cortico-NAc inputs after in vivo morphine (Zheng et al 2014). This is also in contrast to the DStr, where D1Rs are required for NMDAR-dependent LTP (Centonze et al 2001).…”

Section: Interaction Of Nmdars With Other Receptor Typesmentioning

confidence: 99%

Do specific NMDA receptor subunits act as gateways for addictive behaviors?

Hopf

2016

Genes Brain and Behavior

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Addiction to alcohol and drugs is a major social and economic problem, and there is considerable interest in understanding the molecular mechanisms that promote addictive drives. A number of proteins have been identified that contribute to expression of addictive behaviors. NMDA receptors (NMDARs), a subclass of ionotropic glutamate receptors, have been of particular interest because their physiological properties make them an attractive candidate for gating induction of synaptic plasticity, a molecular change thought to mediate learning and memory. NMDARs are generally inactive at the hyperpolarized resting potentials of many neurons. However, given sufficient depolarization, NMDARs are activated and exhibit long-lasting currents with significant calcium permeability. Also, in addition to stimulating neurons by direct depolarization, NMDARs and their calcium signaling can allow strong and/or synchronized inputs to produce long-term changes in other molecules (such as AMPA-type glutamate receptors) which can last from days to years, binding internal and external stimuli in a long-term memory trace. Such memories could allow salient drug-related stimuli to exert strong control over future behaviors and thus promote addictive drives. Finally, NMDARs may themselves undergo plasticity, which can alter subsequent neuronal stimulation and/or the ability to induce plasticity. This review will address recent and past findings suggesting that NMDAR activity promotes drug- and alcohol-related behaviors, with a particular focus on GluN2B subunits as possible central regulators of many addictive behaviors, as well as newer studies examining the importance of non-canonical NMDAR subunits and endogenous NMDAR cofactors.

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“…Acute morphine exposure induced analgesia, while the underlying mechanism might be the rapid neural adaptations and the changes of synaptic transmission (Beckerman et al 2013, Zheng et al 2014. The amygdala, a forebrain structure that is positioned to influence pain-modulating circuits (Manning 1998), was involved in morphine analgesia, morphine-induced withdrawal, and morphine-induced conditioned place preference (Calvino et al 1982, Freedman and Aghajanian 1985, Good and Westbrook 1995, Helmstetter et al 1993, Lin et al 2011, Stinus et al 1990.…”

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Influences of Morphine on the Spontaneous and Evoked Excitatory Postsynaptic Currents in Lateral Amygdala of Rats

Zhang

Liu²,

2016

Physiol Res

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Acute morphine exposure induces antinociceptive activity, but the underlying mechanisms in the central nervous system are unclear. Using whole-cell patch clamp recordings, we explore the role of morphine in the modulation of excitatory synaptic transmission in lateral amygdala neurons of rats. The results demonstrate that perfusion of 10 μM of morphine to the lateral amygdala inhibits the discharge frequency significantly. We further find that there are no significant influences of morphine on the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs). Interestingly, morphine shows no marked influence on the evoked excitatory postsynaptic currents (eEPSCs) in the lateral amygdala neurons. These results indicate that acute morphine treatment plays an important role in the modulation on the excitatory synaptic transmission in lateral amygdala neurons of rats.

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Activation of the D1 receptors inhibits the long-term potentiation in vivo induced by acute morphine administration through a D1–GluN2A interaction in the nucleus accumbens

Cited by 7 publications

References 23 publications

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

Do specific NMDA receptor subunits act as gateways for addictive behaviors?

Influences of Morphine on the Spontaneous and Evoked Excitatory Postsynaptic Currents in Lateral Amygdala of Rats

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