Naloxone reversed cognitive impairments induced by repeated morphine under heavy perceptual load in the 5‐choice serial reaction time task

Guo, Hao; Xie, Qiaoli; Cui, Jingjing; Xu, Dakang; Deji, Cuola; Chen, Yuanyuan; Wang, Yunpeng; Lai, Jianghua

doi:10.1002/jnr.24427

Cited by 11 publications

(11 citation statements)

References 49 publications

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“…We have previously demonstrated that 7 days of morphine exposure (10 mg/kg, i.p.) impaired attention in mice 27,28 . This study confirmed that repeated morphine administration for 14 days results in severe deficits in attentional function.…”

Section: Discussionsupporting

confidence: 82%

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Modafinil rescues repeated morphine‐induced synaptic and behavioural impairments via activation of D1R–ERK–CREB pathway in medial prefrontal cortex

Yin

Zhang

et al. 2021

Addiction Biology

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Long‐term opioid abuse causes a variety of long‐lasting cognitive impairments such as attention, impulsivity and working memory. These cognitive impairments undermine behavioural treatment for drug abuse and lead to poor treatment retention and outcomes. Modafinil is a wake‐promoting drug that shows potential in improving attention and memory in humans and animals. However, modafinil's effect on opioid‐induced cognitive impairments remains unclear, and the underlying mechanism is poorly understood. This study showed that repeated morphine administration significantly impairs attention, increases impulsivity and reduces motivation to natural rewards in mice. Systemic modafinil treatment at low dose efficiently ameliorates morphine‐induced attention dysfunction and improves motivation and working memory in mice. High dose of modafinil has adverse effects on impulsive action and attention. Local infusion of D1R antagonist SCH‐23390 reverses the morphine‐induced synaptic abnormalities and activation of the D1R–ERK–CREB pathway in medial prefrontal cortex (mPFC). This study demonstrated a protective effect of modafinil in mPFC neurons and offered a therapeutic potential for cognitive deficits in opioid abuse.

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Section: Discussionsupporting

confidence: 82%

“…impaired attention in mice. 27,28 This study confirmed that repeated morphine administration for 14 days results in severe deficits in attentional function.…”

Section: Discussionsupporting

confidence: 72%

Modafinil rescues repeated morphine‐induced synaptic and behavioural impairments via activation of D1R–ERK–CREB pathway in medial prefrontal cortex

Yin

Zhang

et al. 2021

Addiction Biology

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“…However, erastin, a ferroptosis activator, accelerates the development of chronic morphine tolerance at day 3 after morphine injection (data are shown in Supplementary Figure S1). Moreover, we found that naloxone (5 mg/kg, ip), an opioid receptor antagonist, 25 had no effect on the Lip-1 mediated antinociception in morphine tolerant mice (data are shown in Supplementary Figure S2).…”

Section: ■ Results and Discussionmentioning

confidence: 96%

Liproxstatin-1 Attenuates Morphine Tolerance through Inhibiting Spinal Ferroptosis-like Cell Death

Chen

Zhang

Liu

et al. 2019

ACS Chem. Neurosci.

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Morphine tolerance is a classic, challenging clinical issue. However, the mechanism underlying this phenomenon remains poorly understood. Recently, studies have shown that ferroptosis correlates with drug resistance. Therefore, this study investigated whether spinal cord ferroptosis contributes to morphine tolerance. C57BL/6 mice were continuously subcutaneously injected with morphine, with or without the ferroptosis inhibitor liproxstatin-1. We found that chronic morphine exposure led to morphine antinociception tolerance, accompanied by loss of spinal cord neurons, increase in the levels of iron, malondialdehyde, and reactive oxygen species, and decreases in the levels of superoxide dismutase. Additionally, inflammatory response and mitochondrial shrinkage, processes that are involved in ferroptosis, were observed. Simultaneously, we found that 10 mg/kg of liproxstatin-1 could alleviate iron overload by balancing transferrin receptor protein 1/ferroportin expression and attenuate morphine tolerance by increasing glutathione peroxidase 4 levels, while reducing the levels of malondialdehyde and reactive oxygen species. It also downregulated the expression of extracellularly regulated protein kinases that had been induced by chronic morphine exposure. Our results indicate that spinal cord ferroptosis contributes to morphine tolerance, while liproxstatin-1 attenuates the development of morphine tolerance. These findings suggest that ferroptosis may be a potential therapeutic target for morphine tolerance.

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“…Animals were conducted a series of behavioral tests throughout the experimental procedure: CUMS, forced swim test (FST), tail suspension test (TST), open‐field test (OFT), elevated plus maze (EPM), Y‐maze and novel objects recognition (NOR). OFT, EPM, Y‐maze and NOR have been fully described in Supporting Information and our previous studies 26,27 …”

Section: Methodsmentioning

confidence: 99%

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

Guo

Deji

Han

et al. 2021

Genes Brain and Behavior

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Previous investigations have implicated the basolateral amygdala (BLA) epigenetic mechanisms in the pathophysiology of depression. SIRT1 is a NAD+‐dependent class III histone deacetylase, widely expresses in BLA. However, epigenetic mechanisms in the BLA under the regulation of SIRT1 in the depression are largely uncharacterized. Under the chronic unpredictable chronic mild stress (CUMS) mouse model, we used adeno‐associated viral vectors (AAV) that encoded SIRT1‐shRNA or SIRT1 to specifically knockdown or overexpress SIRT1 in BLA neurons, respectively. CUMS procedure induced significant depression symptoms including the decreased sucrose preference, the less bodyweight gained, the decreased immobile latency and the increased immobile time both in forced swim test (FST) and tail suspension test (TST). Knockdown of SIRT1 in BLA glutamatergic neurons reversed these depression‐like behaviors and restored the synaptic abnormalities. Overexpression of SIRT1 in BLA glutamatergic neurons induced depression‐like behaviors in non‐stressed control mice. The result of protein expressions and ultrastructural changes were consistent with the behavioral results. Our study suggested that downregulation of SIRT1 in BLA has certain beneficial effect on CUMS‐induced depression‐like behaviors such as anorexia, anhedonia, hopelessness and despair. In addition, the increased expression of SIRT1 may be the immediate cause of depressive‐like symptoms. The abnormal expression of SIRT1 may affect the transcriptional regulation mechanism and signaling protein acetylation, affecting neuroplasticity and ultimately contribute to MDD. In the stress‐susceptible mice, these two mechanisms may co‐exist, but the specific mechanism needs further research.

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Naloxone reversed cognitive impairments induced by repeated morphine under heavy perceptual load in the 5‐choice serial reaction time task

Cited by 11 publications

References 49 publications

Modafinil rescues repeated morphine‐induced synaptic and behavioural impairments via activation of D1R–ERK–CREB pathway in medial prefrontal cortex

Modafinil rescues repeated morphine‐induced synaptic and behavioural impairments via activation of D1R–ERK–CREB pathway in medial prefrontal cortex

Liproxstatin-1 Attenuates Morphine Tolerance through Inhibiting Spinal Ferroptosis-like Cell Death

The role of SIRT1 in the basolateral amygdala in depression‐like behaviors in mice

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