Anxiety-like behavior in acute and protracted withdrawal after morphine-induced locomotor sensitization in C57BL/6 male mice: The role of context

Masukawa, Márcia Yuriko; Correa-Netto, Nelson Francisco; Silva-Gomes, Alessandro Marcos; Linardi, Alessandra; Santos-Junior, Jair Guilherme

doi:10.1016/j.pbb.2020.172941

Cited by 7 publications

(3 citation statements)

References 56 publications

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“…Each rat was placed on the central platform and allowed to explore the apparatus for 5 min while facing one of the open arms. The time spent in the open arms was recorded by JLBehv-EPMG-4 (Shanghai Jiliang Software Technology Co., Ltd., Shanghai, China) based on previous literature [ 39 ]; behavior tests and evaluation were performed in a blinded manner.…”

Section: Methodsmentioning

confidence: 99%

STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex

Zhang

Wang

et al. 2022

Cancers

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The medial prefrontal cortex (mPFC) is the main cortical area for processing both sensory and affective aspects of pain. Recently, mPFC was reported to participate in cancer-induced bone pain (CIBP) via the mechanism of central inflammation. STING is a key component of neuroinflammation in the central neuron system by activating downstream TBK1 and NF-κB signaling pathways. We aimed to investigate whether STING regulated neuroinflammation in the mPFC in rat models of CIBP. It is worth noting that we found a significant upregulation of STING in the mPFC after CIBP, accompanied by activation of TBK1 and NF-κB signaling pathways. In addition, pain and anxiety-like behaviors were alleviated by intraperitoneal injection of the STING inhibitor C-176. Furthermore, in microglia GMI-R1 cells, C-176 reversed LPS-induced M1 polarization. Collectively, this evidence indicated that STING may contribute to cancer-induced bone pain by activating TBK1 and NF-κB, and by promoting M1 polarization of microglia in the mPFC.

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Section: Methodsmentioning

confidence: 99%

STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex

Zhang

Wang

et al. 2022

Cancers

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“…In rodents, the EPM is one of the most common protocols used to screen the anxiolytic effects of drugs (Lister, 1987 ). The EPM is also useful for investigating the biological basis of addiction and withdrawal (Schulteis et al, 1998 ; Zanos et al, 2016 ; Masukawa et al, 2020 ). In our study, anxiety-like behaviors appeared during the first 2 weeks after morphine withdrawal and affected stress-induced reinstatement to drug seeking.…”

Section: Discussionmentioning

confidence: 99%

The Basolateral Amygdala to Ventral Hippocampus Circuit Controls Anxiety-Like Behaviors Induced by Morphine Withdrawal

Deji

Peng

et al. 2022

Front. Cell. Neurosci.

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Anxiety is one of the most common comorbid conditions reported in people with opioid dependence. The basolateral amygdala (BLA) and ventral hippocampus (vHip) are critical brain regions for fear and anxiety. The kappa opioid receptor (KOR) is present in the mesolimbic regions involved in emotions and addiction. However, the precise circuits and molecular basis underlying anxiety associated with chronic opioid use are poorly understood. Using a mouse model, we demonstrated that anxiety-like behaviors appeared in the first 2 weeks after morphine withdrawal. Furthermore, the BLA and vHip were activated in mice experiencing anxiety after morphine withdrawal (Mor-A). KORs in the BLA to vHip projections were significantly increased in the Mor-A group. Optogenetic/chemogenetic inhibition of BLA inputs ameliorated anxiety-like behaviors and facilitated conditioned place preference (CPP) extinction in Mor-A mice. Knockdown of the BLA to vHip circuit KOR alleviated the anxiety-like behaviors but did not affect CPP extinction or reinstatement. Furthermore, combined treatment of inhibition of the BLA to vHip circuit and KOR antagonists mitigated anxiety-like behaviors and prevented stress-induced CPP reinstatement after morphine withdrawal. These results revealed a previously unknown circuit associated with the emotional component of opioid withdrawal and indicated that restoration of synaptic deficits with KOR antagonists might be effective in the treatment of anxiety associated with morphine withdrawal.

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“…Each rat was placed on the central platform facing one of the open arms and allowed to explore the apparatus for 5 min. We analyzed the time spent in the open arms and total numbers of entries by JLBehv-EPMG software, based on previous literature ( Masukawa et al, 2020 ).…”

Section: Methodsmentioning

confidence: 99%

Neuroinflammation in the medial prefrontal cortex exerts a crucial role in bone cancer pain

Wang

Zhang

et al. 2022

Front. Mol. Neurosci.

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Bone cancer pain (BCP) is one of the most common types of pain in cancer patients which compromises the patient’s functional status, quality of life, and survival. Central hyperalgesia has increasingly been identified as a crucial factor of BCP, especially in the medial prefrontal cortex (mPFC) which is the main cortical area involved in the process of pain and consequent negative emotion. To explore the genetic changes in the mPFC during BCP occurrence and find possible targets for prediction, we performed transcriptome sequencing of mPFC in the BCP rat model and found a total of 147 differentially expressed mRNAs (DEmRNAs). A protein-protein interaction (PPI) network revealed that the DEmRNAs mainly participate in the inflammatory response. Meanwhile, microglia and astrocytes were activated in the mPFC of BCP rats, further confirming the presence of neuroinflammation. In addition, Gene Ontology (GO) analysis showed that DEmRNAs in the mPFC are mainly involved in antigen processing, presentation of peptide antigen, and immune response, occurring in the MHC protein complex. Besides, the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed that DEmRNAs are mainly enriched in the pathways of phagosome, staphylococcus aureus infection, and antigen processing, in which MHCII participate. Furthermore, immunostaining showed that MHCII is mainly located in the microglia. Microglia are believed to be involved in antigen processing, a key cause of BCP. In vivo, minocycline (MC) treatment inhibits the activation of microglia and reduces the expression of MHCII and proinflammatory cytokines, thereby alleviating BCP and pain-related anxiety. Taken together, our study identified differentially expressed genes in the BCP process and demonstrated that the activation of microglia participates in the inflammatory response and antigen process, which may contribute to BCP.

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Anxiety-like behavior in acute and protracted withdrawal after morphine-induced locomotor sensitization in C57BL/6 male mice: The role of context

Cited by 7 publications

References 56 publications

STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex

STING Contributes to Cancer-Induced Bone Pain by Promoting M1 Polarization of Microglia in the Medial Prefrontal Cortex

The Basolateral Amygdala to Ventral Hippocampus Circuit Controls Anxiety-Like Behaviors Induced by Morphine Withdrawal

Neuroinflammation in the medial prefrontal cortex exerts a crucial role in bone cancer pain

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