Brain-derived neurotrophic factor (BDNF) is one of the neurotrophic factors that promotes the survival and protection of neurons in many disorders. The potential protective effect of BDNF and its mechanisms on morphine addiction are unclear. In this study, morphine-induced conditioned place preference (CPP) in mice was used to show the effect of BDNF on rewarding behavior. Western blot assays were used to determine the changes caused by BDNF, for example, changes in total BDNF, tropomyosin-related kinase receptor B (TrkB), and cAMP response element binding protein (CREB) in the ventral tegmental area (VTA) and nucleus accumbens (NAc). The results showed that the BDNF-adeno-associated viral vector (BDNF-AAV) injected in the VTA, attenuated morphine-induced CPP with synergistic changes in BDNF/TrkB/CREB concentrations in the VTA and NAc in the CPP acquisition and recurrence phases; however, the attenuation was lower in the extinction phase, with different changes in molecules downstream of the BDNF.
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http://dx.doi.org/10.1016/j.neulet.2022.136701 | DOI Listing |
Sci Rep
January 2025
Department of Neuroscience and Addiction Studies, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, No. 38, Italia Ave., Ghods St, Keshavarz Boulevard, Tehran, Iran.
Substance Use Disorder (SUD) is a medical condition where an individual compulsively misuses drugs or alcohol despite knowing the negative consequences. The anterior cingulate cortex (ACC) has been implicated in various types of SUDs, including nicotine, heroin, and alcohol use disorders. Our research aimed to investigate the effects of deep brain stimulation (DBS) in the ACC as a potential therapeutic approach for morphine use disorder.
View Article and Find Full Text PDFNeuroscience
January 2025
Research Center of Physiology, Semnan University of Medical Sciences, Semnan, Iran; Department of Physiology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. Electronic address:
Corticosteroid signaling plays a critical role in modulating the neural systems underlying reward and addiction, but the specific contributions of glucocorticoid receptors (GRs) and mineralocorticoid receptors (MRs) in the medial prefrontal cortex (mPFC) to opioid reward and dopaminergic plasticity remain unclear. Here, we investigated the effects of intra-mPFC injection of corticosteroid receptor ligand (corticosterone; CORT), glucocorticoid receptor antagonist (RU38486; RU), and mineralocorticoid receptor antagonist (spironolactone; SP) on morphine-induced conditioned place preference (CPP) and dopamine transporter (DAT) expression in the mPFC. Adult male Wistar rats received intra-mPFC injections of CORT, RU, SP, or their respective vehicles prior to morphine CPP conditioning.
View Article and Find Full Text PDFBiomed Pharmacother
December 2024
School of Cognitive Sciences, Institute for Research in Fundamental Sciences, IPM, Tehran, Iran; Department of Physiology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran. Electronic address:
bioRxiv
October 2024
Department of Pharmacology & Physiology, Drexel University College of Medicine, 245 North 15th Street, Philadelphia, PA, USA.
Morphine and other synthetic opioids are widely prescribed to treat pain. Prolonged morphine exposure can paradoxically enhance pain sensitivity in humans and nociceptive behavior in rodents. To better understand the molecular mechanisms underlying opioid-induced hyperalgesia, we investigated changes in miRNA composition of small extracellular vesicles (sEVs) from the serum of mice after a morphine treatment paradigm that induces hyperalgesia.
View Article and Find Full Text PDFFEBS Open Bio
December 2024
Department of Neuroscience, Beijing Institute of Basic Medical Sciences, China.
Morphine is an opioid commonly used to treat pain in clinic, but it also has the potential to be highly addictive, which can lead to abuse. Despite these known risks, the cellular and molecular mechanism of morphine conditioned place preference (CPP) is still unclear. In this study, using a rat model of chronic morphine administration, we found that compared with the control group, the mRNA and protein expression of HCN2 channel in the ventral tegmental area (VTA) were upregulated.
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