The α2-adrenoceptor antagonist yohimbine reduces glial fibrillary acidic protein upregulation induced by chronic morphine administration
Section snippets
Acknowledgements
We thank Linda Hamalainem for her help in the preparation of the manuscript. This study was supported by grants from Laboratorios ESTEVE, Agencia Antidroga CAM and Plan Nacional sobre Drogas.
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2022, Drug and Alcohol DependenceCitation Excerpt :Our results are consistent with prior studies showing enhanced astrocyte reactivity and increased expression of pro-inflammatory cytokines during both opioid exposure and withdrawal (Campbell et al., 2013; García-Pérez et al., 2013). Indeed, dosing regimens of morphine that produce tolerance and dependence enhance GFAP immunoreactivity in multiple brain regions, including the NAC (Garrido et al., 2005; García-Pérez et al., 2013, 2014, 2015). In our study, the increase in GFAP mRNA levels during morphine abstinence was specific to the NAC as no significant changes were detected in the VTA or PFC. It is not clear if the increase in GFAP mRNA levels, quantified 24 h after discontinuation of morphine exposure, was due to morphine exposure or withdrawal, as previous studies have detected an increase in astrocyte reactivity across multiple stages of opioid exposure and withdrawal (i.e., following acute exposure, during chronic exposure, and during abstinence) (García-Pérez et al., 2015).
Astroglial correlates of neuropsychiatric disease: From astrocytopathy to astrogliosis
2018, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :GFAP protein and mRNA levels have been reported to be upregulated in the striatum after chronic morphine administration (Marie-Claire et al., 2004) and in the whole brain following naloxone-induced withdrawal of chronic morphine treatment (Pajohanfar et al., 2017). Moreover, chronic (but not acute) morphine treatment increased GFAP expression in the NAc shell, VTA and frontal cortex, which is prevented by the α2-adrenoceptor antagonist yohimbine (Garrido et al., 2005). Additionally, increased GFAP expression in the hippocampus, spinal cord, midbrain and posterior cingulate cortex has been reported in morphine tolerant rats, while no difference was found in the thalamus (Wen et al., 2008; Song and Zhao, 2001; Harada et al., 2013; Takemoto et al., 2016).
The effects of pioglitazone, a PPARγ receptor agonist, on the abuse liability of oxycodone among nondependent opioid users
2016, Physiology and BehaviorCitation Excerpt :Alternatively, it has been shown that opioids cause direct glial cell activation in a non-classical opioid receptor fashion, possibly via opioid-induced activation of a class of pattern recognition receptors referred to as toll-like receptors [17]. For example, chronic morphine administration has been associated with an increase in proinflammatory cytokine protein and/or mRNA [18], glial fibrillary acid protein [19,20], and proliferation (astrogliosis) and migration of astrocytes [21,22,23,24,25]. Although the cause of these discrepant findings is still under debate, investigators have begun to study opioid and glial interactions as a means to separate the beneficial effects of opioids (analgesia) from their detrimental effects (abuse potential).
Influence of morphine on medial prefrontal cortex alpha2 adrenergic system in passive avoidance learning in rats
2015, Pharmacology Biochemistry and BehaviorGlial cell activation in the spinal cord and dorsal root ganglia induced by surgery in mice
2013, European Journal of PharmacologyChanges of protein expression profiles in the amygdala during the process of morphine-induced conditioned place preference in rats
2011, Behavioural Brain ResearchCitation Excerpt :Previous studies demonstrated that chronic morphine treatment could dose-dependently inhibit the proliferation of astrocytes in vitro directly via its receptor [39,40], in contrary to in vivo experiment. Treatment with chronic morphine increased the levels of GFAP in ventral tegmental area, the shell of nucleus accumbens and frontal cortex [41]. Chronic morphine administration enhanced the gene and protein expression of GFAP in rat striatum [42].