Introduction: We have previously demonstrated that alcohol has the ability to release low levels of endogenously expressed, chemically authentic, morphine from neural tissues.
Material And Methods: Presently, we demonstrate that chronic exposure of Mytilus edulis pedal ganglia tissues maintained in organotypic culture to very concentrations of 1 mM and 10 mM ethanol induces a time dependent increase in both endogenous morphine and dopamine (DA) levels.
Results: Chronic incubation of M. edulis pedal ganglia with 3 concentrations of DA resulted in statistically significant elevations of cellular morphine levels, thereby confirming previous studies from our laboratory establishing DA as an essential precursor in the morphine biosynthetic pathway.
Conclusions: By understanding multiple debilitating effects of alcohol on "morphinergic" signaling, we may understand the ravages of neural processes associated with alcohol abuse and how its treatment may be made more effective.
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http://dx.doi.org/10.5114/aoms.2010.14249 | DOI Listing |
BMC Med Genomics
December 2024
Pharmaceutical Care, Department of Pharmaceutical Sciences, University of Basel, Basel, Switzerland.
Background: Postoperative pain is a common complication following surgery, with severity and duration varying between patients. Chronic postoperative pain after inguinal hernia surgery has an incidence rate of approximately 10%. Risk factors for acute and chronic pain following hernia surgery include age, sex, psychosocial factors, and demographic background.
View Article and Find Full Text PDFACS Chem Neurosci
January 2025
Edward F Domino Research Center, Department of Pharmacology, University of Michigan, Ann Arbor, Michigan 48109, United States.
Positive allosteric modulation of the mu-opioid receptor is a promising strategy to address the ever-growing problem of acute and chronic pain management. Positive allosteric modulators (PAMs) of the mu-opioid receptor could be employed to enhance the efficacy of endogenous opioid peptides to a degree that provides pain relief without the need for traditional opioid drugs. Alternatively, PAMs might be used to enhance the action of opioid drugs and so provide an opioid-sparing effect, allowing for the use of lower doses of opioid agonists and potentially decreasing associated side effects.
View Article and Find Full Text PDFNeuroscience
December 2024
Institute of Physiology, School of Basic Medical Sciences, and State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, 199 Donggang West Road, Lanzhou 730000, PR China. Electronic address:
Increasing evidence indicates that neuropeptide FF (NPFF) produces analgesic effects and augments opioid-induced analgesia at the spinal level. However, our recent research demonstrated that NPFF exerted complex opioid-modulating effects in an inflammatory pain model after intrathecal (i.t.
View Article and Find Full Text PDFBiochem Pharmacol
November 2024
Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Lodz, Poland. Electronic address:
The antinociceptive effect of the opioid drugs is achieved through activation of the µ-opioid receptor (MOP). The orthosteric and allosteric sites of opioid receptors may be modulated, orthosteric site by endogenous i.e.
View Article and Find Full Text PDFMol Psychiatry
November 2024
Department of Anatomy and Neurobiology, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.
Distinguishing the brain mechanisms affected by distinct addictive drugs may inform targeted therapies against specific substance use disorders (SUDs). Here, we explore the function of a drug-associated, transcriptionally repressive transcription factor (TF), ZFP189, whose expression in the nucleus accumbens (NAc) facilitates cocaine-induced molecular and behavioral adaptations. To uncover the necessity of ZFP189-mediated transcriptional control in driving cocaine-induced behaviors, we created synthetic ZFP189 TFs of distinct transcriptional function, including ZFP189, which activates the expression of target genes and exerts opposite transcriptional control to the endogenously repressive ZFP189.
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