Aim: Prescription opioids are psychoactive substances that can elicit many neuropsychological effects. There are no studies that directly demonstrate the effects of prescription opioid addiction (POA) on the human brain. This study aimed to quantify γ-aminobutyric acid (GABA) and glutamate (Glu) levels in the prefrontal cortex (PFC) of POA patients using proton magnetic resonance spectroscopy ( H-MRS), and to explore their association with impulsive behavior and cognitive impairment.
Methods: Thirty-five patients with a definitive clinical diagnosis of codeine-containing cough syrup dependence and 35 matched healthy controls underwent neuropsychological assessments, namely the Barratt Impulsiveness Scale (BIS-11) and the Montreal Cognitive Assessment Scale (MoCA). Point-resolved spectroscopy was performed to detect GABA and glutamate within the medial PFC, and the corresponding levels were estimated using jMRUI and corrected for fraction of cerebrospinal fluid in the H-MRS voxel. The difference in metabolite levels between groups and the correlation between metabolite levels and psychometric scores in patients were analyzed statistically.
Results: The peak level predominantly consisting of GABA with a relatively small influence of other chemicals (GABA+) was lower and that of glutamate was higher in the PFC of POA patients than in healthy controls. GABA+ levels correlated negatively with BIS-11 scores but correlated positively with MoCA scores. In contrast, glutamate levels showed a positive correlation with BIS-11 scores but no significant correlation with MoCA scores.
Conclusion: The quantitative in vivo measurement of GABA and glutamate levels in the PFC by H-MRS could be a reliable way to evaluate impulsivity and cognitive function of POA.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1111/pcn.12940 | DOI Listing |
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2024
Department of Anesthesiology, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing 210008.
Objectives: Sleep deprivation (SD) is a risk factor for the development of chronic pain in adolescents, significantly affecting pain management and prognosis; however, the mechanisms by which SD influences postoperative pain outcomes remain unclear. This study aims to investigate the molecular mechanism through which the spinal 5-hydroxytryptamine 1 receptor (5-HT1R) regulates the excitation/inhibition (E/I) balance in the dorsal horn to modulate postoperative chronic pain induced by SD in adolescent mice.
Methods: A pain model combining 4.
Neurobiol Aging
March 2025
Neuroscience and Behavioural Diseases and Eye-ACP, SERI/SNEC, Centre for Vision Research, Duke-NUS Medical School, 8 College Road, 169857, Singapore; Save Sight Institute, University of Sydney, Sydney, NSW, Australia. Electronic address:
Increasing age and elevated intraocular pressure (IOP) are the two major risk factors for glaucoma, the most common cause of irreversible blindness worldwide. Accumulating evidence is pointing to metabolic failure predisposing to neuronal loss with advancing age and IOP injury. Many neurotransmitters are synthesized from endogenous metabolites and are essential for correct cell to cell signaling along the visual pathways.
View Article and Find Full Text PDFActas Esp Psiquiatr
March 2025
Department of Pediatric, The First People's Hospital of Taizhou, 318020 Taizhou, Zhejiang, China.
Background: Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by deficits in social communication and limited behavior. Despite the association of numerous synaptic gene mutations with ASD, the presence of behavioral abnormalities in mice expressing autism-associated R617W mutation in synaptic adhesion protein neuroligin-3 (NL3) has not been established. This work focuses on establishing a mouse model of ASD caused by NL3 R617W missense mutation (NL3R617W) and characterizing and profiling the molecular as well as behavioral features of the animal model.
View Article and Find Full Text PDFAnnu Rev Neurosci
March 2025
Center for Cognition and Sociality, Institute for Basic Science (IBS), Daejeon, South Korea; email:
Astrocytes, traditionally viewed as supportive cells within the central nervous system (CNS), are now recognized as dynamic regulators of neural signaling and homeostasis. They actively engage in synaptic transmission and brain health by releasing gliotransmitters such as glutamate, GABA, ATP, adenosine, lactate, and d-serine. Astrocytes also play a critical role in ion homeostasis and immune response through cytokine modulation and reactive oxygen species regulation.
View Article and Find Full Text PDFJ Neurochem
March 2025
Department of Drug Design and Pharmacology, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Synaptic homeostasis of the principal neurotransmitters glutamate and GABA is tightly regulated by an intricate metabolic coupling between neurons and astrocytes known as the glutamate/GABA-glutamine cycle. In this cycle, astrocytes take up glutamate and GABA from the synapse and convert these neurotransmitters into glutamine. Astrocytic glutamine is subsequently transferred to neurons, serving as the principal precursor for neuronal glutamate and GABA synthesis.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!