The effects of acute and chronic morphine treatment on the incorporation of 3H-lysine into synaptic proteins were studied. No changes related to tolerance development were observed in the total incorporation of 3H-lysine into cortical or subcortical synaptic plasma membrane (SPM) or synaptic soluble proteins. Two populations of subcortical SPM were prepared, one from light (L) and one from heavy (H) nerve ending particles. When the labeled SPM-L proteins were separated by means of sodium dodecyl sulfate disc gel electrophoresis, an increased amount of label was found in the high molecular weight region of the gel. This increase depended on the rate of tolerance development. In contrast to the results found in the SPM-L gels, chronic morphinization significantly decreased the amount of high molecular weight labeled protein recovered from SPM-H gels.

Download full-text PDF

Source

Publication Analysis

Top Keywords

synaptic plasma
8
incorporation 3h-lysine
8
tolerance development
8
high molecular
8
molecular weight
8
influence morphine
4
morphine protein
4
protein synthesis
4
synaptic
4
synthesis synaptic
4

Similar Publications

Polyunsaturated fatty acids in particular omega-3 fatty acids, such as docosahexaenoic acid (DHA), are essential nutrients and components of the plasma membrane. They are involved in various processes, including synaptic development, functionality, integrity, and plasticity, and are therefore thought to have general neuroprotective properties. Considerable research evidence further supports the beneficial effects of omega-3 fatty acids, specifically on mitochondria, through their antioxidant and anti-apoptotic properties, making them an attractive addition in treatment options for neurodegenerative disorders in which mitochondrial alterations are commonly observed.

View Article and Find Full Text PDF

Physical activity, cathepsin B, and cognitive health.

Trends Mol Med

January 2025

Body-Brain-Mind Laboratory, School of Psychology, Shenzhen University, Shenzhen, 518060, China. Electronic address:

Regular physical activity (PA) is beneficial for cognitive health, and cathepsin B (CTSB) - a protease released by skeletal muscle during PA - acts as a potential molecular mediator of this association. PA-induced metabolic and mechanical stress appears to increase plasma/serum CTSB levels. CTSB facilitates neurogenesis and synaptic plasticity in brain regions (e.

View Article and Find Full Text PDF

Loss of neuronal activity facilitates surface accumulation of p75NTR and cell death in avian cochlear nucleus.

Neurosci Res

January 2025

Department of Cell Physiology, Graduate School of Medicine, Nagoya University, Nagoya 466-8550, Japan. Electronic address:

Sensorineural hearing loss causes cell death in central auditory neurons, but molecular mechanisms of triggering this process are not fully understood. We report here that loss of afferent activity promotes cell death by facilitating proBDNF-p75NTR signals in cochlear nucleus of chicks around hatch. RNA-seq analyses revealed up-regulation of genes related to proBDNF-p75NTR-JNK signals as well as apoptosis at the nucleus within 24hours after unilateral cochlea deprivation.

View Article and Find Full Text PDF

Understanding the role and mode of action of nutrient transporters requires information about their dynamic associations with plant membranes. Historically, apoplastic nutrient export has been associated with proteins localized at the plasma membrane (PM), while the role of endomembrane localization has been less explored. However, recent work on the PHOSPHATE 1 (PHO1) inorganic phosphate (Pi) exporter demonstrated that, although primarily localized at the Golgi and trans-Golgi network (TGN) vesicles, PHO1 does associate with the PM when clathrin-mediated endocytosis (CME) was inhibited, supporting a mechanism for Pi homeostasis involving exocytosis.

View Article and Find Full Text PDF

APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.

Mol Neurodegener

January 2025

Department of Neurobiology and Behavior, Charlie Dunlop School of Biological Sciences, University of California, Irvine, CA, 92697-4545, USA.

Background: Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer's Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!