Synenkephalin (proenkephalin 1-70) is produced and secreted as an intact molecule or as a part of precursors in the adult brain and adrenal medulla, respectively. However, it is cleaved to low molecular weight peptides in proliferating immune cells. Considering that the pre-proenkephalin gene is expressed in the embryonic rat brain during the cell proliferation stage, we studied the processing of synenkephalin in embryonic rat brains (E18) and compared it with the processing in adult rat brains. IR-synenkephalin was measured by RIA using a C-terminally directed antiserum. Adult rat brains contained higher concentrations of immunoreactive (IR)-synenkephalin (2,612 + 264) than embryonic rat brain (1,361 + 100) (results in fmol/mg proteins, n = 5). Gel filtration chromatography (Sephadex G-50) showed that in the extracts of adult rat brain, 50% of the IR-synenkephalin eluted in the position of the authentic peptide (8 kDa) and the rest of the immunoreactivity corresponded to partially processed peptides of 4.0 and 2.5 kDa. In embryonic rat brains synenkephalin was processed to intermediate peptides of 2.5, 1.7 and mainly to a low molecular weight peptide of 1.0 kDa. The concentration of this last peptide, which was further characterized by affinity column and HPLC, represented 45% of the total immunoreactivity. IR-met-enkephalin in embryonic rat brains (analyzed before and after enzymatic digestion with trypsin and carboxypeptidase B) corresponded principally to non-processed or partially processed products. However, these were cleaved to free met-enkephalin in adult rat brains.(ABSTRACT TRUNCATED AT 250 WORDS)
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/0165-3806(94)90191-0 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Graft ischemia post cell transplantation to the brain: Glucose deprivation as the primary driver of rapid cell death.
Neurotherapeutics
January 2025
School of Pharmacy and Pharmaceutical Sciences, Cardiff University, King Edward VII Avenue, Cardiff, CF10 3NB, UK; Leibniz-Institut für Polymerforschung Dresden, Max Bergmann Center of Biomaterials Dresden, Hohe Straße 6, D-01069 Dresden, Germany. Electronic address:
Replacing cells lost during the progression of neurodegenerative disorders holds potential as a therapeutic strategy. Unfortunately, the majority of cells die post-transplantation, which creates logistical and biological challenges for cell therapy approaches. The cause of cell death is likely to be multifactorial in nature but has previously been correlated with hypoxia in the graft core.
View Article and Find Full Text PDFExtractable organic matter from PM inhibits cardiomyocyte differentiation via AHR-mediated mA RNA methylation.
J Hazard Mater
January 2025
The First Affiliated Hospital, MOE Education Key Laboratory of Geriatric Diseases and Immunology, Suzhou Medical College of Soochow University, Suzhou, China; Jiangsu Key Laboratory of Preventive and Translational Medicine for Major Chronic Non-Communicable Diseases, China. Electronic address:
An ever-increasing body of research has established a link between maternal PM2.5 exposure and congenital heart diseases in the offspring, but the underlying mechanisms remain elusive. We recently reported that activation of the aryl hydrocarbon receptor (AHR) by PM2.
View Article and Find Full Text PDFComparative Analysis of the Effects of Maternal Hypoxia and Placental Ischemia on HIF1-Dependent Metabolism and the Glucocorticoid System in the Embryonic and Newborn Rat Brain.
Int J Mol Sci
December 2024
Laboratory of Regulation of Brain Neuronal Functions, Pavlov Institute of Physiology, Russian Academy of Sciences, Makarova emb. 6, 199034 Saint-Petersburg, Russia.
Prenatal hypoxia, often accompanied by maternal glucocorticoid stress, can predispose offspring to neurological disorders in adulthood. If placental ischemia (PI) primarily reduces fetal oxygen supply, the maternal hypoxia (MH) model also elicits a pronounced fetal glucocorticoid exposure. Here, we compared MH and PI in rats to distinguish their unique and overlapping effects on embryonic and newborn brain development.
View Article and Find Full Text PDFThe effect of Naringin on cognitive function, oxidative stress, cholinergic activity, CREB/BDNF signaling and hippocampal cell damage in offspring rats with utero-placental insufficiency-induced intrauterine growth restriction.
Brain Res
January 2025
Physiology, Department of Biology, Marvdasht Branch, Islamic Azad University, Marvdasht, Iran.
Intrauterine growth restriction (IUGR) induced by utero-placental insufficiency (UPI) results in delayed neural development and impaired brain growth. This study investigates the effects of Naringin (Nar) on memory, learning, cholinergic activity, oxidative stress markers, hippocampal CREB/BDNF signal pathway and cell damage in offspring of rats exposed to UPI. Twenty pregnant Wistar rats were randomly assigned to four groups: control, sham surgery, UPI + NS (UPI + normal saline as a vehicle), and UPI + Nar (UPI + Nar at 100 mg/kg/day).
View Article and Find Full Text PDFThe potential ameliorative effect of mesenchymal stem cells-derived exosomes on cerebellar histopathology and their modifying role on PI3k-mTOR signaling in rat model of autism spectrum disorder.
J Mol Histol
January 2025
Department of Histology, Faculty of Medicine, Assiut University, Assiut, Egypt.
Article Synopsis
- Autism spectrum disorder (ASD) is a serious neurodevelopmental issue, and this study investigates the effects of administering MSCs-derived exosomes after birth on a rat model of ASD.
- The research involved dividing male rat pups into control, VPA (exposed to a neurotoxin), and VPA treated with exosomes, assessing changes in behavior and cerebellar structure.
- Results showed that VPA groups exhibited increased activity, social impairments, and disrupted cerebellar structure, while those treated with exosomes showed improvements in histological integrity and behaviors, supported by changes in specific signaling pathways.
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!