B-50/GAP-43 is an intraneuronal membrane-associated growth cone protein with an important role in axonal growth and regeneration. By using adenoviral vector-directed expression of B-50/GAP-43 we studied the morphogenic action of B-50/GAP-43 in mature primary olfactory neurons that have established functional synaptic connections. B-50/GAP-43 induced gradual alterations in the morphology of olfactory synapses. In the first days after overexpression, small protrusions originating from the preterminal axon shaft and from the actual synaptic bouton were formed. With time the progressive formation of multiple ultraterminal branches resulted in axonal labyrinths composed of tightly packed sheaths of neuronal membrane. Thus, B-50/GAP-43 is a protein that can promote neuronal membrane expansion at synaptic boutons. This function of B-50/GAP-43 suggests that this protein may subserve an important role in ongoing structural synaptic plasticity in adult neurons and in neuronal membrane repair after injury to synaptic fields.
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http://dx.doi.org/10.1523/JNEUROSCI.17-17-06575.1997 | DOI Listing |
Sci Rep
January 2025
Neuroscience Graduate Program, The Ohio State University, Columbus, OH, 43210, USA.
Postpartum depression (PPD) affects up to 20% of new mothers and has adverse consequences for the well-being of both mother and child. Exposure to stress during pregnancy as well as dysregulation in the mesolimbic dopamine (DA) reward system and its upstream modulator oxytocin (OT) have been independently linked to PPD. However, no studies have directly examined DA or OT signaling in the postpartum brain after gestational stress.
View Article and Find Full Text PDFFree Radic Biol Med
January 2025
Department of Neurology, Columbia University Medical Center, New York, NY, 10032, USA. Electronic address:
Coenzyme Q (CoQ) is a critical component of the mitochondrial respiratory chain. CoQ deficiencies often cause a variety of clinical syndromes, often involving encephalopathies. The heterogeneity of clinical manifestations implies different pathomechanisms, reflecting CoQ involvement in several biological processes.
View Article and Find Full Text PDFExp Neurol
January 2025
Traumatic Brain Injury & Metabolomics Department, DRDO, Institute of Nuclear Medicine and Allied Sciences (INMAS), S. K Mazumdar Road, Timarpur, New Delhi 110054, India. Electronic address:
Head trauma from blast exposure is a growing health concern, particularly among active military personnel, and is considered the signature injury of the Gulf War. However, it remains elusive whether fundamental differences exist between blast-related traumatic brain injuries (TBI) and TBI due to other mechanisms. Considering the importance of lipid metabolism associated with neuronal membrane integrity and its compromise during TBI, we sought to find changes in lipidomic profiling during blast or blunt (Stereotaxically Controlled Contusison-SCC)-mediated TBI.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Department of Health Sciences, Section of Clinical Pharmacology and Oncology, University of Florence, Italy. Electronic address:
Cannabis derivatives are among the most widely used psychoactive substances in the world, which leads to growing medical concerns regarding its chronic use and abuse especially among adolescents. Exposure to THC during formative years produces long-term behavioral alterations that share similarities with symptoms of psychiatric and neurodevelopmental disorders. In this study, we have analyzed the functional and molecular mechanisms that might underlie these alterations.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Osaka University Graduate School of Medicine, Toyonaka, Japan.
Background: We have developed a technology for isolating extracellular vesicles (EVs) released from the central nervous system present in plasma.
Method: Initially, we differentiated induced pluripotent stem cells (iPS) into neurons to examine the membrane surface molecules of neuron-derived EVs in culture media. Our analysis revealed a specific interest in neuron-specific APLP1.
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