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Journal of Neurobiology and Physiology
ISSN: 2692-546X
Featured Article
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology
Featured Article
Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers
Featured Article
Duration and magnitude of bidirectional fluctuation in blood pressure: the link between cerebrovascular dysfunction and cognitive impairment following spinal cord injury
About this Journal
Journal of Neurobiology and Physiology is an international, multidisciplinary open access, peer-reviewed journal that publishes groundbreaking novel research articles, comprehensive review articles, short commentary, case reports, and editorials written by leading researchers in the field of neurology and neuroscience.
Articles
Evaluation of chondrocyte dedifferentiation mechanisms using confocal Raman microscopy
Human chondrocytes were isolated from articular cartilage harvested from a patient's knee during surgery, following informed consent. Cells were enzymatically digested with collagenase, then expanded directly onto Calcium Fluoride (CaF2) slides in two-dimensional (2D) monolayer cultures. Evaluations using wide-field optical microscopy, as well as Raman spectral measurements at D7, D14, D21, and D28 were performed for each passage from P1 to P4.
Results: Analysis of the different passages showed morphological and biochemical changes associated with cell passages. The greater the number of passages, the more the cells adopted a fibroblastic morphology. Raman bands located at 1063, 1255, and 1665 cm-1 were essential for monitoring changes in the molecular composition of glycosaminoglycans (GAGs), type II collagen and type I collagen over the passages.
Commentary on “Understanding bacterial chondronecrosis with osteomyelitis (BCO) in poultry: Highlights from proteomic analyses and imaging techniques”
Bacterial chondronecrosis with osteomyelitis (BCO) is a leading cause of lameness in broiler chickens, which results in financial losses due to mortality and reduced growth. Due to the nature of the condition, it raises animal welfare and food safety concerns as well. The pathology in the commercial setting is derived from a combination of weak bone and bacterial translocation and infection. Multiple genetic, nutritional, and managerial strategies have been employed to help mitigate the negative consequences of BCO; however, without understanding of the underlying causes of onset and progression, any benefit of these interventions is likely tempered. Compounding our dearth of knowledge is the fact that current methods of identification rely on subjective gait scores for lameness that may not show changes until the problem is severe or require diagnosis of BCO at necropsy. Therefore, our research group has aimed to tackle both facets of this important poultry concern.
The genetical genomic path to understanding why rats and humans consume too much alcohol
At the invitation of the Journal, we are providing a summary of our published work that has followed the publication in 2009 of our manuscript entitled “Genetical Genomic Determinants of Alcohol Consumption in Rats and Humans”. Our initial premise, which has been maintained throughout, is that knowledge regarding gene transcription would greatly enhance GWAS of alcohol-related phenotypes. We chose to concentrate our studies on the quantitative phenotype of alcohol consumption since high levels of alcohol consumption are a prerequisite for the development of alcohol use disorder (AUD). We also structured our studies to focus on “predisposition” to higher levels of alcohol consumption. We defined predisposition as a genetic structure and transcriptional pattern that is inherent in an organism and present prior to exposure to an environmental stimulus that engenders a physiological/behavioral response. In studies using humans, this interest in predisposition usually requires prolonged periods of cohort follow-up.
Commentary on “Identification of CD19 as a shared biomarker via PPARγ/β-catenin/Wnt3a pathway linking psoriasis and major depressive disorder”
This study presents a comprehensive exploration into the shared molecular mechanisms linking psoriasis and major depressive disorder (MDD), two conditions that are increasingly recognized as having potential comorbidities. It offers new insights into the immune and genetic pathways that may contribute to both disorders, emphasizing the potential of CD19 as a biomarker and therapeutic target through the PPARγ/β-catenin/Wnt3a signaling pathway. The study's findings underscore the need for further investigation into how inflammation and immune dysregulation may drive both the physical and mental health symptoms observed in patients with psoriasis and MDD. In this commentary, I will analyze the key findings of this study, explore its implications, and discuss areas for future research.
Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers
Gating of voltage-dependent sodium channels involves coordinated movements of the voltage sensors in the voltage-sensing modules (VSMs) of the four domains (DI-DIV) in response to membrane depolarization. Zhu et al. have recently examined the effects of charge reversal substitutions at the VSM of domain III on the action of scorpion alpha- and beta-toxins that intercept the voltage sensors in domains IV and II, respectively. The increased activity of both toxin types on the mutant channels has suggested that the VSM module at domain III interacts allosterically with the VSM modules in domains IV and II during channel gating thus affecting indirectly the action of both scorpion toxin classes.
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology
Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases.
Duration and magnitude of bidirectional fluctuation in blood pressure: the link between cerebrovascular dysfunction and cognitive impairment following spinal cord injury
Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators.
Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers
Gating of voltage-dependent sodium channels involves coordinated movements of the voltage sensors in the voltage-sensing modules (VSMs) of the four domains (DI-DIV) in response to membrane depolarization. Zhu et al. have recently examined the effects of charge reversal substitutions at the VSM of domain III on the action of scorpion alpha- and beta-toxins that intercept the voltage sensors in domains IV and II, respectively. The increased activity of both toxin types on the mutant channels has suggested that the VSM module at domain III interacts allosterically with the VSM modules in domains IV and II during channel gating thus affecting indirectly the action of both scorpion toxin classes.
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology
Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases.
Duration and magnitude of bidirectional fluctuation in blood pressure: the link between cerebrovascular dysfunction and cognitive impairment following spinal cord injury
Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators.
Allosteric interactions among voltage-sensor modules of sodium channels probed by scorpion toxin modifiers
Gating of voltage-dependent sodium channels involves coordinated movements of the voltage sensors in the voltage-sensing modules (VSMs) of the four domains (DI-DIV) in response to membrane depolarization. Zhu et al. have recently examined the effects of charge reversal substitutions at the VSM of domain III on the action of scorpion alpha- and beta-toxins that intercept the voltage sensors in domains IV and II, respectively. The increased activity of both toxin types on the mutant channels has suggested that the VSM module at domain III interacts allosterically with the VSM modules in domains IV and II during channel gating thus affecting indirectly the action of both scorpion toxin classes.
Endoplasmic reticulum stress and mitochondrial dysfunctions in metal-induced neurological pathology
Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases.
Duration and magnitude of bidirectional fluctuation in blood pressure: the link between cerebrovascular dysfunction and cognitive impairment following spinal cord injury
Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators.