It has been proposed that reactive oxygen species and lipid peroxidation have a role in the delayed neuronal death of pyramidal cells in the CA1 region. To explore the in situ localization and serial changes of 4-hydroxy-2-nonenal-modified proteins, which are major products of membrane peroxidation, we used immunohistochemistry of the gerbil hippocampus after transient forebrain ischemia with or without preconditioning ischemia. The normal gerbil hippocampus showed weak immunoreactivity for 4-hydroxy-2-nonenal-modified proteins in the cytoplasm of CA1 pyramidal cells. 4-hydroxy-2-nonenal immunoreactivity showed no marked changes after preconditioning ischemia. In the early period after ischemia and reperfusion, there was a transient increase of nuclear 4-hydroxy-2-nonenal immunoreactivity in CA1 pyramidal neurons. In contrast, cytoplasmic immunoreactivity transiently disappeared during same period and then increased markedly from 8h to seven days. One week after ischemia, 4-hydroxy-2-nonenal immunoreactivity was observed within reactive astrocytes in the CA1 region. Early nuclear accumulation of 4-hydroxy-2-nonenal in CA1 neurons may indicate a possible role in signal transduction between the nucleus and cytoplasm/mitochondria, while delayed accumulation of 4-hydroxy-2-nonenal-modified proteins in the cytoplasm may be related to mitochondrial damage. We conclude that 4-hydroxy-2-nonenal may be a key mediator of the oxidative stress-induced neuronal signaling pathway and may have an important role in modifying delayed neuronal death.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/s0306-4522(00)00264-5 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Impact of Astroglia Kir4.1 Channel Dysfunction on Neuronal Activity and Autism-Related Behavioral Abnormalities.
Glia
January 2025
Neurophysiology Research Center, Institute of Neuroscience and Cognition, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Autism spectrum disorder (ASD) is marked by neurobehavioral developmental deficits, potentially linked to disrupted neuron-glia interactions. The astroglia Kir4.1 channel plays a vital role in regulating potassium levels during neuronal activation, and mutations in this channel have been associated with ASD.
View Article and Find Full Text PDFCerebrolysin treatment improved short-term memory deficits while simultaneously increasing hippocampal spine density in hypertensive female rats.
Behav Brain Res
January 2025
Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Unidad Tlaxcala, Mexico. Electronic address:
Hypertension, if untreated, can disrupt the blood-brain-barrier (BBB) and reduce cerebral flow in the central nervous system (CNS) inducing hippocampal atrophy, potentially leading to cognitive deficits and vascular dementia. Spontaneous hypertensive rats (SHR) demonstrated neuroplastic alterations in the hippocampus, hyperlocomotion and memory deficits in males. Cerebrolysin (CBL), a neuropeptide preparation, induces synaptic and neuronal plasticity in various populations of neurons and repairs the integrity of the BBB.
View Article and Find Full Text PDFProlonged incubation with Δ-tetrahydrocannabinol but not with cannabidiol induces synaptic alterations and mitochondrial impairment in immature and mature rat organotypic hippocampal slices.
Biomed 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 PDFPlural molecular and cellular mechanisms of pore domain encephalopathy.
Elife
January 2025
Department of Neurology, Baylor College of Medicine, Houston, United States.
Article Synopsis
- Variants associated with neurodevelopmental impairments in children are complex and challenging to evaluate due to their diverse nature and unclear causes.
- The study highlights a case of a child with neonatal-onset epilepsy and a specific genetic variant (G256W) that impacts ion channel function and leads to reduced cell stability and conduction in nervous tissue.
- The research also establishes a mouse model that exhibits epilepsy and hyperexcitability in brain cells, linking the genetic variant to observable neurological behaviors and suggesting potential wider implications for understanding similar conditions in other patients.
Development of differential sublaminar feedforward inhibitory circuits in CA1 hippocampus requires .
J Neurosci
January 2025
Department of Neuroscience, The Ohio State University College of Medicine, Columbus, OH 43210
Pyramidal cells (PCs) in CA1 hippocampus can be classified by their radial position as deep or superficial and organize into subtype-specific circuits necessary for differential information processing. Specifically, superficial PCs receive fewer inhibitory synapses from parvalbumin (PV)-expressing interneurons than deep PCs, resulting in weaker feedforward inhibition of input from CA3 Schaffer collaterals. Using mice, we investigated mechanisms underlying CA1 PC differentiation and the development of this inhibitory circuit motif.
View Article and Find Full Text PDFWant 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!