Mapping immediate early gene (IEG) expression levels to characterize changes in neuronal activity patterns has become a golden standard in neuroscience research. Due to straightforward detection methods such as in situ hybridization and immunohistochemistry, changes in IEG expression can be easily visualized across brain regions and in response to physiological and pathological stimulation. Based on in-house experience and existing literature, zif268 represents itself as the IEG of choice to investigate the neuronal activity dynamics induced by sensory deprivation. In the monocular enucleation mouse model of partial vision loss, zif268 in situ hybridization can be implemented to study cross-modal plasticity by charting the initial decline and subsequent rise in neuronal activity in visual cortical territory deprived of direct retinal visual input. Here, we describe a protocol for high-throughput radioactive zif268 in situ hybridization as a readout for cortical neuronal activity dynamics in response to partial vision loss in mice.
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http://dx.doi.org/10.1007/978-1-0716-3012-9_4 | DOI Listing |
Clin Sci (Lond)
January 2025
Center for Interdisciplinary Research in Biology, College de France, Institut National de la Santé et de la Recherche Médicale, Paris, France.
Apelin, a (neuro) vasoactive peptide, plays a prominent role in controlling water balance and cardiovascular functions. Apelin and its receptor co-localize with vasopressin in magnocellular vasopressinergic neurons. Apelin receptors (Apelin-Rs) are also expressed in the collecting ducts of the kidney, where vasopressin type 2 receptors are also present.
View Article and Find Full Text PDFJ Vis Exp
January 2025
Genetics and Aging Research Unit, MassGeneral Institute for Neurodegenerative Disease, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, Harvard Medical School;
A method to quantitate the stabilization of Mitochondria-Associated endoplasmic reticulum Membranes (MAMs) in a 3-dimensional (3D) neural model of Alzheimer's disease (AD) is presented here. To begin, fresh human neuro progenitor ReN cells expressing β-amyloid precursor protein (APP) containing familial Alzheimer's disease (FAD) or naïve ReN cells are grown in thin (1:100) Matrigel-coated tissue culture plates. After the cells reach confluency, these are electroporated with expression plasmids encoding red fluorescence protein (RFP)-conjugated mitochondria-binding sequence of AKAP1(34-63) (Mito-RFP) that detects mitochondria or constitutive MAM stabilizers MAM 1X or MAM 9X that stabilize tight (6 nm ± 1 nm gap width) or loose (24 nm ± 3 nm gap width) MAMs, respectively.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
School of Pharmacy, Jiangxi University of Chinese Medicine, Nanchang, China.
Microglia-mediated neuroinflammation plays a crucial role in Alzheimer's disease (AD). Tinosinenside A (Tis A) is a novel sesquiterpene glycoside isolated from the dried rattan stem of Tinospora sinensis (Lour.) Merr.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Cell Biology, Emory University, 615 Michael St, Atlanta, GA, USA, 30322.
Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.
View Article and Find Full Text PDFACS Chem Neurosci
January 2025
Sensor Engineering Department, Faculty of Science and Engineering, Maastricht University, 6200 MD Maastricht, The Netherlands.
As the main inhibitory neurotransmission system, the GABAergic system poses an interesting yet underutilized target for molecular brain imaging. While PET imaging of postsynaptic GABAergic neurons has been accomplished using radiolabeled benzodiazepines targeting the GABA receptor, the development of presynaptic radioligands targeting GABA transporter 1 (GAT1) has been unsuccessful thus far. Therefore, we developed a novel GAT1-addressing radioligand and investigated its applicability as a PET tracer in rodents.
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