Female rats were allowed to consume ethanol during gestation and lactation, and brain polyphosphoinositides of the 21-day-old pups were quantified. Ethanol intake prevented the disappearance of the metabolically labile pools of phosphatidylinositol-4-phosphate and phosphatidylinositol-4,5-bis-phosphate, which are rapidly degraded in the control group. In contrast, preweaning undernutrition left the size of these pools virtually unchanged, indicating a differential effect of the two nutritional regimens.
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http://dx.doi.org/10.1111/j.1471-4159.1984.tb02762.x | DOI Listing |
Proc Natl Acad Sci U S A
December 2024
Department of Neuroscience, Section of Pharmacology, University of Naples Federico II, Naples 80131, Italy.
Pathogenic variants in encoding Kv7.2 voltage-gated potassium channel subunits cause developmental encephalopathies (-encephalopathies), both with and without epilepsy. We herein describe the clinical, in vitro, and in silico features of two encephalopathy-causing variants (A317T, L318V) in Kv7.
View Article and Find Full Text PDFNat Commun
August 2024
Department of Brain Sciences, Daegu Gyeongbuk Institute of Science and Technology (DGIST), Daegu, 42988, Republic of Korea.
Proton-activated chloride (PAC) channels, ubiquitously expressed in tissues, regulate intracellular Cl levels and cell death following acidosis. However, molecular mechanisms and signaling pathways involved in PAC channel modulation are largely unknown. Herein, we determine that phosphatidylinositol 4,5-bisphosphate [PI(4,5)P] of the plasma membrane inner leaflet is essential for the proton activation of PAC channels.
View Article and Find Full Text PDFNat Commun
June 2024
Division of Medical Physics and Biophysics, Medical University of Graz, Graz, Austria.
The transient receptor potential canonical type 3 (TRPC3) channel plays a pivotal role in regulating neuronal excitability in the brain via its constitutive activity. The channel is intricately regulated by lipids and has previously been demonstrated to be positively modulated by PIP. Using molecular dynamics simulations and patch clamp techniques, we reveal that PIP predominantly interacts with TRPC3 at the L3 lipid binding site, located at the intersection of pre-S1 and S1 helices.
View Article and Find Full Text PDFJ Hazard Mater
August 2024
Department of Cell Biology & Institute of Biomedicine, College of Life Science and Technology, Jinan University, Guangzhou 510632, China; Guangdong Provincial Key Laboratory of Bioengineering Medicine, Jinan University, Guangzhou 510632, China; National Engineering Research Center of Genetic Medicine, Jinan University, Guangzhou 510632, China. Electronic address:
The fetus and infants are particularly vulnerable to Cadmium (Cd) due to the immaturity of the blood-brain barrier. In utero and early life exposure to Cd is associated with cognitive deficits. Although such exposure has attracted widespread attention, its gender-specificity remains controversial, and there are no reports disclosing the underlying mechanism of gender‑specific neurotoxicity.
View Article and Find Full Text PDFSTAR Protoc
June 2024
Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Robert-Rössle-Str. 10, 13125 Berlin, Germany; Faculty of Biology, Chemistry, Pharmacy, Freie Universität Berlin, 14195 Berlin, Germany; NeuroCure Cluster of Excellence, Charité Universitätsmedizin Berlin, 10117 Berlin, Germany. Electronic address:
The minor phospholipid phosphatidylinositol 4,5-bisphosphate [PI(4,5)P] is crucial for neurotransmission and has been implicated in Parkinson's disease. Here, we present a staining protocol for the analysis of activity-dependent changes of PI(4,5)P at synapses. We describe steps for stimulating and fixing murine hippocampal neurons, staining with probes for PI(4,5)P and a synaptic marker, and analysis by high-resolution microscopy.
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