Results 91 to 100 of about 153,025 (224)
Responsive Materials, EarlyView.This review presents the structure and transport routes of the blood‐brain barrier, summarizes the ischemic stroke pathophysiological cascade, and discusses the BBB‐crossing mechanisms and multitarget therapeutic effects of carbon dots, demonstrating their promising theranostic potential for ischemic stroke.
Yanhan Huang +6 more
wiley +1 more source
An Experimental Study on the Protective Effect of Memantine in Noise‐Induced Hearing Loss
World Journal of Otorhinolaryngology - Head and Neck Surgery, EarlyView.ABSTRACT Objective This study examined the potential protective effects of memantine, an N‐methyl‐D‐aspartate (NMDA) receptor antagonist, against acoustic trauma (AT) in guinea pigs, using electrophysiological and histopathological analyses. Methods Thirty guinea pigs with normal hearing were divided into six groups (n = 5 per group): Group 1 (control),
Begüm Arda +6 more
wiley +1 more source
Insight into Glutamate Excitotoxicity from Synaptic Zinc Homeostasis [PDF]
International Journal of Alzheimer’s Disease, 2010 Zinc is released from glutamatergic (zincergic) neuron terminals in the hippocampus, followed by the increase in Zn2+ concentration in the intracellular (cytosol) compartment, as well as that in the extracellular compartment. The increase in Zn2+ concentration in the intracellular compartment during synaptic excitation is mainly due to Zn2+ influx ...
openaire +2 more sources
In vivo evidence for NMDA receptor mediated excitotoxicity in a murine genetic model of Huntington Disease [PDF]
, 2008 N-methyl-D-aspartate receptor (NMDAR) mediated excitotoxicity is implicated as a proximate cause of neurodegeneration in Huntington Disease (HD). However, this hypothesis has not been tested rigorously in vivo. NMDAR NR2B-subunits are the predominant NR2
Joe Tsien +4 more
core
L-lactate-mediated neuroprotection against glutamate- induced excitotoxicity requires ARALAR/AGC1 [PDF]
, 2017 ARALAR/AGC1/Slc25a12, the aspartate-glutamate carrier from brain mitochondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS. MAS is used to oxidize cytosolic NADH in mitochondria, a process required to maintain oxidative glucose ...
Pardo, Beatriz +4 more
core +1 more source
Brain Pathology, EarlyView.Divergent remodeling of TRPC channels occurs in Alzheimer's disease, with TRPC3 increased in neurons and reactive astrocytes and TRPC6 reduced in pyramidal neurons. These alterations may contribute to calcium dysregulation, neuroinflammation, and synaptic dysfunction during AD progression.
Xingyong Chen +8 more
wiley +1 more source
Investigating the Effect of SER-1 in a Caenorhabditis elegans Model of Glutamate Excitotoxicity
, 2016 vi, 30 p.Excitotoxicity, the underlying mechanism common to all neurodegenerative diseases, is the pathology of necrotic effects caused by the prolonged activation of excitatory neurotransmitter receptors in the central nervous system.
Alzouhayli, Suma
core +1 more source
Peripheral targets for neuropathic pain
British Journal of Pharmacology, EarlyView.Neuropathic pain represents a significant clinical challenge, with still limited pharmacological approaches to symptomatic relief. This review focuses on molecular targets implicated in neuropathic pain, particularly those involved in peripheral mechanisms. Using the IUPHAR/BPS database of biological targets, their occurrence together with ‘neuropathic
Amirhossein Afsharipour +3 more
wiley +1 more source
British Journal of Pharmacology, EarlyView.Disruption of intracellular ionic homeostasis is a convergent pathological feature across diverse neurological injuries and disorders, including ischaemic and haemorrhagic stroke, hypoxic–ischaemic brain injury, traumatic brain injury, epilepsy and brain tumour.
Xinyang Zhang +5 more
wiley +1 more source
NMDA receptor-dependent glutamate excitotoxicity in human embryonic stem cell-derived neurons [PDF]
, 2013 Thanks to the development of efficient differentiation strategies, human pluripotent stem cells (HPSC) offer the opportunity for modelling neuronal injury and dysfunction in human neurons in vitro.
Hardingham, G.E. +2 more
core +1 more source