Results 41 to 50 of about 57,791 (292)
Astrocytic FABP5 promotes mitochondrial stress, cGAS‐STING pathway activation, pyroptosis, and neuroinflammation in epilepsy, contributing to seizure pathology. Genetic targeting of FABP5 or pharmacological inhibition of STING alleviates epileptic phenotypes, highlighting a potential therapeutic strategy for epilepsy.
Chen Chen +10 more
wiley +1 more source
.: We have previously demonstrated an important role of influx of Cl− rather than Ca2+ in acute excitotoxicity in adult rat retina. As p53 has been implicated in delayed apoptotic cell death, here we examined the appearance of p53 immunoreactivity in a ...
Yasuhiro Hama +4 more
doaj +1 more source
Protective effect of naringenin on glutamate-induced neurotoxicity in cultured hippocampal cells [PDF]
Monosodium glutamate induces excitotoxicity in the central nervous system through hyperactivation of both ionotropic and metabotropic glutamate receptors, which leads to neuronal cell death.
Xu Xiao-Hui +8 more
doaj +1 more source
Functionalized Biomimetic Scaffolds for Human‐Derived Auditory Neural Circuit Construction
In Vitro Auditory Circuit Model. ABSTRACT Damage to auditory circuits results in sensorineural hearing loss. However, the scarcity of human inner ear tissue significantly hinders the development of therapies to preserve auditory function, creating a critical need for reliable in vitro models.
Pan Feng +12 more
wiley +1 more source
Background Excitotoxicity induced by glutamate contributes significantly to ischemic brain injury. The role of enriched environment (EE) in promoting neurological recovery post-stroke is well-established, yet its impact on excitotoxicity remains unclear.
Yi Zhang +4 more
doaj +1 more source
Polydopamine nanoparticles enable a precise, non‐genetic, and transcranial neuromodulation strategy via near‐infrared photothermal stimulation. By activating TRPV1 channels, this approach specifically enhances hippocampal gamma oscillations, thereby rescuing spatial memory deficits in models of perioperative neurocognitive disorder.
Yan‐Bo Zhou +10 more
wiley +1 more source
Excitotoxicity due to excessive glutamate release causes oxidative stress and neuronal death, and is a feature of many brain diseases. Here the authors show that protein kinase D1 is inactivated by excitotoxicity in a model of stroke and that its ...
Julia Pose-Utrilla +18 more
doaj +1 more source
Background Hyperexcitability of neuronal networks can lead to excessive release of the excitatory neurotransmitter glutamate, which in turn can cause neuronal damage by overactivating NMDA-type glutamate receptors and related signaling pathways.
Takashi Miyamoto +7 more
doaj +1 more source
Impaired MEC astrocytic Ca2+ signaling is associated with fragmented spatial exploration in AD mice. Region‐specific glial progenitor transplantation generates engrafted astrocytes that are accompanied by improved AQP4 polarization, reduced amyloid‐β‐associated pathology, attenuated neuroinflammation, preserved synaptic integrity, and ameliorated ...
Fengjuan Wu +16 more
wiley +1 more source
VEGFD Protects Retinal Ganglion Cells and, consequently, Capillaries against Excitotoxic Injury
In the central nervous system, neurons and the vasculature influence each other. While it is well described that a functional vascular system is trophic to neurons and that vascular damage contributes to neurodegeneration, the opposite scenario in which ...
Annabelle Schlüter +4 more
doaj +1 more source

