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Noradrenergic regulation of synaptic plasticity in the hippocampal CA1 region.
TLDR
Results show that NE plays a modulatory role in the induction of hippocampal synaptic plasticity and indicates that activation of both alpha1 and beta-receptors is required in determining effects on previously potentiated synapses.
A critical role of TRPM2 in neuronal cell death by hydrogen peroxide.
TLDR
The results suggest that TRPM2 plays a pivotal role in H2O2-induced neuronal death as redox-sensitive Ca2+-permeable channels expressed in neurons.
3‐Hydroxykynurenine, an Endogenous Oxidative Stress Generator, Causes Neuronal Cell Death with Apoptotic Features and Region Selectivity
TLDR
3‐HK, depending on transporter‐mediated cellular uptake and on intracellular generation of oxidative stress, induces neuronal cell death with brain region selectivity and with apoptotic features, which may be relevant to pathology of neurodegenerative disorders.
Endogenous Monocarboxylates Sustain Hippocampal Synaptic Function and Morphological Integrity during Energy Deprivation
TLDR
Results suggest that endogenous monocarboxylates rather than glucose maintain neuronal integrity during energy deprivation, and EPSPs supported by 2–3.3 mm glucose were sensitive to 4-CIN, suggesting that endogenousMonocar boxylates are involved in maintaining neuronal function even under conditions of mild glucose deprivation.
Hydrogen peroxide-mediated neuronal cell death induced by an endogenous neurotoxin, 3-hydroxykynurenine.
TLDR
It is demonstrated that micromolar concentrations of 3-HK cause cell death in primary neuronal cultures prepared from rat striatum, suggesting that this endogenous compound should be regarded as an important factor in pathogenesis of neurodegenerative disorders.
Nicotinic Acetylcholine Receptor-Mediated Neuroprotection by Donepezil Against Glutamate Neurotoxicity in Rat Cortical Neurons
TLDR
The results suggest that donepezil not only protects cortical neurons against glutamate neurotoxicity via α4β2- and α7-nAChRs but also prevents apoptotic neuronal death.
Protective effects of 1 alpha,25-(OH)(2)D(3) against the neurotoxicity of glutamate and reactive oxygen species in mesencephalic culture.
TLDR
It is suggested that 1 alpha,25-(OH)(2)D(3) provides protection of dopaminergic neurons against cytotoxicity induced by glutamate and dopamine toxins by facilitating cellular functions that reduce oxidative stress.
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