Publications by authors named "J M Hernandez-Guijo"

Article Synopsis
  • - The study highlights that while excitatory amino acids like glutamate and aspartate are known to contribute to brain damage during ischemia, the impact of non-excitatory amino acids (like L-alanine and glycine) is not well understood, despite their potential role in worsening brain injuries.
  • - Findings show that exposure to a combination of specific non-excitatory amino acids during transient hypoxia can cause irreversible neuronal damage, highlighting a new aspect of brain injury that needs further exploration.
  • - The researchers suggest that the swelling of astrocytes due to these amino acids might activate certain channels that release excitotoxins, leading to further neuron damage, indicating that these mechanisms could be important for developing new treatments for conditions
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The present work, using chromaffin cells of bovine adrenal medullae (BCCs), aims to describe what type of ionic current alterations induced by lead (Pb) underlies its effects reported on synaptic transmission. We observed that the acute application of Pb lead to a drastic depression of neurotransmitters release in a concentration-dependent manner when the cells were stimulated with both K or acetylcholine, with an IC of 119,57 μM and of 5,19 μM, respectively. This effect was fully recovered after washout.

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The aim of this review is to explore the relationship between melatonin, free radicals, and non-excitatory amino acids, and their role in stroke and aging. Melatonin has garnered significant attention in recent years due to its diverse physiological functions and potential therapeutic benefits by reducing oxidative stress, inflammation, and apoptosis. Melatonin has been found to mitigate ischemic brain damage caused by stroke.

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The contribution of excitatory amino acids (AA) to ischemic brain injury has been widely described. In addition, we reported that a mixture of non-excitatory AA at plasmatic concentrations turns irreversible the depression of synaptic transmission caused by hypoxia. Here, we describe that the presence of seven non-excitatory AA (L-alanine, L-glutamine, glycine, L-histidine, L-serine, taurine, and L-threonine) during hypoxia provokes an irreversible neuronal membrane depolarization, after an initial phase of hyperpolarization.

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Aluminum (Al ) has long been related to neurotoxicity and neurological diseases. This study aims to describe the specific actions of this metal on cellular excitability and neurotransmitter release in primary culture of bovine chromaffin cells. Using voltage-clamp and current-clamp recordings with the whole-cell configuration of the patch clamp technique, online measurement of catecholamine release, and measurements of [Ca ] with Fluo-4-AM, we have observed that Al reduced intracellular calcium concentrations around 25% and decreased catecholamine secretion in a dose-dependent manner, with an IC of 89.

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