Mercury chronic toxicity might be associated to some cases of hydrocephalus in adult humans?

Sieger, Federico Arturo Silva; Silva, Gustavo Adolfo Díaz; Ardila, Gustavo; García, Ronald G.

doi:10.1016/j.mehy.2012.03.022

Cited by 2 publications

(1 citation statement)

References 15 publications

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“…The choices of these experimental doses were based on the studies showing that in the Minamata Bay exposure in Japan, the mercury concentration in the brains of patients was found to be around 1.7 μM to 26 μM, whereas in non-exposed controls its levels averaged around 30 nM [33,34]. Additionally, several studies have revealed that mercury levels in brain tissues are 2–10 fold higher in patients with dental amalgam fillings, Alzheimer’s disease, autism spectrum disorders, epilepsy or hydrocephalus [35-38]. Figure 1A shows a typical culture dish grown under control conditions (no mercury) yielding a healthy population of both neurons and glial cells (indicated by a circle) with extensive neurite outgrowth and network formation (indicated by an arrow).…”

Section: Resultsmentioning

confidence: 99%

Mercury-induced toxicity of rat cortical neurons is mediated through N-methyl-D-Aspartate receptors

Farkas

Kortbeek

et al. 2012

Mol Brain

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BackgroundMercury is a well-known neurotoxin implicated in a wide range of neurological or psychiatric disorders including autism spectrum disorders, Alzheimer’s disease, Parkinson’s disease, epilepsy, depression, mood disorders and tremor. Mercury-induced neuronal degeneration is thought to invoke glutamate-mediated excitotoxicity, however, the underlying mechanisms remain poorly understood. Here, we examine the effects of various mercury concentrations (including pathological levels present in human plasma or cerebrospinal fluid) on cultured, rat cortical neurons.ResultsWe found that inorganic mercuric chloride (HgCl2 –at 0.025 to 25 μM) not only caused neuronal degeneration but also perturbed neuronal excitability. Whole-cell patch-clamp recordings of pyramidal neurons revealed that HgCl2 not only enhanced the amplitude and frequency of synaptic, inward currents, but also increased spontaneous synaptic potentials followed by sustained membrane depolarization. HgCl2 also triggered sustained, 2–5 fold rises in intracellular calcium concentration ([Ca2+]i). The observed increases in neuronal activity and [Ca2+]i were substantially reduced by the application of MK 801, a non-competitive antagonist of N-Methyl-D-Aspartate (NMDA) receptors. Importantly, our study further shows that a pre incubation or co-application of MK 801 prevents HgCl2-induced reduction of cell viability and a disruption of β-tubulin.ConclusionsCollectively, our data show that HgCl2-induced toxic effects on central neurons are triggered by an over-activation of NMDA receptors, leading to cytoskeleton instability.

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