Cadmium inhibits GABA-activated ion currents by increasing intracellular calcium level in snail neurons

Molnár, Gábor; Salánki, J.; Kiss, Tibor

doi:10.1016/j.brainres.2004.02.035

Cited by 17 publications

(9 citation statements)

References 29 publications

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“…Among these agents, heavy metals have been well documented in terms of their toxicity on ionic channels and the ability to bioaccumulate in the tissues [27]. For example, cadmium has been demonstrated to inhibit GABA-activated ion currents by increasing intracellular calcium levels in snail neurons [28] and to induce apoptosis in the hemocytes of the oyster, Crassostrea virginica , through a mitochondria/caspase-independent pathway [29]. Like heavy metals, saxitoxin and its analogs, all potent Na + channel blockers, may be responsible for the apoptosis observed here.…”

Section: Resultsmentioning

confidence: 99%

Exposure to the Neurotoxic Dinoflagellate, Alexandrium catenella, Induces Apoptosis of the Hemocytes of the Oyster, Crassostrea gigas

et al. 2013

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This study assessed the apoptotic process occurring in the hemocytes of the Pacific oyster, Crassostrea gigas, exposed to Alexandrium catenella, a paralytic shellfish toxins (PSTs) producer. Oysters were experimentally exposed during 48 h to the toxic algae. PSTs accumulation, the expression of 12 key apoptotic-related genes, as well as the variation of the number of hemocytes in apoptosis was measured at time intervals during the experiment. Results show a significant increase of the number of hemocytes in apoptosis after 29 h of exposure. Two pro-apoptotic genes (Bax and Bax-like) implicated in the mitochondrial pathway were significantly upregulated at 21 h followed by the overexpression of two caspase executor genes (caspase-3 and caspase-7) at 29 h, suggesting that the intrinsic pathway was activated. No modulation of the expression of genes implicated in the cell signaling Fas-Associated protein with Death Domain (FADD) and initiation-phase (caspase-2) was observed, suggesting that only the extrinsic pathway was not activated. Moreover, the clear time-dependent upregulation of five (Bcl2, BI-1, IAP1, IAP7B and Hsp70) inhibitors of apoptosis-related genes associated with the return to the initial number of hemocytes in apoptosis at 48 h of exposure suggests the involvement of strong regulatory mechanisms of apoptosis occurring in the hemocytes of the Pacific oyster.

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Section: Resultsmentioning

confidence: 99%

Exposure to the Neurotoxic Dinoflagellate, Alexandrium catenella, Induces Apoptosis of the Hemocytes of the Oyster, Crassostrea gigas

et al. 2013

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“…CRHSP24 has been suggested to be involved in calcium-mediated signal transduction (39). As cadmium has been reported to interfere with calcium homeostasis in nerve cells (23)(24)(25), we suggest that PIPPin might be a novel and central target of cadmium action in the brain. …”

Section: Discussionmentioning

confidence: 79%

“…Cadmium enters the central nervous system either through the olfactory pathway or by altering the permeability of the blood-brain barrier (18)(19)(20)(21), and has been reported to cause lipid peroxidation (15), damage to DNA (22), and alteration of calcium homeostasis (23)(24)(25). Cadmium was also demonstrated to affect metabolism, release and re-uptake of different neurotransmitters (26)(27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

The effect of cadmium on brain cells in culture

Gerspacher

Scheuber²,

Schiera³

et al. 2009

Int J Mol Med

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Abstract. Cadmium is a long-living heavy metal, abundantly present in the environment, which accumulates in the body. In this study, we investigated the effects of cadmium on the expression of molecular chaperones, and of certain cell-specific proteins, in a variety of brain cell types in culture, namely primary cultures of rat cortical neurons and astrocytes, a brain capillary endothelial cell line (RB4E.B cells), and pheochromocytoma cells (PC12), induced or not to differentiate by NGF treatment. The metal induces a dose-dependent increase of Hsp70 in all cell types. Responses to the metal are cellspecific in the case of Hsc70 and Hsp90: i) in astrocytes, as well as in PC12 cells, cadmium has no significant effect; ii) in endothelial cells, an increase of both proteins is clearly observable from 20 μM cadmium; iii) both Hsp90 and Hsc70 decrease in neurons treated with high doses of cadmium. Damage to the cytoskeleton in treated cells was also evident. Finally, we report that the metal at high doses induces a decrease of PIPPin (also known as CSD-C2), a putative RNAbinding protein highly expressed in neurons and probably involved in the regulation of histone replacement variant expression.

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“…Collar cells were found to stimulate spermatogenesis in gastropods (Takeda 1982). An in vitro study in L. stagnalis by Molnár et al (2004) also suggested that Cd inhibited GABA-activated chloride currents by increasing intracellular calcium levels in collar cells. These are plausible mechanisms by which Cd may disrupt neurotransmitter control of reproduction in gastropods.…”

Section: Neuroendocrine Disruption In Invertebratesmentioning

confidence: 96%

Neuroendocrine Disruption: More Than Hormones are Upset

Waye

Trudeau

2011

Journal of Toxicology and Environmental Health, Part B

117

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Only a small proportion of the published research on endocrine-disrupting chemicals (EDC) directly examined effects on neuroendocrine processes. There is an expanding body of evidence that anthropogenic chemicals exert effects on neuroendocrine systems and that these changes might impact peripheral organ systems and physiological processes. Neuroendocrine disruption extends the concept of endocrine disruption to include the full breadth of integrative physiology (i.e., more than hormones are upset). Pollutants may also disrupt numerous other neurochemical pathways to affect an animal's capacity to reproduce, develop and grow, or deal with stress and other challenges. Several examples are presented in this review, from both vertebrates and invertebrates, illustrating that diverse environmental pollutants including pharmaceuticals, organochlorine pesticides, and industrial contaminants have the potential to disrupt neuroendocrine control mechanisms. While most investigations on EDC are carried out with vertebrate models, an attempt is also made to highlight the importance of research on invertebrate neuroendocrine disruption. The neurophysiology of many invertebrates is well described and many of their neurotransmitters are similar or identical to those in vertebrates; therefore, lessons learned from one group of organisms may help us understand potential adverse effects in others. This review argues for the adoption of systems biology and integrative physiology to address the effects of EDC. Effects of pulp and paper mill effluents on fish reproduction are a good example of where relatively narrow hypothesis testing strategies (e.g., whether or not pollutants are sex steroid mimics) have only partially solved a major problem in environmental biology. It is clear that a global, integrative physiological approach, including improved understanding of neuroendocrine control mechanisms, is warranted to fully understand the impacts of pulp and paper mill effluents. Neuroendocrine disruptors are defined as pollutants in the environment that are capable of acting as agonists/antagonists or modulators of the synthesis and/or metabolism of neuropeptides, neurotransmitters, or neurohormones, which subsequently alter diverse physiological, behavioral, or hormonal processes to affect an animal's capacity to reproduce, develop and grow, or deal with stress and other challenges. By adopting a definition of neuroendocrine disruption that encompasses both direct physiological targets and their indirect downstream effects, from the level of the individual to the ecosystem, a more comprehensive picture of the consequences of environmentally relevant EDC exposure may emerge.

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Cadmium inhibits GABA-activated ion currents by increasing intracellular calcium level in snail neurons

Cited by 17 publications

References 29 publications

Exposure to the Neurotoxic Dinoflagellate, Alexandrium catenella, Induces Apoptosis of the Hemocytes of the Oyster, Crassostrea gigas

Exposure to the Neurotoxic Dinoflagellate, Alexandrium catenella, Induces Apoptosis of the Hemocytes of the Oyster, Crassostrea gigas

The effect of cadmium on brain cells in culture

Neuroendocrine Disruption: More Than Hormones are Upset

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