Interaction of Metals with Brain Calmodulin Purified from Normal and Cadmium Exposed Rats

Vig, P. J. S.; Ravi, K.; Nath, R.

doi:10.3109/01480549109017877

Cited by 13 publications

(10 citation statements)

References 21 publications

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“…Cadmium was deposited in the brain and in other tissues, and caused neuronal death when injected 6 mg/kg to rats (2). It was also reported that cadmium (0.4 mg/kg) has neurotoxic effects in all regions of the brain except hippocampus when it was given into cerebra-spinal fluid of mature rats (3).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of nicardipine on cadmium‐induced Purkinje cell death in rat cerebellum

Bağirici

Genç

Tan

et al. 2001

Neuroscience Res Communica

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SUMMARYThe present study was designed to investigate the effects of nicardipine on cadmium-induced Purkinje cell loss in cerebellum of rats. Animals were divided into three groups as control, cadmium and cadmium + nicardipine groups. Saline, cadmium sulphate (0,0021 mg/kg) and cadmium sulphate (0,002 1 mg/kg) + nicardipine (1 mg/kg) were intracortically administered respectively. All rats were observed for one week, but only the rats in the third group were injected nicardipine (10 n&kg/day, i.p.) during this period. One week later, all rats were perfused intracardially. Series of frontal sections from cerebella were stained with Thionin staining. Purkinje cells were counted under x400 magnification via a light microscope.Cadmium administration caused 25-35 % decrease in Purkinje cell density in Crus I, Crus II and Lobulus Simplex areas of cerebellum in cadmium group (pcO.05). The Purkinje cell density was 16-23 % less in nicardipine-treated group than control and cells were partially protected from toxic effects of cadmium significantly (pcO.05).These results suggest that cadmium has neurotoxic effects on Purkinje cells in cerebellum and nicardipine may protect neurons from cadmium-induced toxicity 6~0.05).

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Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of nicardipine on cadmium‐induced Purkinje cell death in rat cerebellum

Bağirici

Genç

Tan

et al. 2001

Neuroscience Res Communica

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“…Brain CaM activity was determined by measuring the stimulation of phosphodiesterase activity. A [58,61]. Lead was also found to interfere with CaM activity in vitro and in vivo.…”

Section: Disruption Of Long-term Potentiation Bymentioning

confidence: 99%

“…Calmodulin (CaM) activity is affected by aluminum, cadmium, and inorganic lead. Both aluminum and cadmium inhibited CaM activity [20,58,[60][61][62][63] whereas inorganic lead first increased CaM activity at lower concentrations (possibly by mimicking calcium), but then at higher concentrations it decreased CaM activity [59,232]. CaM is the central modulator of NMDARmediated synaptic plasticity and a majority of the regulators of synaptic plasticity depend on CaM for their activation.…”

Section: Summary Of Long-term Effectsmentioning

confidence: 99%

Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

Ghazala

Sadiq

Chowdhury

et al. 2010

Qatar Foundation Annual Research Forum Proceedings

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Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+ , Cd 2+ , and Hg + ) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+ , Pb 2+ , Cu 2+ , Cd 2+ , Ni 2+ , Co 2+ , Li 3+ , Hg + , and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+ , Pb 2+ , Cd 2+ , and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

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“…CaM bound to Cd 2+ was also detected in the brains of rats exposed to CdCl 2 . It was proposed that, since Cd 2+ has an ionic radius similar to Ca 2+ , it might interact with the Ca 2+ -binding sites on the CaM [58, 61]. …”

Section: Disruption Of Synaptic Plasticitymentioning

confidence: 99%

Metal Toxicity at the Synapse: Presynaptic, Postsynaptic, and Long-Term Effects

Sadiq

Ghazala

Chowdhury

et al. 2012

Journal of Toxicology

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Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+, Cd 2+, and Hg +) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+, Pb 2+, Cu 2+, Cd 2+, Ni 2+, Co 2+, Li 3+, Hg +, and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+, Pb 2+, Cd 2+, and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

show abstract

Interaction of Metals with Brain Calmodulin Purified from Normal and Cadmium Exposed Rats

Cited by 13 publications

References 21 publications

Neuroprotective effect of nicardipine on cadmium‐induced Purkinje cell death in rat cerebellum

Neuroprotective effect of nicardipine on cadmium‐induced Purkinje cell death in rat cerebellum

Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

Metal Toxicity at the Synapse: Presynaptic, Postsynaptic, and Long-Term Effects

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