Effect of manganese and copper interaction on behavior and biogenic amines in rats fed a 10% casein diet.

@article{Murthy1981EffectOM,
  title={Effect of manganese and copper interaction on behavior and biogenic amines in rats fed a 10\% casein diet.},
  author={Ramesh Chandra Murthy and S Lal and Daya Krishna Saxena and Girja S. Shukla and M. M. Ali and Satya V. Chandra},
  journal={Chemico-biological interactions},
  year={1981},
  volume={37 3},
  pages={
          299-308
        }
}

Effect of daily oral intake of manganese on free polysomal protein synthesis of rat brain.

The data suggest that the previously reported retardation in learning and memory of manganese treated immature rats may partly be due to alteration of cerebral RNA and protein synthesis.

Monoamine uptake in brain synaptosomes after administration of copper to rats.

  • H. Komulainen
  • Biology, Chemistry
    Acta pharmacologica et toxicologica
  • 1983
The results indicate that Cu is not liable to affect monoamine uptake in nerve endings in vivo, which may be explained by effective endogenous protective mechanisms against Cu.

Supersensitivity of the cholinergic muscarinic system in the rat's brain is induced by high concentrations of Cu+2.

45 days of Cu2+ or PA treatment induced brain hypercuprosis, which was associated with MR binding supersensitivity; however, change in ME was only observed in PA treated rats suggesting that might be still another factor in these experiments besides Cu2- (i.e., Zn2- or PA itself) involved in memory modulation.

Effect of cadmium exposure on lipids, lipid peroxidation and metal distribution in rat brain regions.

Results suggest that the increased peroxidation decomposition of structural lipids and the altered distribution of the essential trace metals in brain may play a significant role in Cd-induced neurotoxicity.

Copper sulfate prevents tyrosine hydroxylase reduced activity and motor deficits in a Parkinson's disease model in mice.

Results suggest that preservation of THA participates in the neuroprotective effects derived from the copper supplementation, a phenomenon that avoid the hypokinetic state induced by the MPP+ experimental model of PD.

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