Time-dependent inhibition of rat brain monoamine oxidase by an analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP),4-(4-chlorophenyl)-1,2,3,6-tetrahydropyridine

@article{Arai1986TimedependentIO,
  title={Time-dependent inhibition of rat brain monoamine oxidase by an analogue of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP),4-(4-chlorophenyl)-1,2,3,6-tetrahydropyridine},
  author={Yuichiro Arai and Norimitsu Hamamichi and Hiroyasu Kinemuchi},
  journal={Neuroscience Letters},
  year={1986},
  volume={70},
  pages={255-260}
}

MPTP-induced duodenal ulcers in rat. Prevention by reuptake blockers for serotonin and norepinephrine, but not dopamine.

The data suggest that abnormally low levels of synaptic transmission in serotonergic and possibly noradrenergic neurons play an important role in the pathogenesis of duodenal ulcer while the role of dopamine may be limited to modulation of ulcer severity.

Pyridine derivatives: structure-activity relationships causing parkinsonism-like symptoms.

Data is discussed concerning the effects of metabolite structure on the major steps in the neurotropic action mechanism of MPTP-like compounds and special attention is focused on the key steps defining the selectivity ofMPTP's neuronal action.

IN VITRO ANTI-INFLAMMATORY ACTIVITY OF 4-BENZYLPIPERIDINE

The in vitro anti-inflammatory activity of 4-benzylpiperidine is evaluated and shows dose-dependent significant activity when compared with a standard drug, giving an idea that it can be used as a lead compound for designing a potent anti- inflammation drug.

References

SHOWING 1-10 OF 21 REFERENCES

Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase inhibitors

It is reported that pargyline, nialamide and tranylcypromine, which inhibit both MAO-A andMAO-B, when administered to mice before MPTP, protect against MPTP-induced dopaminergic neurotoxicity.

Comparison of 1-methyl-4-(p-chlorophenyl)-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and p-chloroamphetamine as monoamine depletors.

According to this data, the addition of a p-chloro substituent to MPTP eliminates its neurotoxicity to striatal dopamine neurons, and replacement of the aminoisopropyl side chain of PCA with a 1-methyl-1,2,3,6-tetrahydropyridin-4-yl group eliminates its Neurotoxicity to brain serotonin neurons.

Relations between MPTP (1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine), the Neurotoxin MPP+ (1-Methyl-4-Phenylpyridinium Ion), and MAO in Rat Brain

A fundamental biological characteristic of Parkinson’s disease is a damaged dopamine system between the substantia nigra and the corpus striata, and the precise reason for the loss of DA producing cells in this region remains obscure.

Studies on the Oxidation of the Dopaminergic Neurotoxin 1‐Methyl‐4‐Phenyl‐1,2,5,6‐Tetrahydropyridine by Monoamine Oxidase B

In vitro oxidation of 1‐Methyl‐4‐phenyl‐ 1,2,5,6 ‐tetrahydropyridine and the fact that MAO‐B inhibitors can protect against MPTP‐induced dopami nergic neurotoxicity in vivo point to an important role for MAO-B in MPTP metabolism in vivo.