Patricia K. Sonsalla

TL;DR: A potential neural basis for the inverse association of caffeine with the development of PD is established and the potential of A(2A) antagonists as a novel treatment for this neurodegenerative disease is enhanced.

TL;DR: MK-801, phencyclidine, and ketamine, noncompetitive antagonists of one subtype of excitatory amino acid receptor, the N-methyl-D-aspartate receptor, provided substantial protection against neurotoxicity produced by methamphetamine but not that produced by MPTP.

TL;DR: The data suggest that PD and MPTP both destroy the same population of midbrain DA neurons within nuclei A8, A9, and A10, and that perhaps CaBP protects the DA neurons from cell death caused by both PD andMPTP.

TL;DR: D dopamine plays an important role in the changes mediated by the administration of methamphetamine in both the dopaminergic and serotonergic systems, and the ability of a single administrations of methamphetamine to depress tryptophan hydroxylase was also dependent on catecholamine synthesis.

TL;DR: The data presented here clearly highlight the complexity of using adenosinergic agents therapeutically in PD and other neurodegenerative disorders and point out many areas for further inquiry, and confirm that adenosine receptor ligands, particularly A2A receptor ligand, have many promising characteristics that encourage the pursuit of their therapeutic potential.