Abstract
Parkinson's disease has been described as a multisystem disorder that includes alterations in the function of the autonomic nervous system. The activity of the adrenal medulla in this disease has not been thoroughly investigated. Previous reports are reviewed that demonstrate that the adrenal medullae of parkinsonian patients are compromised, having a decreased content of all catecholamines and several neuropeptides. An animal model was used to investigate whether the observations made in human patients were related to extended treatment with antiparkinsonian medications or were a natural concomitant of the disease. Administration of Lβdopa and/or carbidopa to C57BL mice for 4β16 weeks had no significant effect on the level of any of the adrenal medullary catecholamines. Treatment with MPTP 4β16 weeks prior to sacrifice did not deplete adrenal medullary catecholamines in these animals, thus not fully mimicking Parkinson's disease in this animal model. The only significant effect was an interaction between group (MPTP or control) and treatment with antiparkinsonian medications; Lβdopa, in the absence and presence of carbidopa, had opposite effects in the two groups. Based primarily on the lack of effect of antiparkinsonian medications on adrenal medullary catecholamines, it was concluded that the adrenal medullary depletion observed in human patients was a peripheral concomitant of Parkinson's disease. Β© 1994 WileyβLiss, Inc.