CNS Compensation to Dopamine Neuron Loss in Parkinson’s Disease

  • Kenneth G. Lloyd
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 90)


Postmortem studies in brains from parkinsonian patients consis tently reveal a minimum loss of 75% of the nigrostriatal dopamine neurons. This indicates that over a prolonged period, before Parkinson’s disease is clinically evident, there is a physiological compensation for the slow loss of dopamine neurons (i.e. compensated stage of Parkinson’s disease). Only when the dopamine neuron loss is sufficiently severe (greater than 75% of nigrostriatal dopamine neurons) does the disease become clinically evident (decompensated state). Postmortem examination of Parkinson’s disease brains and study of animal models indicate that the following mechanisms may contribute to this CNS compensation:

1) A decrease in striatal cholinergic activity, in an attempt to maintain a critical DA:ACh balance; and 2) A decrease in activity of GABA neurons in the striatum and substantia nigra, resulting in an increased firing rate of nigral dopamine cells. These mechanisms allow the brain to readjust to the initial dopamine cell loss in Parkinson’s disease.


Substantia Nigra Dopamine Neuron Gaba Neuron Tyrosine Hydroxylase Activity Choline Acetyl Transferase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Plenum Press, New York 1977

Authors and Affiliations

  • Kenneth G. Lloyd
    • 1
    • 2
  1. 1.Departments of Psychiatry and PharmacologyUniversity of TorontoTorontoCanada
  2. 2.Department of PsychopharmacologyClarke Institute of PsychiatryTorontoCanada

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