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Changes in benzodiazepine and acetylcholine receptors in the globus pallidus in Parkinson's disease

Lookup NU author(s): Emeritus Professor Robert Perry

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Abstract

Experiments are described in which the benzodiazepine portion of the gamma-aminobutyric acid (GABA)/benzodiazepine receptor and the muscarinic cholinergic receptor were investigated in Parkinson's disease and control brains. Tritiated flunitrazepam and tritiated quinuclidinyl benzilate (QNB) were used to locate and quantify the receptors by autoradiographic and homogenate binding techniques. Densitometric analysis of autoradiographs of the basal ganglia allowed comparison of receptor densities in the post-mortem control and parkinsonian tissue, while homogenate binding experiments gave information concerning receptor affinity and maximum binding capacity. The results indicate that: 1) Binding of flunitrazepam to the benzodiazepine receptor is reduced in the lateral segment of the globus pallidus in Parkinson's disease. This suggests that the GABA-ergic pathway from the putamen to the lateral pallidal segment is overactive in Parkinson's disease. 2) Binding of QNB to the cholinergic receptors of the medial pallidal segment is increased in Parkinson's disease. This finding suggests underactivity of the cholinergic pathway from the pedunculopontine nucleus of the medial pallidal segment. 3) Binding of these ligands in the caudate and putamen of Parkinson's disease is not significantly different from controls. We reviewed the literature concerning the activity of these projections in parkinsonian conditions assessed by different methods and discuss here their implications for the pathogenesis of parkinsonian symptons.


Publication metadata

Author(s): Griffiths PD, Sambrook MA, Perry R, Crossman AR

Publication type: Article

Publication status: Published

Journal: Journal of the Neurological Sciences

Year: 1990

Volume: 100

Issue: 1-2

Pages: 131-136

Print publication date: 01/12/1990

ISSN (print): 0022-510X

ISSN (electronic): 1878-5883

Publisher: Elsevier

URL: http://dx.doi.org/10.1016/0022-510X(90)90023-G

DOI: 10.1016/0022-510X(90)90023-G


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