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CL 218,872 Binding to Benzodiazepine Receptors in Rat Spinal Cord: Modulation by γ‐Aminobutyric Acid and Evidence for Receptor Heterogeneity
Author(s) -
Villiger John W.
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12823.x
Subject(s) - spinal cord , gabaa receptor , receptor , chemistry , cerebral cortex , muscimol , benzodiazepine , cortex (anatomy) , gamma aminobutyric acid , aminobutyric acid , cord , central nervous system , medicine , endocrinology , biophysics , biology , neuroscience , biochemistry , surgery
The binding of the triazolopyridazine CL 218,872 to central benzodiazepine receptors identified with [ 3 H]Ro 15–1788 was studied in extensively washed homogenates of rat spinal cord and cerebral cortex. CL 218,872 displacement curves were shallow in both spinal cord (n H = 0.67) and cortex (n H = 0.54), suggesting the presence of type 1 and type 2 benzodiazepine receptors in both tissues. CL 218,872 had lower affinity in spinal cord (IC 50 = 825 n M ) than cortex (IC 50 = 152 n M ), possibly reflecting the presence of fewer type 1 sites in the cord. Activating γ‐aminobutyric acid (GABA) receptors with 10 μ M muscimol resulted in a two‐ to threefold increase in CL 218,872 affinity in both tissues without changes in the displacement curve slope. This indicates that GABA enhances CL 218,872 affinity for both type 1 and type 2 sites in both spinal cord and cerebral cortex.