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Chronic treatment with clorgyline, a type A monoamine oxidase (MAO) inhibitor (1 mg/kg/day for 11 days), reduced the number (Bmax) but not the affinity (Kd) of [3H]tryptamine binding sites in rat frontal/parietal cortical membranes. Binding was reduced for at least 36 days following the last injection. The reduction in [3H]tryptamine binding was dose-related and appeared to be maximal following a daily dose of 3 mg/kg. Chronic treatment with deprenyl, a type B MAO inhibitor (1 mg/kg/day for 11 days), did not affect [3H]tryptamine binding. Acute clorgyline administration (11 mg/kg) also had no effect. These data suggest that [3H]tryptamine binds to neurotransmitter receptors for tryptamine since mere chemical recognition sites would not be expected to be modulated by chronic drug treatment. Also, since [3H]tryptamine binding was down-regulated by a type A, but not a type B, MAO inhibitor, tryptamine may be selectively metabolized by type A MAO in vivo.
L L Martin, and
R F Neale, and
P L Wood
October 1989,
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L L Martin, and
R F Neale, and
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June 1988,
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L L Martin, and
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P L Wood
December 2000,
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L L Martin, and
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P L Wood
October 1988,
European journal of pharmacology,
L L Martin, and
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P L Wood
September 1984,
Neurology,
L L Martin, and
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P L Wood
August 1982,
European journal of pharmacology,
L L Martin, and
R F Neale, and
P L Wood
January 1990,
Progress in clinical and biological research,
L L Martin, and
R F Neale, and
P L Wood
January 1990,
Biochemical pharmacology,
L L Martin, and
R F Neale, and
P L Wood
February 1953,
The Journal of physiology,
L L Martin, and
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P L Wood
September 1987,
European journal of pharmacology,
