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Chronic ACTH treatment increases striatal dopamine D-2 receptor binding in developing rat brain
C A Chiriboga1, M R Pranzatelli, D C De Vivo
1Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY.
Brain & Development
|January 1, 1989
Summary
Adrenocorticotropic hormone (ACTH) therapy significantly increased D-2 dopamine receptor binding in rat pups. This suggests a potential mechanism for ACTH
Area of Science:
- Neuroendocrinology
- Pharmacology
- Dopamine receptor research
Background:
- Adrenocorticotropic hormone (ACTH) therapy is linked to decreased dopamine metabolites in infantile spasms patients.
- The precise mechanism of ACTH's effect on the dopamine system remains unclear.
Purpose of the Study:
- To investigate the role of dopamine receptors in the therapeutic effects of ACTH.
- To determine if ACTH influences dopamine receptor binding in developing rats.
Main Methods:
- Rat pups were treated subcutaneously with porcine ACTH (40 IU/kg) or saline for 30 days.
- Specific binding of D-2 receptors was measured using [3H]-spiperone.
- Nonspecific binding was determined using unlabeled spiperone and sulpiride.
- Protein concentration in brain tissue was assessed.
Main Results:
- ACTH treatment significantly increased D-2 dopamine receptor specific binding by 46% in the striata of rat pups compared to controls.
- No significant changes in D-2 receptor binding were observed in the nucleus accumbens.
- Protein concentration in the striata was significantly decreased following ACTH treatment.
Conclusions:
- High-dose ACTH administration in rats leads to increased D-2 dopamine receptor binding in the striatum.
- Further studies, including saturation analyses, are needed to clarify whether this increase reflects altered receptor density or affinity.
- The impact of lower, clinically relevant doses of ACTH on dopamine receptors warrants investigation.