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Andrew P Thompson

Publications and source records attributed to Andrew P Thompson.

2 recordsLinked to original sources

Transient dopamine synthesis modulation in prefrontal cortex: in vitro studies.

The present study provides further evidence for transient D1 autoreceptor-like synthesis modulation in prefrontal cortex, but not striatum, of developing rats. DOPA accumulation was attenuated in a concentration-dependent manner in slices from the prefrontal cortex and striatum at 15 days of age by the partial D1 agonist SKF 38393 (0.01-10 microM) and the full D1 agonist SKF-81297 (0.01-10 microM) following NSD-1015; the response was no longer apparent by 40 days. Both agonists had greater potency in prefrontal cortex than striatum, and SKF-81297 exerted greater maximal inhibitory effects than SKF-38393. The inhibitory effects of both agonists were antagonized by pre-incubation with the D1 antagonist SCH-23390 in cortex, but not in striatum.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Pubertal changes in gonadal hormones do not underlie adolescent dopamine receptor overproduction.

Males, but not females, overproduce dopamine receptors in the striatum of rats across the periadolescent period followed by their elimination during young adulthood. In order to investigate the role that gonadal hormones play in this pubertal process, rats were castrated or ovariectomized at postnatal day (P) 28 when estrogen and testosterone levels are beginning to surge. Dopamine D1 and D2 striatal receptor density was then determined with autoradiography at P40 (adolescence) and P80 (young adulthood) to determine if either testosterone stimulates the overproduction of receptors in males or if estrogen inhibits this process in females. Neither castration nor ovariectomy altered dopamine receptor density, although enhanced testosterone levels increased D1 receptor binding 4.2% and 19.5% in males and females, respectively. The results of this study suggest that the endogenous rise in gonadal steroid hormones during puberty is not responsible for the overproduction of receptors in males or the lack of overproduction in females.

Aging↗