Preliminary reliability and validity of a new time-sensitive ADHD symptom scale in adolescents with ADHD.

OBJECTIVES: To validate the Time-Sensitive ADHD Symptom Scale (TASS) in the assessment of symptom change during the day in adolescents with attention-deficit/hyperactivity disorder (ADHD). METHODS: A total of 40 participants with ADHD aged 13 to 17 years completed 1 or 2 visits, 1 to 9 weeks apart. The TASS and the ADHD Rating Scale-IV (ADHD-RS-IV) were completed twice at each visit: at the time of the clinic visit (in-clinic assessment) and 2 to 6 hours afterwards (evening assessment). RESULTS: Internal consistency of the TASS was high, with Cronbach's alpha coefficients of 0.91 (in-clinic) and 0.90 (evening) for visit 1, and 0.88 (in-clinic) and 0.86 (evening) for visit 2. Pearson's correlation coefficients between the TASS and ADHD-RS-IV were significant at both visits (P < 0.0001). Stability analyses of the TASS found no significant effect between ratings performed at different visits (P = 0.936), but there was a significant effect of the assessment time within visits (P < 0.0001). There was not a significant visit by assessment time interaction (P = 0.924). CONCLUSIONS: The TASS showed high internal consistency and high concurrent validity with the ADHD-RS-IV. Results of this preliminary study indicate that the TASS is a valid and reliable self-report scale for adolescents with ADHD.

Testosterone differentially alters cocaine-induced ambulatory and rearing behavioral responses in adult and adolescent rats.

Little is known about the physiological and behavioral effects of testosterone when co-administered with cocaine during adolescence. The present study aimed to determine whether exogenous testosterone administration differentially alters psychomotor responses to cocaine in adolescent and adult male rats. To this end, intact adolescent (30-days-old) and adult (60-day-old) male Fisher rats were pretreated with vehicle (sesame oil) or testosterone (5 or 10mg/kg) 45 min prior to saline or cocaine (20mg/kg) administration. Behavioral responses were monitored 1h after drug treatment, and serum testosterone levels were determined. Serum testosterone levels were affected by age: saline- and cocaine-treated adults in the vehicle groups had higher serum testosterone levels than adolescent rats, but after co-administration of testosterone the adolescent rats had higher serum testosterone levels than the adults. Pretreatment with testosterone affected baseline activity in adolescent rats: 5mg/kg of testosterone increased both rearing and ambulatory behaviors in saline-treated adolescent rats. After normalizing data to % saline, an interaction between hormone administration and cocaine-induced behavioral responses was observed; 5mg/kg of testosterone decreased both ambulatory and rearing behaviors among adolescents whereas 10mg/kg of testosterone decreased only rearing behaviors. Testosterone pretreatment did not alter cocaine-induced behavioral responses in adult rats. These findings suggest that adolescents are more sensitive than adults to an interaction between testosterone and cocaine, and, indirectly, suggest that androgen abuse may lessen cocaine-induced behavioral responses in younger cocaine users.

Effects of RU 486 and tamoxifen on cocaine-induced behavioral and endocrinologic activations in male and female Fischer rats.

Evidence suggests that sex differences in response to cocaine administration may be regulated by activation of progesterone and estrogen receptors. To test this hypothesis, rats were pretreated with either RU 486 (progesterone antagonist; 0, 3, or 25 mg/kg), tamoxifen (estrogen antagonist; 0, 1, or 3 mg/kg), or vehicle followed by saline or cocaine administration (15 mg/kg). Although RU 486 did not affect cocaine-induced locomotor activity in female rats, it dose-dependently decreased such activity in males (3 mg/kg significantly attenuated locomotor responses in cocaine-treated rats as compared with vehicle treatment or 25 mg/kg of RU 486). RU 486 also affected baseline serum levels of corticosterone. Males treated with 3 mg/kg of RU 486 plus cocaine had higher progesterone and corticosterone serum levels than vehicle-treated groups. In females, both doses (3 and 25 mg/kg) of RU 486 significantly attenuated corticosterone serum levels compared with vehicle treatment. For both sexes overall, tamoxifen neither significantly influenced cocaine-induced ambulatory and rearing responses nor altered cocaine-induced progesterone and corticosterone serum levels. Taken together, our results suggest that progesterone receptors have a sexually dimorphic role in cocaine-induced effects, but estrogen receptors have only a limited role. Moreover, both receptor antagonists modulate neurochemical responses differentially.

Testosterone plays a limited role in cocaine-induced conditioned place preference and locomotor activity in male rats.

Growing evidence suggests that sex differences in cocaine reward responses are regulated by endogenous gonadal hormones. However, few studies have addressed the role of testosterone on cocaine reward and psychomotor activation. This study aimed to determine whether testosterone influences the development of psychomotor and reward responses to cocaine. Castrated 8-week-old male Fisher rats received placebo or testosterone via Silastic capsules (1-3 capsules of 100% testosterone) or subcutaneous injections (400, 800, or 1200 microg/kg) concurrent with cocaine administration. Although chronic testosterone administration did not alter cocaine-induced conditioned place preference (CPP), concurrent administration of testosterone and cocaine affected the development of cocaine CPP dose-dependently; 400 microg/kg blocked the expression of cocaine-induced CPP. Testosterone did not affect cocaine-induced locomotor activity. Furthermore, testosterone-saline-treated controls did not develop CPP, suggesting that at these doses, testosterone does not produce rewarding or motor responses. These data suggest that testosterone may play a limited role in cocaine-induced reward associations and locomotor responses and thus has a limited effect in the previously reported sexually dimorphic responses to cocaine.