Ritanserin blocks DOI-altered embryonic motility and posthatch learning in the developing chicken.

Developing chicken embryos exposed to cocaine show altered motility, hatchability, and posthatch detour learning. Pretreating such subjects with the serotonin2 (5-HT2) antagonist ritanserin (RIT) can block the motility suppression and reduced hatchability, indicating 5-HT2 receptor involvement in these cocaine effects. To study behavioral consequences of more selective 5-HT2 receptor stimulation and its blockade during development and to compare such exposure with that of cocaine, we injected eggs with 15-day-old chicken embryos with the 5-HT2 agonist dimethoxyiodophenylaminopropane (DOI, 1.0 mg/kg egg) and 1 h later, with RIT (0.3 and 0.9 mg/kg egg). Motility was recorded 2.5 or 24 h after DOI. This DOI dose suppressed motility 2.5 h but not 24 h after administration. Both RIT doses blocked DOI's motility suppression. No treatment affected hatchability. Subjects were tested on posthatch days 6-9 for detour learning acquisition. DOI "enhanced" learning (i.e., reduced latency), a cocaine-like effect observed in prior work, which was also blocked by both RIT doses. Thus, some consequences of DOI exposure late during embryonic development resemble cocaine's and are blocked by RIT, suggesting a therapeutic role for RIT-like drugs against cocaine's potential developmental toxicity.