{'fraction_non_alphanumeric': 0.03857280617164899, 'fraction_numerical': 0.01253616200578592, 'mean_word_length': 5.178571428571429, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Ontogeny of two cholinergically mediated central effects: stereotyped yawning and potentiation of head-shaking.

The ontogenetic course of two cholinergically mediated central neuropharmacological effects, yawning and potentiation of head-shaking induced by D-amphetamine (5 mg/kg), was explored in developing rats. Physostigmine (0.1 mg/kg) and pilocarpine (4 mg/kg) evoke stereotyped yawning in neonatal rats, the effect declining in the middle of the second week of life. Both cholinomimetic drugs strongly potentiate amphetamine induced head-shaking between the 4th and 10th postnatal days. Pilocarpine per se is capable of inducing head-shaking, in the absence of amphetamine, in rats from 8 to 12 days. Infant rat yawning and head-shaking are blocked by scopolamine (5 mg/kg). Nicotine (0.1 mg/kg) potentiates head-shaking but inhibits yawning. Yawning is also depressed by D-amphetamine. The early maturation of these cholinergic effects is discussed in comparison to the later maturation of several forebrain cholinergic systems.