{'fraction_non_alphanumeric': 0.028963414634146343, 'fraction_numerical': 0.003048780487804878, 'mean_word_length': 5.404878048780488, '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}}
Modulation of dopamine-induced hypermotility following injection of various opioids into the nucleus accumbens.

The aim of the present work was to obtain some data on the eventual role of nucleus accumbens in the antidopamine action of some opioids. Classical neuroleptics are known to inhibit the dopamine-elicited hypermotility when injecting them into the nucleus accumbens of rats pretreated with MAO inhibitors. In the present study the effects of some opioids have been examined in this model. The opioids examined were morphine, a mu-selective classical opiate, D-Ala2, Nle5-enkephalin sulphonic acid (ES), a delta selective opioid peptide and D-Met2, Pro5-enkephalinamide (EA), a non-selective opioid peptide. Haloperidol and chlorpromazine have been used for comparison. EA and morphine, especially the former, potently antagonized the dopamine-induced hyperactivity, similarly to haloperidol and chlorpromazine. ES exerted biphasic effect, the initial inhibition was followed by potentiation of the dopamine-elicited excitation. Thus the order of potency was: EA greater than haloperidol approximately equal to morphine greater than chlorpromazine greater than EA. The data indicate that the antidopamine action of opioids might be mediated, at least in part, by mu-receptors in the nucleus accumbens.