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   <subfield code="a">(NATIONALLICENCE)springer-10.1007/BF00168948</subfield>
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   <subfield code="u">Unit of Additive Drug Research, School of Pharmacology, Victorian College of Pharmacy, 381 Royal Parade, 3052, Parkville, Victoria, Australia</subfield>
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   <subfield code="a">Effect of α2-adrenoceptor agonists on the expression of morphine-withdrawal in rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Ian Coupar]</subfield>
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   <subfield code="a">Summary: Previous studies using clonidine indicate that α2-adrenoceptors are involved in suppressing opiate-withdrawal symptoms. However, clonidine may act as a partial agonist at α2-adrenoceptors and it also possesses significant α1-receptor agonist activity. The aim of this study was to determine the role of α2-adrenoceptors in the expression of opiate withdrawal signs using morphine-dependent rats. A range of agonists were selected for study on the basis of their differential preferences for α-adrenoceptors. Hooded Wistar rats were made physically dependent on morphine (s.c. injection of an emulsion releasing a total of 250 mg/kg of morphine base over 48 h). Test drugs were injected s.c. followed by naloxone (10 mg/kg i.p.) 20 min later. The incidence of 5 selected withdrawal signs was recorded during the following 20 min. The α2-adrenoceptor agonists displayed different profiles of activity. Azepexole (1-10 mg/kg) reduced all signs. Clonidine (80-800 μg/kg) reduced all signs except paw shakes while guanfacine (25-250 μg/kg) reduced all except jumping and diarrhoea. Talipexole (0.1-1 mg/kg) reduced all signs except diarrhoea which was not affected and jumping which was markedly enhanced. UK 14,304 (80-800 μg/kg) reduced jumps, potentiated paw shakes but did not affect body shakes, teeth chattering or diarrhoea. The results suggest that there are subpopulations of α2-adrenoceptors that modulate the expression of opiate withdrawal signs and/or that some of the drugs used affect receptors other than α2-adrenoceptors.</subfield>
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   <subfield code="a">Springer-Verlag, 1992</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Opiate addiction</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">Morphine withdrawal</subfield>
   <subfield code="2">nationallicence</subfield>
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  <datafield tag="690" ind1=" " ind2="7">
   <subfield code="a">α2-adrenoceptor agonists</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Clonidine</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="t">Naunyn-Schmiedeberg's Archives of Pharmacology</subfield>
   <subfield code="d">Springer-Verlag</subfield>
   <subfield code="g">345/5(1992-05-01), 553-557</subfield>
   <subfield code="x">0028-1298</subfield>
   <subfield code="q">345:5&lt;553</subfield>
   <subfield code="1">1992</subfield>
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   <subfield code="o">210</subfield>
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   <subfield code="u">Unit of Additive Drug Research, School of Pharmacology, Victorian College of Pharmacy, 381 Royal Parade, 3052, Parkville, Victoria, Australia</subfield>
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   <subfield code="B">NATIONALLICENCE</subfield>
   <subfield code="P">773</subfield>
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   <subfield code="t">Naunyn-Schmiedeberg's Archives of Pharmacology</subfield>
   <subfield code="d">Springer-Verlag</subfield>
   <subfield code="g">345/5(1992-05-01), 553-557</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
   <subfield code="2">nationallicence</subfield>
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