Endomorphin-1, an endogenous μ-opioid receptor agonist, improves apomorphine-induced impairment of prepulse inhibition in mice

• Published in: Peptides (New York, N.Y. : 1980) Vol. 24; no. 5; pp. 741 - 744
• Main Authors: Ukai, Makoto, Okuda, Ami
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-05-2003; Elsevier Science
• Subjects: Animals; Apomorphine; Apomorphine - antagonists & inhibitors; Apomorphine - pharmacology; Biological and medical sciences; Endomorphin-1; Fundamental and applied biological sciences. Psychology; Male; Mice; Mouse; Naloxonazine; Naltrexone - agonists; Naltrexone - analogs & derivatives; Oligopeptides - pharmacology; Opioid receptor; Prepulse inhibition; Receptors, Opioid, mu - agonists; Reflex, Startle - drug effects; Vertebrates: endocrinology; β-Funaltrexamine; β-Funaltrexamine; Naloxonazine; Endomorphin-1; Mouse; Opioid receptor; Apomorphine; Prepulse inhibition; Vertebrata; Agonist; Mammalia; Endogenous; Endomorphin 1; Dopamine receptor; Animal; Rodentia; Dopamine agonist; μ Opioid receptor; Inhibition
• ISSN: 0196-9781; 1873-5169
• DOI: 10.1016/S0196-9781(03)00123-2

The present study was designed to examine the effects of the endogenous μ-opioid receptor agonist endomorphin-1 on prepulse inhibition (PPI) in mice. Although apomorphine (1
mg/kg) produced a marked decrease in PPI, endomorphin-1 (17.5
μg) had no marked effects on PPI or startle amplitude in normal mice. Endomorphin-1 (17.5
μg) inhibited the apomorphine (1
mg/kg)-induced decrease in PPI. β-Funaltrexamine (5
μg), a μ-opioid receptor antagonist, did not significantly antagonize the effects of endomorphin-1 (17.5
μg). Naloxonazine (35
mg/kg), a μ
1-opioid receptor antagonist, antagonized the effects of endomorphin-1 (17.5
μg) on the apomorphine (1
mg/kg)-induced decrease in PPI, whereas naloxonazine (35
mg/kg) itself was without significant effects on the apomorphine (1
mg/kg)-induced decrease. These results suggest that endomorphin-1 alleviates the impairment of PPI resulting from the hyperactivity of dopaminergic neurotransmission through the mediation of μ
1-opioid receptors.