Further characterization of opioid receptors in the striatum mediating muscular rigidity in rats

Summary

In previous studies, we had found that opioid receptors in the striatum can mediate muscular rigidity which can be recorded as a tonic EMG activity in the gastrocnemiussoleus muscle of rats. We have now tried to evaluate the type of opioid receptors mediating the EMG activity. For this purpose, opioids regarded to be selective agonists at one type of opioid receptors were injected into the striatum of unanesthesized rats.

Morphine, a μ-type agonist, in the dose of 40 nmol induced a pronounced EMG activity, while 10 or 40 nmol of [D-Ala², D-Leu⁵] enkephalin, a δ-type agonist, led to no or little effect, respectively. β-Endorphin, which reacts with the ε-type of receptors, was completely ineffective in doses of 3 or 15 nmol. The benzomorphan compound Mr 2033-Cl, which is a ν-type agonist, induced a moderate activity in the dose of 15 nmol; 3 nmol were ineffective. β-Casomorphin-4 was the most potent of the drugs studied in our system, since 9 nmol induced a pronounced rigidity, which was naloxone-reversible (2 mg/kg i.p.). The doses of these opioids effective in comparison with their known in vitro potencies suggest that the rigidity is mediated by a group of striatal opioid receptors, which has some similarity to the μ-type, but also shows some differences.

In contrast, haloperidol, injected either into the striatum (30 nmol) or systemically (2 mg/kg i.p.), did not induce any EMG activity, suggesting that a decrease in dopaminergic neurotransmission is not the primay mechanism inducing the rigidity. β-LPH_62–67 and β-LPH_66–77 (15 nmol) intrastritally] were also completely inactive.