Gen Comp Endocrinol. 2015 Jan 1;210:81-6. doi: 10.1016/j.ygcen.2014.09.021.
Endocannabinoids and their receptors are found throughout the brain of all vertebrates. By virtue of their wide distribution, endocannabinoids have the potential to affect many behaviors. Prior research has shown that cannabinoids inhibit courtship-clasping and mediate behavioral responses to stress in male rough-skinned newts, Taricha granulosa, and cannabinoid signaling is initiated by rapid actions of the steroid corticosterone (CORT) at its specific membrane receptor (mCR). This same mCR also recognizes κ-opioid receptor agonists and antagonists. Prior behavioral studies show that κ-opioid agonists suppress clasping behavior in a dose dependent manner. Combined, these studies suggest that κ-opioid agonists might suppress clasping behavior via the same pathway initiated by CORT: up-regulation of endocannabinoid signaling. We examined whether pretreatment with a CB1 antagonist, AM281, would block κ-opioid-mediated suppression of clasping. We found that the CB1 antagonist did not reverse κ-opioid-induced suppression of clasping, revealing that while endocannabinoids mediate CORT-induced suppression of clasping, endocannabinoids do not mediate the κ-opioid-induced suppression of clasping.
内源性大麻素及其受体存在于所有脊椎动物的大脑中。由于它们的广泛分布，内源性大麻素有可能影响许多行为。先前的研究表明，大麻素抑制求爱性握持，并介导糙皮新蝾螈 Taricha granulosa 雄性对压力的行为反应，大麻素信号是由类固醇皮质酮（CORT）在其特定的膜受体（mCR）上的快速作用引发的。同一个 mCR 也识别 κ-阿片受体激动剂和拮抗剂。先前的行为研究表明，κ-阿片受体激动剂以剂量依赖的方式抑制握持行为。综上所述，这些研究表明，κ-阿片受体激动剂可能通过 CORT 启动的相同途径抑制握持行为：内源性大麻素信号的上调。我们研究了 CB1 拮抗剂 AM281 的预处理是否会阻断 κ-阿片受体介导的握持抑制。我们发现，CB1 拮抗剂并没有逆转 κ-阿片受体诱导的握持抑制，这表明虽然内源性大麻素介导 CORT 诱导的握持抑制，但内源性大麻素不介导 κ-阿片受体诱导的握持抑制。
