Tsang D, Tan A T, Henry J L, Lal S
Brain Res. 1978 Sep 8;152(3):521-7. doi: 10.1016/0006-8993(78)91107-1.
Morphine and the opioid peptides leucine-enkephalin (leu-enk), methionine-enkephalin (met-enk) and beta-endorphin had no effect on basal cyclic AMP levels in rat cerebral cortex and hypothalamus, but each inhibited noradrenaline (NA)-stimulated cyclic AMP formation in both brain regions. This inhibition was reversed by naloxone. Naloxone did not reverse phentolamine- or propranolol-induced inhibition of NA-stimulated cyclic AMP formation. The increase in cyclic AMP formation induced by NaF or MnCl2 was unaffected by met-enk or morphine. These data suggest that in rat cerebral cortex and hypothalamus opiates bind to opiate receptors and that the opiate-receptor complex interferes with noradrenergic receptor activity.
吗啡以及阿片肽亮氨酸脑啡肽(亮脑啡肽)、甲硫氨酸脑啡肽(甲脑啡肽)和β-内啡肽对大鼠大脑皮层和下丘脑的基础环磷酸腺苷(cAMP)水平没有影响,但它们均抑制这两个脑区中去甲肾上腺素(NA)刺激的cAMP生成。这种抑制作用可被纳洛酮逆转。纳洛酮不能逆转酚妥拉明或普萘洛尔诱导的对NA刺激的cAMP生成的抑制。由氟化钠(NaF)或氯化锰(MnCl2)诱导的cAMP生成增加不受甲脑啡肽或吗啡的影响。这些数据表明,在大鼠大脑皮层和下丘脑中,阿片类药物与阿片受体结合,且阿片受体复合物会干扰去甲肾上腺素能受体的活性。