Morales T, Shapiro E, Marina N, Mena F
Centro de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM, Apdo. Postal 1-1140 76230 Juriquilla, Querétaro, Qro., Mexico.
Physiol Behav. 2001;74(1-2):37-43. doi: 10.1016/s0031-9384(01)00559-5.
Previous work has shown that physiologic activation of the sympathetic system may inhibit milk yield (ME) in rats. Thus, adrenal catecholamines (CAs) are released by suckling, but it is not known whether such inhibition results also from reflex activation by the same stimulus of neural sympathetics upon the mammary gland. The present experiments were designed to determine whether suckling inhibits ME induced by oxytocin (OT) in the urethane-anesthetized lactating rat, and whether such inhibition results from adrenal and/or neurally released CAs. Rats were isolated (6 h) from their pups and then anesthetized. OT (0.8 mU every 2 min) was administered intravenously to the mothers during suckling. Rats were either chronically implanted with cannulae into the lateral cerebral ventricles (intracerebroventricularly), bilaterally adrenalectomized (ADX), hypophysectomized (HX), spinal cord transected (SCT: T3-T4), or had the nipple area (NA) locally anesthetized before suckling. MEs were low in control, sham, ADX and HX rats, but not in rats given the beta-adrenergic blocker propranolol (PROP; intravenously or intracerebroventricularly injected), nor in SCT, NA or PROP-HX rats. As revealed by ductal resistance measurements as an indicator of ductal tone, suckling-induced inhibition of ME was due to ductal constriction within the mammary glands. These effects of suckling, however, could be prevented by prior activation of ductal mechanoreceptors. Together, these results indicate that suckling inhibits ME through the reflex activation of neurally mediated central beta-adrenergic mechanisms, and that these effects, in turn, can be regulated by ductal mechanoreceptor activation.
先前的研究表明，交感神经系统的生理激活可能会抑制大鼠的产奶量（ME）。因此，哺乳会促使肾上腺释放儿茶酚胺（CAs），但尚不清楚这种抑制是否也源于相同刺激对乳腺的神经交感神经反射激活。本实验旨在确定哺乳是否会抑制氨基甲酸乙酯麻醉的泌乳大鼠中催产素（OT）诱导的ME，以及这种抑制是否源于肾上腺和/或神经释放的CAs。将大鼠与幼崽隔离（6小时），然后进行麻醉。在哺乳期间，向母鼠静脉注射OT（每2分钟0.8 mU）。大鼠要么长期植入侧脑室插管（脑室内），双侧肾上腺切除（ADX），垂体切除（HX），脊髓横断（SCT：T3-T4），要么在哺乳前对乳头区域（NA）进行局部麻醉。对照组、假手术组、ADX组和HX组大鼠的ME较低，但静脉注射或脑室内注射β-肾上腺素能阻滞剂普萘洛尔（PROP）的大鼠、SCT组、NA组或PROP-HX组大鼠的ME不低。作为导管张力指标的导管阻力测量结果显示，哺乳诱导的ME抑制是由于乳腺内的导管收缩。然而，哺乳的这些作用可通过预先激活导管机械感受器来预防。总之，这些结果表明，哺乳通过神经介导的中枢β-肾上腺素能机制的反射激活来抑制ME，而且反过来，这些作用可由导管机械感受器激活来调节。
