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T Morales

Publications and source records attributed to T Morales.

21 records · Page 2Linked to original sources
PubMedDate not supplied

Sympathetic innervation of mammary glands mediates suckling-induced reflex inhibition of milk yield in rats.

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.

Adrenalectomy↗
PubMedDate not supplied

beta-adrenergic mechanisms modulate central nervous system effects of prolactin on milk ejection.

It is known that prolactin (PRL) is produced within the brain and numerous central actions of the hormone have been reported. In anesthetized lactating rats, central administration of PRL, i.e., intracerebroventricular (icv) or intrathecally (it), facilitated milk ejection (ME) by depressing the sympathetically mediated facilitatory tone of the mammary ductal system. However, it is not known whether or not the same effects and similar mechanisms take place in conscious rats after PRL administration. In the present study, the effects of centrally administered PRL, i.e., icv or it, on ME was determined in both conscious and anesthetized rats. In conscious rats, the rate of ME was determined by applying a 15-min period of suckling by the litter, following a 6-h period of isolation. In anesthetized rats, intramammary pressure (IMP) responses of the mammary glands to exogenous oxytocin (OT) were recorded. The results showed that, whereas in anesthetized rats, increased responsiveness of the mammary glands to OT were observed after PRL administration, an intense inhibition of ME occurred in conscious rats. Because, in conscious and anesthetized rats, these effects were prevented by prior administration of the beta-adrenergic blocker propranolol (PROP) to the mothers, this suggests that the PRL effects on ME are modulated through sympathomimetic and sympatholytic actions in conscious and anesthetized rats, respectively. Thus, as shown by ductal tone measurements, in conscious, but not in anesthetized rats, the effect of PRL was associated with increased ductal constriction within the mammary glands; an effect that was mimicked by icv administration of the beta-adrenergic agonist isoproterenol (ISOP) and that was prevented by PROP. Further, the sympatholytic action of icv-PRL in anesthetized rats prevented the effect on ductal tone of both icv-PRL in conscious rats and of ISOP in anesthetized rats. Taken together, these results clearly suggest that the central effects of PRL on ME are modulated by adrenergic mechanisms.

Anesthesia↗