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SUMMARY
Placental lactogen has been detected in the field vole, Microtus agrestis, and the bank vole, Clethrionomys glareolus, using a co-culture technique. In field voles this activity could be detected from about day 8 of pregnancy to shortly before term, and stimulated both mouse and vole mammary gland to secrete in vitro. Partial immunological cross-reaction was detected in a radioimmunoassay system between rat prolactin and either extracts of vole pituitaries or media on which vole pituitaries had been cultured; vole placental lactogen showed no cross-reaction with rat prolactin. One site of origin for this hormone is probably the trophoblastic giant cells.
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Discrete, transverse stereotaxic cuts in the forebrain of the anaesthetized lactating rabbit caused spontaneous milk-ejection responses repeated at intervals of 1–5 min. The region of the brain in which cuts were effective included the diagonal band of Broca, the entire rostrocaudal extent of the dorsal medial septum, part of the cingulum and part of the hippocampal fimbria. It is proposed that severance of a septo-hippocampal pathway frees the hippocampus from inhibition and allows oxytocin release to occur. It remains to be determined whether the hippocampus itself is directly responsible for periodic activation of neurosecretory cells.
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Recording electrodes were implanted in contact with the dura mater overlying the parietal cortex of six female goats, four of which were lactating. After recovery from surgery and complete familiarization with the housing conditions, the personnel and the recording technique, each goat was observed continuously for 24 h with simultaneous recording of the cortical electroencephalogram (EEG). Remote blood sampling was carried out every 30 min without disturbing the animal. Apart from the release of growth hormone (GH) associated with morning milking in two of the goats, there was no consistent relationship between the apparently spontaneous, episodic release of GH and behaviour, stages of sleep, cortical EEG, air temperature, time of day or night, obvious environmental stimuli which arose from the normal husbandry routine, or the levels of prolactin, insulin, glucose or free fatty acids in the blood. There was also no relationship between the release of prolactin and the stages of sleep.
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Adults who were affected by intrauterine growth restriction (IUGR) suffer from reductions in muscle mass and insulin resistance, suggesting muscle growth may be restricted by molecular events that occur during fetal development. To explore the basis of restricted fetal muscle growth, we used a sheep model of progressive placental insufficiency-induced IUGR to assess myoblast proliferation within intact skeletal muscle in vivo and isolated myoblasts stimulated with insulin in vitro. Gastrocnemius and soleus muscle weights were reduced by 25% in IUGR fetuses compared to those in controls (CON). The ratio of PAX7+ nuclei (a marker of myoblasts) to total nuclei was maintained in IUGR muscle compared to CON, but the fraction of PAX7+ myoblasts that also expressed Ki-67 (a marker of cellular proliferation) was reduced by 23%. Despite reduced proliferation in vivo, fetal myoblasts isolated from IUGR biceps femoris and cultured in enriched media in vitro responded robustly to insulin in a dose- and time-dependent manner to increase proliferation. Similarly, insulin stimulation of IUGR myoblasts upregulated key cell cycle genes and DNA replication. There were no differences in the expression of myogenic regulatory transcription factors that drive commitment to muscle differentiation between CON and IUGR groups. These results demonstrate that the molecular machinery necessary for transcriptional control of proliferation remains intact in IUGR fetal myoblasts, indicating that in vivo factors such as reduced insulin and IGF1, hypoxia and/or elevated counter-regulatory hormones may be inhibiting muscle growth in IUGR fetuses.