The onset of oestrus and ovulation in lactating rats

Lactation delays the re-initiation of oestrous cyclicity in rats, resulting in physiological sterility for the duration of suckling. During this phase, the secretion of pituitary gonadotrophins is suppressed by an unknown mechanism. Continued application of the suckling stimulus by litter replacement (Bruce, 1958; Nicoll & Meites, 1959), or injections of prolactin (Meites & Nicoll, 1959), have been shown to prolong lactation considerably beyond the usual period. The present study aimed to demonstrate the role of prolactin in inhibiting the gonadotrophin secretion necessary for the re-establishment of oestrous cyclicity during lactation. Pregnant rats weighing approximately 300 g were obtained from the Institute colony and housed in individual cages. At parturition, the number of young in the litter was adjusted to eight, two or one as required. The day following the post-partum oestrus was regarded.

Prolactin suppresses release of luteinising hormone during lactation in the monkey

STUDIES with rats have shown that during lactation there is an inhibition of luteinising hormone (LH)-dependent physiological events, such as implantation1, and a return to oestrus cyclicity2. This inhibition has been shown to occur only during the intense suckling phase and it has been correlated with the high levels of prolactin present in the circulation at this time. Although exogenous prolactin could substitute for the effects of intense suckling, it could do so only under the permissive influence of minimal suckling stimulus. We have shown that there is, in these conditions, a lowering of LH levels, and that this is due to interference by prolactin with the pituitary responsiveness to LH-releasing hormone (LHRH) (K. Muralidhar, R. M. and N. R. M., unpublished). Using the lactating monkey, we have now demonstrated a similar inhibitory effect of prolactin on pituitary responsiveness to LHRH, suggesting a mechanism by which amenorrhoeic conditions are maintained during lactation.

Development of Nonsocial Behaviour in the Asiatic Elephant

The elephant calf, a defended follower is completely dependent on adults till the age of 3 months. It begins to explore and attempts to feed at 3 to 6 months, and then becomes partially independent with some feeding on its own. The characteristics of behavior in adults are examined and the development of this pattern in the calf is traced by analyis of duration, transition and clustering of the behavioural elements. Essential activities like suckling, locomotion and lying down for rest appear soon after birth whereas elements of feeding, grooming and play appear only at a later stage. The calf takes the initiative in suckling and its termination, drinking directly by mouth till the age of 6 months. The first element of feeding appears at about a week in attempts to pick up and hold objects in the trunk. Co-ordination of limb, trunk and mouth movement is achieved by about 1 month. The calf is strong enough to pull out plants by 6 months when independent feeding begins. In about a year feeding, drinking and dusting patterns are well developed.

The ability of prolactin to change the sensitivity of the pituitary of the lactating rat to luteinising hormone releasing hormonein vitro

The ability of prolactin to influence the responsiveness of the lactating rat pituitary to luteinising hormone releasing hormone has been examinedin vitro. The pituitary responsivenessin vivo to luteinising hormone releasing hormone decreased as a function of increase in the lactational stimulus. Prolactin inhibited the spontaneousin vitro release of luteinising hormone and follicle stimulating hormone to a small extent, from the pituitary of lactating rats with the suckling stimulus. However, it significantly inhibited the release of these two hormones from luteinising hormone releasing hormone-stimulated pituitaries. The responsiveness of pituitaries of rats deprived of their litter 24 h earlier, to luteinising hormone releasing hormone was also inhibited by prolactin, although minimal. It was concluded that prolactin could be influencing the functioning of the pituitary of the lactating rat by (a) partially suppressing the spontaneous release of gonadotropin and (b) inhibiting the responsiveness of the pituitary to luteinising hormone releasing hormone.

Quantitative and compositional changes in myelin of undernourished and protein malnourished rat brains

Effects of undernutrition and protein malnutrition on the quantitative and qualitative changes in myelin isolated from rat brain at 3 and 8 weeks of age were investigated. Undernutrition during suckling period was induced by increasing the litter size, and continued from the 3rd to the 8th week by limited food intake, or the rats were rehabilitated with adequate food. Protein malnutrition was induced by feeding the lactating dams 5% protein diet as against 25% protein diet in controls. The protein malnourished rats were rehabilitated from the 3rd to the 8th week with the normal 25% protein diet. Undernutrition produced 16% and 35% reductions in the myelin content at 3 and 8 weeks of age, respectively, and was only partially restored on rehabilitation. Protein malnutrition caused more drastic reduction of 27% in the myelin content at 3 weeks, which was also partially restored on rehabilitation. The specific activity of 2′,3′-cyclic nucleotide 3′-phosphohydrolase was not affected by undernutrition, whereas protein malnutrition caused a 25% reduction at 3 weeks, which was totally reversed by rehabilitation. Undernutrition had not altered the relative composition of myelin proteins, but protein malnutrition resulted in a significant reduction in the proteolipid protein at 3 weeks of age, which could be reversed by rehabilitation.

Protection of adult but not newborn mice against lethal intracerebral challenge with Japanese encephalitis virus by adoptively transferred virus-specific cytotoxic T lymphocytes: Requirement for L3T4(+) T cells

The protective ability of cytotoxic T cells (CTL) raised in vitro against Japanese encephalitis virus (JEV) was examined by adoptive transfer experiments. Adoptive transfer of anti-JEV effecters by intracerebral (i.c.) but not by intraperitoneal (i.p.) or intravenous (i.v.) routes protected adult BALB/c mice against lethal i.c. JEV challenge. In contrast to adult mice, adoptive transfer of anti-JEV effecters into newborn (4-day-old) and suckling (8-14-day-old) mice did not confer protection. However, virus-induced death was delayed in suckling mice compared to newborn mice upon adoptive transfer. The specific reasons for lack of protection in newborn mice are not clear but virus load was found to be higher in newborn mice brains compared to those of adults and virus clearance was observed only in adult mice brains but not in newborn mice brains upon adoptive transfer. Specific depletion of Lyt 2.2(+), L3T4(+) or Thy-1(+) T cell populations before adoptive transfer abrogated the protective ability of transferred effecters. However, when Lyt 2.2(+) cell-depleted and L3T4(+) cell-depleted effecters were mixed and transferred into adult mice the protective activity was retained, demonstrating that both Lyt 2.2(+) and L3T4(+) T cells are necessary to confer protection. Although the presence of L3T4(+) T cells in adoptively transferred effector populations enhanced virus-specific serum neutralizing antibodies, the presence of neutralizing antibodies alone without Lyt 2.2(+) cells was not sufficient to confer protection.