The Response of Plasma Prolactin to Suckling during Normal and Prolonged Lactation in the Rat

In mammals, lactation suppresses GnRH/LH secretion resulting in transient infertility. In rats, GnRH/LH secretion is rescued within 18-48 h after pup separation (PS) and rapidly re-suppressed by subsequent re-exposure of pups. To elucidate the mechanisms underlying these rapid modulations, changes in the expression of kisspeptin, a stimulator of GnRH secretion, in several lactating conditions (normal-lactating; 4-h PS; 18-h PS; 4-h PS C1-h re-exposure of pups; non-lactating) were examined using in situ hybridization. PS for 4 h or 18 h increased Kiss1 expressing neurons in both the anteroventral periventricular nucleus (AVPV) and the arcuate nucleus (ARC), and subsequent exposure of pups re-suppressed Kiss1 in the AVPV. A change in Kiss1 expression was observed prior to the reported time of the change in GnRH/LH, indicating that the change in GnRH/LH results from changes in kisspeptin. We further examined the mechanisms underlying the rapid modulation of Kiss1. We first investigated the possible involvement of ascending sensory input during the suckling stimulus. Injection of the anterograde tracer to the subparafascicular parvocellular nucleus (SPFpc) in the midbrain, which relays the suckling stimulus, revealed direct neuronal connections between the SPFpc and kisspeptin neurons in both the AVPV and ARC. We also examined the possible involvement of prolactin (PRL). Administration of PRL for 1 h suppressed Kiss1 expression in the AVPV but not in the ARC. These results indicate that suckling stimulus rapidly modulates Kiss1 expression directly via neuronal connections and indirectly through serum PRL, resulting in modulation in GnRH/LH secretion.

Section: Discussionsupporting

confidence: 77%

Rapid modulation of hypothalamic Kiss1 levels by the suckling stimulus in the lactating rat

Higo¹,

Aikawa²,

Iijima³

et al. 2015

“…Prolactin levels were within the range reported for lactating animals and showed the characteristic dechne as a function of lac¬ tational age (Mattheij et al 1984). In agreement with previous results (Södersten & Eneroth 1984, Nagy et al 1986), we observed no exact concordance between peaks in PRL levels and suckling episodes.…”

Section: Resultssupporting

confidence: 73%

Suppression of LH secretion in food-restricted lactating females: effects of ovariectomy and bromocryptine treatment

Cd¹,

Mitchell²,

Bc³

1995

It has been shown that restricting food in lactating rats for the first 2 weeks postpartum at a level of 60% of the ad-libitum daily ration increases the length of lactational dioestrus by about 7 days but little is known about correlated changes in hormone levels. In the first experiment we report changes in LH, prolactin (PRL) and ACTH secretion in food-restricted and ad-libitum fed lactating rats at various stages of lactation. Our results demonstrate that food restriction during the first 2 weeks of lactation did not affect PRL or ACTH secretion, but decreased plasma LH levels despite comparable GnRH receptor density between food-restricted and ad-libitum fed females. In the second experiments we investigated a possible causal relationship between the increased secretion of progesterone seen in food-restricted females and the suppression of plasma LH levels, by determining the effects of bromocryptine treatment and ovariectomy on LH secretion in both ad-libitum fed and food-restricted lactating females. LH suppression in food-restricted lactating females was not affected by ovariectomy or bromocryptine treatment, although the latter treatment significantly increased GnRH receptor number. These data suggest that factors other than ovarian steroids, PRL or increased adrenocortical activity modulate LH secretion and the length of lactational dioestrus in food-restricted lactating females.

“…Values for prolactin half-hfe in dairy cows at mid-lactation of 23 and 25 min (Tucker et al 1973) and 23 min (Goodman et al 1979) and of 19 min for injected ovine prolactin in a goat (Bryant et al 1968) are similar to the peak lactation values reported here, but we have found no references to effect of lactation stage or season on prolactin clearance. In women, the half-life of endogenous prolactin is the same at 3 weeks (29 ± 2-5 min) and 3 months (26 ± 3 min) of lactation (Nunley et al 1991) and half-hfe is unaffected by lactation stage in rats infused to steady state with rat prolactin (4-5-5 min in early, mid and late lactation, Mattheij et al 1984). These are both species in which lactation is highly prolactin-dependent (Peters et al 1986, Madon et al 1986).…”

Section: Discussionmentioning

confidence: 99%

Blood prolactin concentrations affect prolactin transfer into goat milk: implications for maintenance of lactation

Forsyth

Taylor²,

Gabai³

et al. 1995

125I-Labelled ovine prolactin was infused for 15 min into a pudic artery supplying one mammary gland of lactating goats (n = 17). Between 0 and 4.25 h significantly more total (P < 0.01) and trichloroacetic acid (TCA)-precipitable (P < 0.001) radioactivity appeared in the milk of the infused compared with the non-infused gland. Gel chromatography and antibody precipitation indicated the presence of undegraded 125I-labelled prolactin in milk whey. Maximum transfer occurred 60-80 min after the end of infusion suggesting passage via a transcellular route. High plasma prolactin concentrations, resulting from infusion of cold prolactin with labelled prolactin in late lactation or from seasonally elevated prolactin at peak lactation, reduced the specific activity of infused prolactin and depressed the difference in secretion of 125I-labelled prolactin into milk of infused and non-infused glands. This suggests the operation of a competitive and saturable mechanism. Together with the increase in the milk to blood ratio of prolactin in goats given long-term (3 week) bromocriptine treatment, the results suggest that the goat mammary gland has a high avidity for prolactin especially when circulating prolactin is low. There was also evidence from TCA precipitation that prolactin may be protected from degradation in these circumstances. These mechanisms may contribute to the resistance of ruminant lactation to reduction in plasma prolactin and protect lactation from seasonal prolactin fluctuations.