The onset of puberty in indigenous male Thai pigs.

Knowledge of puberty plays an important role in planning livestock breeding. The objective of this study was to evaluate the age of the first sexual behavior and the first fertile sperm production, and the changes of reproductive structures in male Thai indigenous pigs, by using a completely randomized design. Male indigenous piglets were randomly divided into 9 groups; each group of 5 piglets was separately sacrificed at the age of 0 (birth), 1.0, 2.0, 3.0, 3.5, 4.0, 4.5, 5.0, and 5.5 months to collect data from the carcasses. The other 3 male pigs were used to test the reproductive ability by natural insemination. The results showed that the first sexual behavior occurred at 2.6 + 0.6 months of age, and the first appearance of fertile sperm mass in the cauda epididymis was in the 4-month group. The semen quality standard was discovered in the 5-month group, and the success of insemination with a fertile female pig was found to be at 5.1 + 0.2 months. The changes in the overall size of reproductive tract and testes occurred in 3 stages of development: slight changes were observed in the first 2 months of age; rapid changes were found from 2 to 4.5 months of age; and gradual changes were detected after 4.5 months of age. Upon examination of semen quality and impregnation ability, it can be concluded that male Thai indigenous pigs attained puberty at the age of 5 months after having manifested sexual behavior for a relatively long period.

The roles of pH in regulation of uterine contraction in the laying hens.

In the laying hens, the uterus (shell gland) plays essential roles in calcium transfer for calcification of the eggshell and expulsion of the egg through the vagina for oviposition. Much is known about the effects of pH changes on eggshell production of the uterus. However, very little is understood about the effects of pH changes on uterine contractility. We investigated the effects of pH changes on uterine contraction in the laying hens. The laying hens were humanely killed, and strips of uterine smooth muscles were isolated. Isometric force was measured and the effects of intracellular and extracellular pH changes studied. The results show that alterations of pH clearly have marked effects on force in the hen uterus. Both intracellular and extracellular acidifications significantly decreased uterine activity, whether it arises spontaneously or in the presence of agonists such as prostaglandin F(2alpha) and arachidonic acid. Alkalinization produced the opposite effects. Thus, changes in pH can regulate uterine contraction. This insight into pH regulation of the uterine activity provides a focus for egg production management directed at physiological and pathological oviposition in the laying hens.

Mechanisms of uterine contractility in laying hens.

The physiological basis of uterine contractility in laying hens is not well understood, but a better understanding is important for understanding the mechanisms governing egg laying. The characteristics of uterine contractility arising spontaneously or by prostaglandin F(2alpha) (PGF(2alpha)) stimulation were therefore examined and the underlying mechanisms investigated. Uterine strips were isolated from laying hens 4h before oviposition and force measured. These strips remained healthy in vitro and produced regular spontaneous contractions. The contractions were phasic and could be recorded for several hours. Exposure to nifedipine, the specific L-type Ca channel blocker, led to the abolition of force. The contraction amplitude and frequency were significantly increased when Bay K8644, an agonist of L-type Ca channels, was applied or when the concentration of extracellular Ca was elevated. Spontaneous contractions were also significantly inhibited by wortmannin, the specific inhibitor of myosin light chain kinase (MLCK). When 1 microM PGF(2alpha) was applied to spontaneously contracting uterus, it significantly increased their amplitude and frequency of the contractions. As with spontaneous contractions, PGF(2alpha)-induced force production was abolished by nifedipine and wortmannin. In the absence of extracellular Ca, a small but tonic force was generated upon application of PGF(2alpha) which was not affected by wortmannin. Thus, extracellular Ca entry and MLCK phosphorylation are essential for uterine force production occurring spontaneously or by PGF(2alpha) stimulation. Our data supports the conclusion that the pathway dependent on extracellular Ca entry and MLCK phosphorylation predominates during PGF(2alpha) stimulation but suggests some involvement of an alternative force-producing pathway, presumably Ca-sensitization.

A mechanism distinct from the L-type Ca current or Na-Ca exchange contributes to Ca entry in rat ventricular myocytes.

The aim of this paper was to characterize the pathways that allow Ca(2+) ions to enter the cell at rest. Under control conditions depolarization produced an increase of intracellular Ca concentration ([Ca(2+)](i)) that increased with depolarization up to about 0 mV and then declined. During prolonged depolarization the increase of [Ca(2+)](i) decayed. This increase of [Ca(2+)](i) was inhibited by nifedipine and the calculated rate of entry of Ca increased on depolarization and then declined with a similar time course to the inactivation of the L-type Ca current. We conclude that this component of change of [Ca(2+)](i) is due to the L-type Ca current. If intracellular Na was elevated then only part of the change of [Ca(2+)](i) was inhibited by nifedipine. The nifedipine-insensitive component increased monotonically with depolarization and showed no relaxation on prolonged depolarization. This component appears to result from Na-Ca exchange (NCX). When the L-type current and NCX were both inhibited (nifedipine and Na-free solution) then depolarization decreased and hyperpolarization increased [Ca(2+)](i). These changes of [Ca(2+)](i) were unaffected by modifiers of B-type Ca channels such as chlorpromazine and AlF(3) but were abolished by gadolinium ions. We conclude that, in addition to L-type Ca channels and NCX, there is another pathway for entry of Ca(2+) into the ventricular myocyte but this is distinct from the previously reported B-type channel.