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Biomedical subjects

W H Yu

Publications and source records attributed to W H Yu.

At least 91 records · Page 5Linked to original sources
PubMed1990

Stimulatory role of substance P on gonadotropin release in ovariectomized rats.

Substance P (SP) has been shown to be present in the hypothalamus and anterior pituitary. To evaluate a possible physiological role of endogenous SP in the control of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release, specific antiserum against SP (anti-SP) was injected intraventricularly (3 microliters into the third ventricle) or intravenously (50 or 200 microliters) into conscious, ovariectomized (OVX) rats. Third ventricular injection of the antiserum induced a significant decrease in both plasma LH and FSH levels when compared to values in control animals injected with normal rabbit serum (p less than 0.01 and p less than 0.025, respectively). The effect was observed within 10 mi and levels remained suppressed for 60 min. In contrast, intravenous injection of large doses of anti-SP had no effect on the release of both hormones. In order to confirm the stimulatory effect of SP itself, synthetic SP was injected intravenously and intraventricularly into estrogen-primed (E-primed), OVX rats. Synthetic SP dramatically stimulated LH release, but not FSH release when injected either intravenously or intraventricularly at doses of 10 and 50 micrograms (p less than 0.001, p less than 0.005 vs. control, respectively). To investigate any direct action of SP on gonadotropin release from the anterior pituitary gland, synthetic SP was incubated with dispersed anterior pituitary cells harvested from E-primed OVX rats. SP did not affect the release of gonadotropins in vitro. These results indicate that endogenous hypothalamic SP exerts a tonic stimulatory hypothalamic control of basal gonadotropin release in OVX rats.

Animals↗
PubMed1990

Physiologically significant inhibitory hypothalamic action of substance P on prolactin release in the male rat.

To evaluate a possible physiological role of endogenous substance P (SP) in the control of prolactin (PRL) release, conscious adult male rats were given injections of a specific antiserum against SP (anti-SP) into the third ventricle (3 microliters) or intravenously (0.5 ml). Third-ventricular injection of anti-SP induced a significant increase in plasma PRL levels when compared to values in control animals injected with normal rabbit serum (p less than 0.02). Plasma PRL concentrations were significantly elevated within 2 h after injection of antiserum and remained elevated for the 4-hour duration of the experiment. In contrast, injections of large doses of anti-SP intravenously had no effect on plasma PRL levels. In order to confirm the effect of SP itself, synthetic SP was injected intravenously and intraventricularly. Opposite effects of SP on PRL release were observed after intravenous and intraventricular injections of low or high doses of the peptide. A lower dose of SP (10 ng, 7.42 pmol) injected into the third ventricle suppressed the release of PRL (p less than 0.01), whereas higher doses (1 microgram, 0.74 nmol, or 5 micrograms, 3.71 nmol) had a stimulatory effect on PRL release (p less than 0.01). Similarly, a low dose of SP (0.1 microgram, 0.07 nmol) injected intravenously lowered plasma PRL (p less than 0.05). Large doses of intravenous SP (50 micrograms, 37.1 nmol) dramatically stimulated PRL release (p less than 0.001). To evaluate a possible direct action of SP on PRL release from the anterior pituitary, the peptide was incubated with dispersed anterior pituitary cells for 1 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Administration of testosterone fails to attenuate axotomy-induced motoneuron loss but results in castration-like effect in young male rats.

It was shown previously that the severity of motoneuron loss induced by nerve transection in rats 3 or 6 weeks of age was correlated inversely with the level of testosterone in circulation [Yu, W.H.A., Exp. Neurol. 102: 230-235, 1988], and that administration of testosterone to female rats attenuated axotomy-induced neuronal cell loss in a dose-dependent manner [Yu, W.H.A., J. Neurosci. 9: 3908-3914, 1989]. The present study was undertaken to examine whether elevation of the level of plasma testosterone in gonadally intact male rats by exogenous testosterone would likewise reduce neuronal cell loss. Following unilateral transection of the hypoglossal and facial nerve at 3 or 6 weeks after birth, rats received subcutaneous injections of 0.5, 1.0, or 2.0 mg testosterone propionate (TP) dissolved in 0.1 ml sesame oil or an equal volume of vehicle alone twice weekly for the first 4 postaxotomy weeks, and once weekly thereafter for additional 6 weeks. Results indicated that males axotomized at 3 weeks of age and treated with 1.0 or 2.0 mg TP had nearly twofold greater neuronal cell loss than oil-treated controls. The resultant cell loss was similar to that of castrated males or females without TP treatment despite the fact that TP treatment significantly elevated the plasma testosterone level. Neuronal cell loss in males axotomized at 6 weeks of age, however, was unaffected by TP treatment. Although testicular atrophy was noted in all TP-treated rats, the damage appeared to be greater in the testis of the 3-week-old than that of 6-week-old rats, as manifested by the castration-like effect of neuronal cell loss in prepubertal rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

A study on an enhancer-like element in Escherichia coli.

An enhancer-like element of 1.0kb (JM103-M) from E. coli JM103 chromosome was isolated using an enhancer-probing vector. The JM103-M fragment was shown to stimulate the nearby CAT or beta-galactosidase gene expression in E. coli in both directions at a stimulation rate of 3-6. The same fragment was also demonstrated to have promoter function when a promoter-probing vector was tested. Results obtained from sequencing data showed that a sequence TGACTAA homologous to the AP-1 binding DNA motif of SV40 and two GC boxes were present.

Base Sequence↗
PubMed1989

Administration of testosterone attenuates neuronal loss following axotomy in the brain-stem motor nuclei of female rats.

This study was undertaken to elucidate whether (1) administration of testosterone to female rats attenuates axotomy-induced neuronal loss; (2) the efficacy of testosterone treatment is related to the age of animals, the dosage given, and the time and duration of the treatment; (3) neurons which project or terminate aberrantly can survive; and (4) the trophic actions of testosterone on neuronal survival and axonal outgrowth are operated under the same mechanisms. The hypoglossal and facial nerves were transected unilaterally at 3 and 6 weeks of age. In order to establish the dose-response curve, testosterone propionate (TP) at doses of 0.5, 1.0, 2.0, or 5.0 mg was injected subcutaneously twice weekly during the first 4 postaxotomy weeks, and once weekly thereafter for an additional 6 weeks. Neuronal numbers in the hypoglossal and facial motor nuclei were counted 10-12 weeks after axotomy in serial paraffin sections stained with cresyl violet. To determine the time course of TP effect, neuronal numbers were counted at 1, 4, 12, and 20 weeks after axotomy. In addition, neuronal loss 12 weeks after axotomy in rats treated with TP for the first 3 postaxotomy weeks only was compared with that in rats withheld TP treatment until the 5th postaxotomy week. To determine axonal projections and terminations of the surviving neurons, HRP retrograde tracing technique was used. Results indicated that TP treatment significantly attenuated neuronal loss in prepubertal and young adult female rats in a dose- and time-dependent manner. Only doses which elevated serum testosterone to levels comparable to or surpassing normal male levels were effective.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Sex difference in neuronal loss induced by axotomy in the rat brain stem motor nuclei.

The magnitudes of axotomy-induced neuronal loss in male, female, and castrated male rats were compared. Ten to twelve weeks after unilateral transection of the hypoglossal and facial nerves in rats of 3 and 6 weeks of age, a significant reduction in cell number occurred in the axotomized motor nuclei. The cell loss was two times greater in females and male castrates than in males, suggesting that higher levels of androgens in males attenuated neuronal loss. The time course of neuronal loss in females axotomized at 6 weeks of age was followed. Results indicated that the neuronal population on the axotomized side sustained a gradual decline during the 1- to 12-week postaxotomy periods, being reduced eventually by 25-30%. No further cell loss was evident thereafter up to 20 weeks postaxotomy. The present study demonstrates that androgens can influence motoneuron survival not only during development as shown by E. J. Nordeen, K. W. Nordeen, D. R. Sengelaub, and A. P. Arnold (1985, Science 229: 671-673) but also in adulthood.

Animals↗
PubMed1988

Synthetic human seminal alpha-inhibin-92 selectively suppresses follicle-stimulating hormone release in vivo.

A 92-amino acid polypeptide, alpha-inhibin-92 (alpha-IB-92), has been isolated and characterized from human seminal plasma and found to be active in suppressing follicle-stimulating hormone (FSH) release in vitro. In the present in vivo study, intravenous injection of synthetic alpha-IB-92 (4 and 20 micrograms) significantly suppressed FSH release (P less than 0.001), whereas this peptide had no effect on luteinizing hormone (LH) release in 1-day orchidectomized male rats. In contrast, third ventricular injection of alpha-IB-92 (0.02, 0.4, 4, or 20 micrograms) had no effect on FSH and LH release in 1- or 2-day orchidectomized rats. These results indicate that alpha-IB-92 exerts a FSH suppressing activity by direct action on the pituitary gland.

Animals↗
PubMed1988

Gonadotropin-releasing hormone-associated peptide exerts a prolactin-inhibiting and weak gonadotropin-releasing activity in vivo.

The in vivo effects of GnRH-associated peptide (GAP) on PRL, LH, and FSH release have been examined by injecting this peptide iv into the following types of conscious rats: 1) ovariectomized steroid-blocked females, 2) ether-stressed males, and 3) lactating females. GAP (2.4 X 10(-10) and 2.4 X 10(-9) mol) suppressed plasma PRL release but did not affect the levels of plasma LH and FSH in ovariectomized steroid-blocked rats. Furthermore, with 1-min etherization, GAP (1.6 X 10(-10) and 8.0 X 10(-10) mol) reduced the stress-induced rise of plasma PRL, but had no effect on the stress-induced decline of plasma gonadotropin levels in male rats. A single iv injection of GAP (8.0 X 10(-10) mol) into lactating rats before the onset of nursing did not block the elevation of plasma PRL induced by suckling. However, a second injection of GAP (1.6 X 10(-10) mol) at 30 min after the onset of suckling partially lowered plasma PRL levels 15 min later. By contrast, plasma FSH levels were significantly elevated by the second injection of GAP, and plasma LH also rose after iv administration of GAP in the nursing rats. These results indicate that the activity of GAP to stimulate FSH and LH release is limited, since GAP stimulated the release of FSH and LH only when plasma gonadotropin levels were extremely low. However, the in vivo evidence that GAP inhibited PRL release in a variety of conditions reinforces the possibility that GAP could be the peptidic PRL-inhibiting factor.

Animals↗
PubMed1987

Purification of FSH-releasing factor: its dissimilarity from LHRH of mammalian, avian, and piscian origin.

Sheep stalk median eminence fragments were lyophylized, extracted and filtered through a column of Sephadex G-25. The fractions were then assayed for the presence of LHRH by radioimmunoassay (RIA) and bioassayed for FSH and LH-releasing activity following their IV injection into ovariectomized, estrogen progesterone-blocked rats. The radioimmunoassayable LHRH emerged from the column at the same position from which it emerged many years before when LH was measured by bioassay. This same region also contained the LH-releasing activity as measured by bioassay. FSH-releasing activity was present in two tubes just preceding the emergence of the bio- and immunoassayable LHRH. The activity was highly significant and there was no LH-releasing activity in the fractions. They contained much less LHRH as determined by RIA than is sufficient to evoke LH release in this assay. The FSH-releasing activity was recovered in the same fractions in which it was found many years ago with this same assay but with measurement of plasma FSH by bio-rather than immunoassay as employed here. A dose-related release of LH was obtained by injection of LHRH in this assay but there was no significant FSH release even with a dose of 27 ng of LHRH per rat. To determine if one of the LHRHs of lower forms might be FSH-RF, Chicken I and II LHRH and Salmon LHRH were also assayed for FSH- and LH-releasing activity. Each of these peptide possessed LH-releasing activity, albeit much less than that of the mammalian peptide but had no FSH-releasing activity whatsoever.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Androgen receptor levels in cranial nerve nuclei and tongue muscles in rats.

Specific in vitro binding of 3H-methyltrienolone (R1881) was demonstrated in 100,000 X g supernatant (cytosol) of hypoglossal, facial, and cochlear nuclei and tongue muscles of adult rats. Binding sites in these cranial nerve nuclei and tongue muscles were of high affinity, limited capacity, with steroid specificity; and they were capable of translocation to the cell nuclei in vivo. Accordingly, an androgen receptor system with properties very much akin to the androgen receptors described in the forebrain limbic regions has been quantitatively demonstrated for the first time in brain stem nuclei. Because of its widespread presence in neurons of the brain stem and spinal cord, androgen receptors may have important roles in regulation of neuron physiology beyond the sphere of reproductive function, including mediating androgen effects on regeneration of the hypoglossal nerve reported previously.

Animals↗
PubMed1984

Responsiveness of hypoglossal neurons to testosterone in pre-pubertal rats.

We have shown previously that administration of testosterone propionate (TP) to adult rats accelerated regeneration of the hypoglossal nerve. This study was made to determine whether TP had a similar effect in pre-pubertal rats, in order to establish the ontogeny of the responsiveness of the hypoglossal neurons to androgenic stimulation. It was found that TP significantly shortened the time course of the regeneration of the hypoglossal nerve in the 4-weeks old but not in the 2- and 3-weeks old rats; and that males of 4-weeks of age responded to TP a few days earlier than females of the same age. The possible causes of the failure of the hypoglossal neurons of younger ages to respond to TP were discussed.

Age Factors↗
PubMed1983

Acceleration of the regeneration of the crushed hypoglossal nerve by testosterone.

The effect of testosterone propionate (TP) on regeneration of the crushed hypoglossal nerve was studied in young adult rats. The TP treatment promoted axonal outgrowth as measured by an increase in the proportion of hypoglossal neurons labeled by retrograde transport of horseradish peroxidase injected into the tongue at selected postlesion periods compared with that in controls. The result indicated that TP exerts its effect on regeneration primarily by increasing the metabolic activity in hormone target neurons. The somatotopic organization of the hypoglossal nucleus and its projection into the major nerve branches were unaltered subsequent to crush injury. The maintenance of specificity was attributed to the intact perineurial and endoneurial sheaths which guided regenerating fibers to their original targets.

Animals↗