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C Desjardins

Publications and source records attributed to C Desjardins.

At least 55 records · Page 3Linked to original sources
PubMed1982

Luteinizing hormone and testosterone secretion in young and old male mice.

This study documents, for the first time, the temporal pattern of luteinizing hormone (LH) release and the relationship between plasma LH concentrations and testicular androgenic responses in young and aged male mice. Both LH and testosterone were measured in the same samples of blood plasma withdrawn at frequent intervals over 9 h from awake, mobile mice through intra-atrial cannulae. The results demonstrate unequivocally that LH and testosterone are discharged into the circulation in discontinuous pulses in this important animal model. Robust episodes of LH release occur at infrequent intervals and increments of circulating LH occasion time-delayed elevations of plasma testosterone. Thus, the frequency of LH release is the major factor determining peripheral concentrations of this gonadotropins. The obvious one-to-one coupling between intermittent LH discharges and testosterone secretion has significant functional and investigative implications. The reduction in circulating testosterone concentrations observed in old male mice is a consequence of fewer LH discharges, which is due most likely to the slowing of a neural GnRH pulse generator. However, age-related declines in copulatory behavior were not associated with altered patterns of hormone secretion. Hence, we suggest that deficits in sexual behavior and episodic LH release in old males result from neural senescence rather than diminished testicular support of reproduction.

Aging↗
PubMed1982

Male rats secrete luteinizing hormone and testosterone episodically.

We studied the temporal aspects of endocrine signaling between the pituitary gland and testes by measuring moment to moment changes in blood LH and testosterone levels in individual male rats. Each rat was fitted with an indwelling vascular cannula, and blood was withdrawn every 5 min for 8-12 h. Rats were maintained throughout the intensive blood-sampling period with an isotonic blood replacement mixture containing rat red blood cells and a human plasma protein preparation. LH and testosterone measurements were made in plasma volumes of 50 and 60 microliters. Most rats released LH in well defined pulses, characterized by a rapid increase in plasma LH within 5-10 min and a gradual decline lasting for the next 50-70 min. LH pulses occurred singly or in trains of two to four. Episodes of testosterone secretion spanned 3-6 h and were marked by a slowly graded rise and fall of plasma testosterone. In several instances, testosterone episodes were preceded (1-2 h) by a train of closely coupled LH pulses. Within a particular animal on different days, hormone episodes varied in number, amplitude, and timing. A particular hormone profile did not serve as a reliable hormone signature for an individual rat. Many rats displayed a characteristic sequence of 1) multiple LH pulses, 2) a sustained testosterone episode, and 3) a period of no LH pulses. This tripartite sequence of events is viewed as the essence of pituitary-testicular stimulation, and testicular negative feedback. Intermittent, short term fluctuations in peripheral levels of LH and testosterone represent the blood-borne, gland to gland signals controlling hypothalamic-pituitary-testicular function in the normal rat.

Animals↗
PubMed1982

Endocrine responses to sexual arousal in male mice.

The endocrine correlates of sexual arousal were explored in male mice. Using indwelling atrial cannulae, temporal changes in the blood levels of six hormones were monitored in sexually rested vs. sexually sated males before and during their exposure to receptive females. The vaginae of some test females were artificially occluded to assess separately the impact of intromission on hormone levels. Sexually rested males responded to receptive females with dramatic increases in their blood levels of corticosterone, epinephrine, and norepinephrine. These changes occurred independently of intromission. Blood titers of these three hormones did not change in sexually sated males when they encountered a receptive female. Both sexually sated and sexually rested males discharged LH in a reflex-like manner immediately upon perceiving a test female. PRL was released only in response to ejaculation, and FSH titers were unaffected by the presence of a female. In general, a receptive female elicits a variety of hormonal responses in a male mouse. Some hormones seem to be discharged in response to sexual arousal per se, whereas others are released with varying degrees of independence of this process. Viewed from another perspective, the present results allow the presentation of a relatively detailed scheme that temporally relates sensory input to hormonal response during the sexual interactions of male mice.

Animals↗
PubMed1980

Classical conditioning: induction of luteinizing hormone and testosterone secretion in anticipation of sexual activity.

A classical conditioning paradigm was used to demonstrate that male rats can learn to secrete luteinizing hormone and testosterone in anticipation of sexual activity. Sexually naïve males were exposed to a neutral stimulus and then to a sexually receptive female once daily. After exposure to the paired stimuli for 14 trials, the neutral stimulus was as effective as the female in triggering luteinizing hormone and testosterone secretion. These findings provide two novel perspectives on the control of reproductive hormone secretion in male rats: (i) environmental cues, which males learn to associate with sexual activity, induce the secretion of hormones that regulate pituitary-testis function, and (ii) classical conditioning may be used as a noninvasive method to evoke functional alterations in the secretion of luteinizing hormone and presumably the neuroendocrine pathways that mediate its release.

Animals↗
PubMed1979

Rabbit lutropin: preparation, characterization of the hormone, its subunits and radioimmunoassay.

The purification of rabbit lutropin is described. A product with a potency of 1.53 X NIH-LH-Sl was obtained as assayed by the ovarian ascorbic acid depletion assay. In a homologous radioimmunoassay, which is described, rabbit lutropin has a potency 4.83 X NIH-LH-Sl. In a radioligand assay, utilizing labeled ovine lutropin as the trace, the relative potency was 0.47 X NIH-LH-Sl measured by 50% inhibition comparison since rabbit lutropin response in this system did not parallel ovine lutropin. A counter-current distribution procedure for separation of rabbit lutropin subunits is described. Amino acid composition of the isolated subunits and intact rabbit lutropin was determined. The carbohydrate composition of the latter is presented; only amino sugar determinations are available for the subunits. The NH2-terminal amino acids are phenylalanine (alpha subunit) and alanine (beta subunit). Preliminary data on COOH-terminal amino acids are provided.

Amino Acid Sequence↗
PubMed1979

Follicle-stimulating hormone-induced, adenosine 3',5'-monophosphate-mediated movement of immature rat sertoli cells in primary culture.

Sertoli cells dissociated from 10-day-old rat testes form colonies in primary culture in response to FSH. FSH and dibutyryl cAMP stimulated the attachment of Sertoli cells to an equal extent; however, FSH-treated cultures contained a small number of large colonies while dibutyryl cAMP-treated cultures contained a large number of small colonies. This relationship was not altered by the addition of a number of other peptide or steroid hormones. Extracellular cAMP levels and colony density were negatively correlated. Colony size at 24 h of culture was diminished in FSH-treated cultures by the addition of a cAMP antibody at 6 or 12 h of incubation. The addition of cAMP at 24 h to FSH-treated cultures caused a dose-dependent stimulation of colony size but not colony density at 48 h of culture. A point source of cAMP (4 x 10(-3) M in agar) inhibited migration of cells toward the agar spot. An agar spot on the dish substratum containing Sepharose-bound FSH exhibited a halo of cells next to the spot, with a zone lacking cells distal to it. Radioautographs of [125I]iodo-FSH-treated cultures exhibited a nonhomogeneous distribution of silver grains; colony size increased faster than the number of labeled cells. Taken together, the results suggest that 1) FSH is stimulating the attachment of Sertoli cells through an increase in intracellular cAMP, 2) FSH is promoting active aggregation of Sertoli cells in culture through a modulation of extracellular cAMP, and 3) cells with a large amount of bound FSH are acting as centers for aggregation.

Animals↗
PubMed1979

Development of Leydig cell tumors and onset of changes in the reproductive and endocrine systems of aging F344 rats.

The age-dependent onset of spontaneous testicular interstitial cell tumors was examined in F344 male rats. Light microscopy of testes established that nodular interstitial cell hyperplasia was evident in 3 of 5 12-month-old rats and in 5 of 5 rats at 15, 18, 21, and 24 months of age. Involution of the seminiferous epithelium was evident in all testes exhibiting extensive interstitial cell proliferation. Striking increments in serum prolactin and estradiol levels were noted with advancing age, whereas serum levels of follicle-stimulating hormone were unequivocally lower at 21 and 24 months than at 6 months of age. No measurable changes were detected in serum testosterone concentrations between 6 and 18 months of age, but marked increments in this androgen, without any measurable change in circulating luteinizing hormone titers, were apparent in 21- and 24-month-old rats. These findings point to a dynamic relationship between testicular interstitial cell tumorigenesis and age-related changes in the synthesis and/or secretion of gonadal and adenohypophyseal hormones.

Aging↗
PubMed1978

Endocrine regulation of reproductive development and function in the male.

Sexual development is an ordered process that begins at the moment of fertilization and terminates with the production and transfer of viable gametes. The formation of the male gonad depends upon genes located on both sex chromosomes and autosomes. Differentiation and growth of the male reproductive system is directed by the fetal testis through the production of a putative peptide which causes the regression of the Mullerian ducts and the secretion of testosterone which virilizes the Wolffian duct and thereby directs the differentiation of the internal accessory structures of reproduction. A third hormone, dihydrotestosterone, is synthesized intracellularly from testosterone within the urogenital sinus and tubercle. The action of this hormone controls the formation of the prostate and the external genitalia characteristic of the male phenotype. The postnatal growth of the testis and accessory sex tissues follows a characteristic curvilinear pattern with the most prominent increments coincident with the onset in testosterone production. Spermatogonial differentiation may proceed in the absence of hypophyseal or gonadal hormones but the respective maturation divisions of primary and secondary spermatocytes and the completion of spermiogenesis are clearly dependent upon testicular steroids produced under the influence of LH. Germ cells differentiate in a unique environment created, in part, by the blood testis barrier which arises as a result of tight-junctional complexes formed between adjacent Sertoli cells. Sertoli cells actively secrete fluids and export an androgen binding protein under the influence of androgens and FSH. Maintenance of spermatogenesis depends on high intratubular concentrations of testosterone, provided in part by the steroidogenic actions of LH on the Leydig cell and, in part, by the production of androgen binding protein by the Sertoli cell. Thus, both gonadotropins act in concert to maintain germ cell production. Selective removal of either LH or FSH curtails sperm production but testosterone supplementation, in adequate amounts, allows spermatogenesis to proceed in the absence of the pituitary gland.

Androgens↗