DEVELOPMENTAL CHANGES IN THE DEGRADATION OF THYROTROPHIN RELEASING HORMONE BY THE SERUM AND BRAIN TISSUES OF THE MALE RAT

1977 ◽  
Vol 74 (2) ◽  
pp. 339-340 ◽  
Author(s):  
C. OLIVER ◽  
C. R. PARKER ◽  
J. C. PORTER

*Laboratoire de Médecine Expérimentale, UER Médecine Nord, Boulevard Pierre Dramard, 13326 Marseille Cedex 3, France and †Department of Obstetrics and Gynecology, Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, Texas 75235, U.S.A. (Received 15 March 1977) Thyrotrophin releasing hormone (TRH) is rapidly degraded when incubated at 37 °C with plasma (Redding & Schally, 1969) or brain homogenates (Bassiri & Utiger, 1974) from adult rats. However, immunoreactive TRH is stable in serum obtained from rats less than 2 weeks old (Oliver, Taurog & Porter, 1974). No loss of biological or immunological TRH activity occurs during incubation with serum from 4- or 16-day-old rats (Neary, Kieffer, Federico, Mover, Maloof & Soodak, 1976). In this report, we have determined the TRH degrading activity of brain homogenates and serum obtained from male rats at various stages of development after birth. Synthetic TRH (1 ng, Beckman Instruments, Inc.) diluted in 50 μl phosphate-buffered saline (0·01

1990 ◽  
Vol 125 (2) ◽  
pp. 263-270 ◽  
Author(s):  
A. E. Pekary ◽  
M. Knoble ◽  
N. H. Garcia ◽  
S. Bhasin ◽  
J. M. Hershman

ABSTRACT Orchidectomy has been reported to decrease concentrations of thyrotrophin (TSH) in the circulation of male rats without affecting serum levels of thyroid hormones. To understand the mechanism underlying this observation, we have measured the effect of gonadal status on the in-vitro release of TSH-releasing hormone (TRH) by male rat hypothalamic fragments. Because hormone release rates can be affected by changes in the post-translational processing of the hormonal precursors, we have also studied the corresponding changes in the concentrations of TRH and TRH-Gly, a TRH precursor peptide in hypothalamus and pituitary, by radioimmunoassay. We observed a significant decline in the in-vitro release of TRH from incubated hypothalami 1 week after castration, which was quantitatively reversed by testosterone replacement. Concentrations of TRH and TRH-Gly in the posterior pituitary, on the other hand, which derive from neurones of hypothalamic origin, increased significantly with castration and were returned to the normal range by testosterone replacement. We conclude that the primary effect of testosterone is the stimulation of hypothalamic TRH release, resulting in the depletion of TRH and TRH precursors from TRH-containing neurones which project into the median eminence and posterior pituitary. Journal of Endocrinology (1990) 125, 263–270


1979 ◽  
Vol 82 (1) ◽  
pp. 53-59 ◽  
Author(s):  
H. J. CHEN ◽  
P. G. WALFISH

SUMMARY Old male rats of 22–24 months and young ones of 3–5 months were studied to find the effects of ageing, of orchidectomy and of orchidectomy and treatment with testosterone propionate (TP) on the basal serum concentrations of thyrotrophin (TSH) and on the total and free concentrations of tri-iodothyronine (T3) and thyroxine (T4) in the serum. The changes in TSH after treatment with thyrotrophin releasing hormone (TRH) were also observed. Intact old rats had significantly (P < 0·001) lower basal T4 and T3 as well as lower (P < 0·05) testosterone concentrations than were present in young rats. They also had higher basal TSH and per cent free T4 but lower absolute free T3 concentrations than had young rats. Two weeks after orchidectomy, basal TSH concentrations were slightly but significantly (P < 0·05) decreased in both young and old rats while T4 decreased significantly (P < 0·05) only in the young. The responses of TSH to TRH were also reduced by orchidectomy in both age groups with the old rats being less responsive than the young. Orchidectomy and treatment with pharmacological doses of TP produced similar effects on the pituitary-thyrotrophic response for both old and young rats but a greater effect occurred in the basal T4 response in young rats. In all groups basal TSH was influenced by orchidectomy or by treatment with TP but was always higher in the aged rat. Tri-iodothyronine concentration was always lower in the older rat and was not altered by orchidectomy or by treatment with TP in either young or old rats. These results indicate that (1) in the male rat these age-specific effects on the thyroid–pituitary system are probably due, not only to a reduction in thyroid gland function and plasma T4 protein-binding, but also to a concomitant hyporesponsiveness of the aged male rat pituitary thyrotroph to TRH stimulation and (2) there is probably a significant influence of testicular function on the pituitary–thyroid system of the male rat.


Author(s):  
O. Tkachenko ◽  
V. Kovalenko

Comparative study of embryo-fetal death in females fertilized by males with metabolic syndrome, induced in adult or juvenile age has shown that the offspring of adult rats did not have significant abnormalities in embrio- and fetogenesis. At the same time it has been revealed 4% postimplantation death of offspring in male rats with metabolic syndrome induced in the juvenile age. The pre-implantation loss in this group was 6 folds higher than in control. Accordingly, the total mortality of the offspring rose 2.4 times in comparison with control.


1998 ◽  
Vol 85 (5) ◽  
pp. 1903-1908 ◽  
Author(s):  
Ronald R. Gomes ◽  
Frank W. Booth

We examined the age-related association in skeletal muscle between atrophy and expression of mRNAs encoding both the γ-subunit of the nicotinic acetylcholine receptor (AChR), and myogenin, a transcription factor that upregulates expression of the γ-subunit promoter. Gastrocnemius and biceps brachii muscles were collected from young (2-mo-old), adult (18-mo-old), and old (31-mo-old) Fischer 344/Brown Norway F1 generation cross male rats. In the gastrocnemius muscles of old vs. young and adult rats, lower muscle mass was accompanied by significantly elevated AChR γ-subunit and myogenin mRNA levels. In contrast, the biceps brachii muscle exhibited neither atrophy nor as drastic a change in AChR γ-subunit and myogenin mRNA levels with age. Expression of the AChR ε-subunit mRNA did not change with age in either gastrocnemius or biceps brachii muscles. Thus changes in skeletal muscle AChR γ-subunit and myogenin mRNA levels may be more related to atrophy than to chronological age in old rats.


2011 ◽  
pp. 961-969 ◽  
Author(s):  
J. TCHEKALAROVA ◽  
H. KUBOVÁ ◽  
P. MAREŠ

Repeated postnatal caffeine treatment of rat pups led to transient developmental changes in cortical epileptic afterdischarges. To know if physiological cortical functions are also affected transcallosal evoked potentials were studied. Rat pups of the Wistar strain were injected daily with caffeine (10 or 20 mg/kg s.c.) from postnatal day (P) 7 to P11, control siblings received saline. Cortical interhemispheric responses were tested at P12, 18, 25 and in young adult rats. Amplitude of initial monosynaptic components was evaluated in averaged responses. Single pulses as well as paired and frequency (five pulses) stimulations were used. Developmental rules – highest amplitude of responses in 25-day-old rats, potentiation with paired and frequency stimulation present since P18 – were confirmed. Caffeine-treated rats exhibited transient changes: single responses were augmented in P25 if high stimulation intensity was used, paired-pulse and frequency responses were higher in experimental than in control animals at P12, the opposite change was observed in 18- and more markedly in 25-day-old rats. No significant changes were found in adult animals, monosynaptic transcallosal responses represent a simple and robust system. The developmental profile of described changes did not exactly correspond to changes in epileptic afterdischarges supporting the possibility that afterdischarges did not arise from early monosynaptic components of responses. In spite of transient nature of changes they can reflect delayed or more probably modified brain development.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 2014 ◽  
Author(s):  
Stefano Sartini ◽  
Davide Lattanzi ◽  
Michael Di Palma ◽  
David Savelli ◽  
Silvia Eusebi ◽  
...  

Creatine plays a crucial role in developing the brain, so much that its genetic deficiency results in mental dysfunction and cognitive impairments. Moreover, creatine supplementation is currently under investigation as a preventive measure to protect the fetus against oxidative stress during difficult pregnancies. Although creatine use is considered safe, posing minimal risk to clinical health, we found an alteration in morpho-functional maturation of neurons when male rats were exposed to creatine loads during brain development. In particular, increased excitability and enhanced long-term potentiation (LTP) were observed in the hippocampal pyramidal neurons of weaning pups. Since these effects were observed a long time after creatine treatment had been terminated, long-lasting modifications persisting into adulthood were hypothesized. Such modifications were investigated in the present study using morphological, electrophysiological, and calcium imaging techniques applied to hippocampal Cornu Ammonis 1 (CA1) neurons of adult rats born from dams supplemented with creatine. When compared to age-matched controls, the treated adult offspring were found to retain enhanced neuron excitability and an improved LTP, the best-documented neuronal substrate for memory formation. While translating data from rats to humans does have limitations, our findings suggest that prenatal creatine supplementation could have positive effects on adult cognitive abilities.


1982 ◽  
Vol 95 (2) ◽  
pp. 267-274 ◽  
Author(s):  
R. N. Clayton ◽  
L. C. Bailey

Measurement of pituitary gonadotrophin releasing hormone (Gn-RH) receptor content provides a qualitative index of prior exposure of the pituitary gland to endogenous Gn-RH. The effect of moderate hyperprolactinaemia (serum prolactin = 95–250 μg/l), achieved with three pituitary grafts beneath the renal capsule, on the pituitary Gn-RH receptor content and serum LH responses to gonadectomy of adult rats has been studied. In males the presence of hyperprolactinaemia for 7 days completely prevented the increase in Gn-RH receptor content 3 days after castration and inhibited the serum LH rise by 45%. By 6 days after castration, Gn-RH receptors had increased in the hyperprolactinaemic castrated animals but values were 33% lower than in sham-grafted controls, while the serum LH increase was attenuated by 30%. Pituitary LH content was also lower in grafted castrated animals 6 days after castration. Hyperprolactinaemia for 3 weeks had no effect on Gn-RH receptors or pituitary LH content of intact male rats, although basal serum LH was decreased by 50%. Hyperprolactinaemia also attenuated the increases in Gn-RH receptors, serum LH and pituitary LH which occurred 6 days after ovariectomy in female rats. In all experiments the pituitary content of prolactin was reduced by 80–90% in animals bearing pituitary grafts. These results suggest that hyperprolactinaemia restricts the Gn-RH receptor response to gonadectomy by decreasing endogenous hypothalamic Gn-RH secretion.


1995 ◽  
Vol 132 (6) ◽  
pp. 765-770 ◽  
Author(s):  
B Díaz López ◽  
MD Colmenero Urquijo ◽  
ME Díaz Rodriguez ◽  
A Arce Fraguas ◽  
A Esquifino Parras ◽  
...  

Díaz López B, Colmenero Urquijo MD, Díaz Rodriguez ME, Arce Fraguas A, Esquifino Parras A, Marín Fernández B, Effect of pinealectomy and melatonin treatment during pregnancy on the sexual development of the female and male rat offspring. Eur J Endocrinol 1995;132:765–70. ISSN 0804–4643 Sexual development of female and male rat offspring of control, pinealectomized (PIN-X) or melatonin (MEL 2 50 μg/100 g body wt)-treated mother rats during pregnancy was studied. Newborns were studied at the following phases of sexual development: neonate (5 days old), infantile (15 days old), juvenile (25 and 30 days old) and pubertal phase (55 days). In female offspring, MEL treatment during pregnancy significantly increased plasma luteinizing hormone (LH) in 15- and 25-day-old rats; however, at the end of the prepubertal period (30 days) the concentration of plasma LH decreased significantly as compared to control rats. This hormonal pattern was different from that observed in offspring of control and PIN-X rats, which had low LH levels at 25 days of age and higher LH levels at 30 days of age. Follicle-stimulating hormone (FSH) did not vary significantly among the three groups. Plasma prolactin levels were affected by PIN-X of the mother, showing significantly higher levels in the 5-day-old offspring than in the controls; plasma prolactin levels were also affected by MEL treatment of the mother, producing hyperprolactinemia in the 30-day-old female offspring. In male offspring, sexual development in control male rats progressed rapidly with significantly increased LH and FSH levels at 25 and 30 days compared to those measured during the neonatal and infantile periods. Pinealectomy of the mother induced the following modifications: in 5-, 15- and 30-day-old male rats, decreased LH levels were measured relative to the other two groups studied in 5- and 25-day-old rats, significantly lower FSH levels than in the control rats were recorded. However, in 5- and 15-day-old rats, significantly higher prolactin levels than in control rats were measured. Melatonin injections during pregnancy decreased FSH levels at 5, 25, 30 and 55 days as compared to the control males. Also, MEL increased LH levels in 25-day-old rats and significantly decreased prolactin levels in 15- and 55-day-old rats as compared to the other two groups. These results indicate that the mother's pineal gland and MEL treatment can act on fetal development and influence the postnatal ontogeny of the hormones involved in the neuroendocrine–reproductive axis in developing rats. The effect of MEL was apparent during pubertal stages of the offspring, while the effect of PIN-X was more apparent during the juvenile period of the young rats. Beatriz Díaz López, Dpt. Biología Funcional, Arca Fisiología, Fac, Medicina, Universidad de Oviedo, 33006-Oviedo, Spain


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