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R Calandra

Publications and source records attributed to R Calandra.

14 recordsLinked to original sources
PubMed1995

Time-dependent effects of dexamethasone on glutamate binding, ornithine decarboxylase activity and polyamine levels in the transected spinal cord.

Evidence exists that the spinal cord is a glucocorticoid-responsive tissue, and glucocorticoids have beneficial effects in cases of spinal cord injury. Using sham-operated rats, spinal cord transected (TRX) rats, and TRX animals receiving dexamethasone (DEX) 5 min or 24 h post-lesion, we have examined the following GC-sensitive parameters 6 h after DEX treatment: (1) binding of glutamate to NMDA-sensitive receptors; (2) the activity of ornithine decarboxylase (ODC); and (3) levels of polyamines. We found that glutamate binding in the dorsal horn (Laminae 1-2) and central canal were upregulated in TRX rats, whereas DEX had an additional stimulatory effect. 24 h post-lesion, glutamate binding was unmodified in TRX or TRX+DEX rats. ODC activity was increased 10-fold in rats killed on the day of transection but only 2-fold 24 h post-lesion. DEX reduced ODC activity on transection day but highly increased it when given 24 h after surgery. The content of the polyamines spermidine and spermine were unchanged after TRX or DEX treatment, in contrast to putrescine which increased in TRX rats and further increased in TRX+DEX rats when measured the day post-lesion. Thus, parallel increases in ODC and putrescine 1 day after the lesion, suggest that glucocorticoid effects on growth responses due to polyamines may develop at a late period. The changes of glutamate binding in the dorsal horn and central canal due to early glucocorticoid treatment, further suggest hormonal modulation of neurotransmission in sensitive areas of the deafferented spinal cord.

Animals↗
PubMed1982

Influence of starvation on the dihydrotestosterone-luteinizing hormone feedback in the male rat.

The suppressing effect of dihydrotestosterone (DHT) on LH secretion in freshly castrated starved and control rats was studied by implanting DHT releasing silastic capsules of various sizes. Lower plasma levels of DHT are needed to suppress the castration induced LH increase in the starved animals. Intravenous injection of tritiated testosterone (18 muCi/100 g b.wt) revealed a significantly longer half-life (12.4 vs 8.9; P less than 0.05) in the starved rat. The ratio [3H]-DHT/[3H]-T in plasma at various times after injection was not significantly different in starved and control animals. The results indicate that the increased sensitivity of the T-LH feedback report earlier [1] cannot be explained by a greater conversion T-DHT in the starved male rat.

Animals↗
PubMed1977

Androgen stimulation of prolactin receptors in rat prostate.

Specific receptors for iodine-labelled human prolactin ([125I]hPrl) are present in membrane preparations of the rat ventral prostate. The binding is saturable with an apparent association constant (Ka) of 2.2 X 10(9) M-1 and a binding capacity of about 1 pmol/100mg prostatic tissue. The binding of [125I]hPrl is inhibited by hPrl, ovine Prl (otprl) and human growth hormone, but not by ovine FSH or LH. Serum from rats having Prl-producing pituitary tumors caused a displacement of the [125I]hPrl from the receptors, and the displacement curve was parallel with that of the hPrl standard. Treatment of immature rats with varying doses of dihydrotestosterone propionate (10-5000 microng) causes a dose-dependent stimulation of Prl receptors calculated both as binding sites per mg of membrane protein and as binding sites per prostate. Androgen stimulation of prostatic Prl receptors increases the tissue sensitivity for circulating Prl and may be one reason for the known increases in endogenous cAMP levels in prostatic tissue after androgen treatment in vivo.

Animals↗
PubMed1977

Prolactin binding in rat testis: specific receptors in interstitial cells.

Specific receptors for [125I]hPrl (human prolactin) are present in membrane preparations of rat testis. The receptors are specific for lactogenic hormones (prolactin and human growth hormone) but do not bind gonadotropins. The prolactin receptors are localized exclusively in the interstitial cell tissue, and are not present in membrane preparations from isolated seminiferous tubules. The localization of prolactin receptors interstitial tissue suggests that the effect of prolactin on LH/hCG-stimulated testosterone production is due to a direct effect of prolactin of Leydig cells.

Animals↗
PubMed1974

Studies on the correlation between androgen binding and activation of rat epididymal tubules in culture.

Rat epididymal tubules maintained in organ culture for 3 or 7 days in media containing androgen showed a marked increase in the incorporation of radioactive amino acids and uridine into acid insoluble material. When the tubules were exposed to these hormones for brief periods, the incorporation of precursors was inhibited initially. In studying the time course of binding of 3H testosterone to the cytoplasmic receptor, a significant amount of radioactivity bound to the receptor was detected only after 12 hr of exposure to the hormone which increased three-fold after 24 hr. The time lag in the binding corresponded closely to the shortest times of observed hormone action wherein a significant increase in the incoporation of uridine (16 hr) and amino acids (24 hr) was produced. Evidence is presented demonstrating that testosterone is bound with high affinity by components of the fetal calf serum present in the culture medium.

Animals↗
PubMedDate not supplied

Effect of an antiestrogen on the testicular response to acute and chronic administration of hCG in normal and hypogonadotropic hypogonadic men: tamoxifen and testicular response to hCG.

The effect of the antiestrogen tamoxifen (Tx) on the acute and chronic hCG administration was evaluated in patients with hypogonadotropic hypogonadism (HH) and in normal men. An hCG test (5000 IU hCG) was performed before, after two months of hCG administration (2000 IU hCG three times weekly) and after two months of hCG + Tx (2000 IU hCG three times weekly plus 20 mg/day of tamoxifen). Blood samples were obtained before and following 24 and 72 h of every test to determine T, E, 17OHP and SHBG. T increased only in HH with both treatments (X +/- SEM: Basal: 97.9 +/- 19.7; hCG: 237.7 +/- 43.2; hCG +/- Tx: 204.7 +/- 10.7 ng/100 ml). 17OHP rose with hCG alone, but not with hCG + Tx in both groups. E, SHBG and 17OHP/T ratio did not change after treatments. hCG tests: E increased 24 h following hCG administration in every test. The ratio 17OHP/T rose at 24 h in the first and second test but in the third test it did not change. These results support the role of E in the acute hCG-induced Leydig cell desensitization. However, the association of Tx does not improve T serum levels, suggesting that E might not be the unique factor involved in the mechanisms for testicular desensitization.

17-alpha-Hydroxyprogesterone↗