PubMed Health⌕ Search

Biomedical subjects

M Arslan

Publications and source records attributed to M Arslan.

At least 19 recordsLinked to original sources
PubMed1992

Studies of the role of the N-methyl-D-aspartate (NMDA) receptor in the hypothalamic control of prolactin secretion.

To further examine the role of excitatory amino acids in the control of prolactin (PRL) secretion, the effects of administering a specific agonist and an antagonist of the N-methyl-D-aspartate (NMDA) receptor on plasma PRL concentrations were examined in the adult male rat. Animals of the Sprague-Dawley strain weighing 250-300 g were implanted with an indwelling cardiac catheter via the right jugular vein. Blood samples were collected through the catheter at 5 min intervals for 40 min, beginning 5 min before the iv administration of drug or the saline vehicle (V). Plasma PRL and luteinizing hormone (LH) concentrations were estimated using RIAs. Groups of animals (n = 5-7) received N-methyl-D,L-aspartate (NMA), D,L-2-amino-5-phosphonopentanoic acid (AP5), AP5 and NMA, norvaline (NOR), or V. The effects of administering the NMDA receptor antagonist alone were studied on two separate occasions. Injection of NMA (4.5 mg/rat) resulted in unambiguous PRL and LH discharges. Treatment with AP5 (9 mg/rat) 1 min prior to NMA administration completely blocked the LH releasing action of NMA, but did not significantly alter the discharge of PRL. Injection of AP5, alone, generally elicited a distinct and robust discharge of PRL, although plasma LH levels in these animals remained unchanged. NOR, an amino acid structurally related to AP5, administered at a dose (5.3 mg/animal) isomolar to that of AP5, was without effect on PRL and LH secretion, as was injection of V alone. These findings suggest that neuroexcitatory amino acids acting at the NMDA receptor may play a role in modulating the activity of neuronal systems that govern the release of both PRL releasing factor (PRF) and PRL inhibiting factor (PIF) into hypophysial portal blood.

Animals↗
PubMed1991

Possible modulation of N-methyl-D,L-aspartic acid induced prolactin release by testicular steroids in the adult male rhesus monkey.

N-methyl-D,L-aspartic acid (NMA), an agonist of the neurotransmitter glutamate has been shown to acutely stimulate the release of prolactin (PRL) in intact rats and monkeys. To further investigate the role of neuroexcitatory amino acids in PRL secretion, the effects of NMA administration were examined on PRL release in long term orchidectomized adult rhesus monkeys, in both the absence and presence of testosterone. Intact and long term castrated adult male monkeys weighing between 8-13 kg, were implanted with a catheter via the saphenous vein for blood withdrawal and drug infusion. Blood samples were collected at 10 min intervals for 50 min before and 70 min after administration of the drug or vehicle. Plasma PRL concentrations were estimated using radioimmunoassay. Whereas a single iv injection of NMA (15 mg/kg BW) induced a prompt discharge of PRL in intact monkeys, an identical dose had surprisingly no effect on PRL secretion in orchidectomized animals. On the other hand, plasma PRL increases in response to a challenge dose of thyrotropin releasing hormone (TRH; 6 micrograms/kg BW, iv) were similar in magnitude in the two groups of monkeys. Testosterone replacement in orchidectomized animals by parenteral administration of testosterone enanthate (200 mg/wk) reinitiated the PRL responsiveness to acute NMA stimulation. These results indicate that N-methyl-D-aspartic acid (NMDA) dependent drive to PRL release in the adult male rhesus monkey may be overtly influenced by the sex steroid milieu.

Animals↗
PubMed1990

Effects of androgens on bioactivity and immunoreactivity of pituitary FSH in GnRH antagonist-treated male rats.

The effects of androgens on the bioactivity and molecular composition of pituitary FSH were examined in intact and GnRH antagonist-suppressed male rats. Eight groups of adult Sprague-Dawley rats were subjected to the following treatments: antagonist (75 micrograms/day by osmotic minipumps; sc), testosterone-filled Silastic implants (3 X 5 cm, sc), dihydrotestosterone-filled Silastic implants (3 X 5 cm, sc), E2 benzoate (15 micrograms/day, sc), and combined administration of antagonist with either steroid for 3 weeks. At the end of the treatment period, pituitaries were dissected out and homogenised. FSH content was determined in the pituitary extracts by an in vitro bioassay and a radioimmunoassay. Individual pituitary extracts from rats treated with vehicle, testosterone and testosterone + antagonist were subjected to isoelectric-focusing on sucrose density gradients performed in the pH range from 3.5 to 7.0. Individual isoelectric-focusing fractions (100-120) were analysed for bioactive and immunoreactive FSH. Treatment with antagonist, E2 or antagonist + E2 caused a significant decrease in pituitary FSH, whereas testosterone and dihydrotestosterone alone or in combination with antagonist prevented the decrease in pituitary FSH. The effects of all treatments on both bioactive and immunoreactive FSH were similar. Testosterone treatment not only maintained FSH synthesis but also altered the molecular composition of pituitary FSH. Following treatment with testosterone there was a shift of maximal FSH bioactivity to the more acidic pH range. On the other hand, less bioactivity was recovered than corresponding immunoreactivity in the higher pH region, resulting in significantly reduced ratios of bioactivity to immunoreactivity of FSH.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗
PubMed1989

Puberty in monkeys is triggered by chemical stimulation of the hypothalamus.

Gonadal quiescence prior to puberty in primates results from a diminished secretion of the pituitary gonadotropic hormones, follicle-stimulating hormone and luteinizing hormone, which, in turn, is occasioned by an interruption of pulsatile release of gonadotropin-releasing hormone (GnRH) from the hypothalamus during this phase of development. A discharge of GnRH may be provoked from the hypothalamus of prepubertal monkeys, however, by an i.v. injection of N-methyl-D-aspartate (NMDA), an analog of the putative excitatory neurotransmitter, aspartate. Since this action of NMDA is blocked by the specific NMDA receptor antagonist, DL-2-amino-5-phosphonopentanoic acid, the release of GnRH is likely mediated by NMDA receptors located either on the GnRH neurons themselves or on afferents to the GnRH cells. We report here that prolonged intermittent NMDA stimulation of GnRH neurons within the hypothalamus of the juvenile monkey for 16-30 wk results, with surprising ease, in the onset of precocious puberty with full activation of the hypothalamic-pituitary-Leydig cell axis and initiation of spermatogenesis. These findings demonstrate that, in primates, the network of hypothalamic GnRH neurons, which in adulthood provides the drive to the gonadotropin-secreting cells of the anterior pituitary gland, must now be viewed together with the pituitary and gonads as a nonlimiting component of the control system that governs the onset of puberty in these species.

Animals↗
PubMed1989

Testosterone and dihydrotestosterone, but not estradiol, selectively maintain pituitary and serum follicle-stimulating hormone in gonadotropin-releasing hormone antagonist treated male rats.

Recently it has been found that testosterone can maintain and restimulate serum and pituitary follicle-stimulating hormone (FSH) in the gonadotropin-releasing hormone (GnRH) antagonist treated adult male rat. The present investigation was undertaken to determine (1) which metabolite of testosterone, dihydrotestosterone (DHT), or estradiol accounts for the effects of testosterone in GnRH antagonist suppressed rats and (2) whether these effects of testosterone are influenced by other testicular factors. Eight groups of 6-8 adult male Sprague-Dawley rats were subjected to the following treatments: vehicle, GnRH antagonist (75 micrograms/day s.c.), testosterone-filled Silastic implants (3 x 5 cm, s.c.), DHT-filled Silastic implants (3 x 5 cm, s.c.), estradiol benzoate (15 micrograms/day s.c.), and combined administration of GnRH antagonist with either steroid. In addition, the GnRH antagonist/testosterone treatment regimen was applied to rats orchidectomized 72 h prior to initiation of treatments. After 3 weeks of treatment, serum was analyzed for concentrations of luteinizing-hormone (LH), FSH, testosterone, DHT, and estradiol. Pituitary extracts were analyzed for LH and FSH content. Except for the vehicle-treated groups, serum and pituitary LH concentrations were markedly suppressed by all treatments. In intact rats treated with GnRH antagonist alone and/or estradiol, the pituitary FSH level was reduced by more than 70% relative to controls, while both testosterone and DHT maintained pituitary FSH. Similarly, testosterone and DHT, but not estradiol, delayed the decline of serum FSH induced with GnRH antagonist alone. In orchidectomized animals, testosterone was also capable of preventing a reduction of pituitary FSH despite concomitant GnRH antagonist administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

DL-2-amino-5-phosphonopentanoic acid, a specific N-methyl-D-aspartic acid receptor antagonist, suppresses pulsatile LH release in the rat.

To determine whether neuroexcitatory amino acids may play a role in generating intermittent hypothalamic GnRH release, the effect of N-methyl-D-aspartate (NMDA) receptor blockade on pulsatile LH secretion was examined in male rats. The ability of the NMDA receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (AP5), to inhibit activation of the hypothalamic-pituitary gonadotroph axis that follows peripheral administration of NMDA, was first established in intact rats. Subsequently, acutely castrated rats (n = 12) bearing venous catheters received four consecutive intravenous injections of AP5 (3.75 mg/injection/rat; approx. 13.6 mg/kg BW/injection) at 15-min intervals. Blood samples were collected at 10-min intervals for 1 h before and 2 h after initiation of AP5 treatment, and plasma LH concentrations were determined by RIA. For control purposes, norvaline, and amino acid structurally related to AP5, was administered to a second group of animals (n = 7) in a quantity (2.25 mg/injection/rat; approx. 8.2 mg/kg BW/injection) equimolar to that of the NMDA receptor antagonist. A third group of animals (n = 8) received only saline, the vehicle employed to inject AP5 and norvaline. AP5, but not norvaline, resulted in a marked suppression of pulsatile LH secretion. These findings suggest that neuroexcitatory amino acids acting at the NMDA receptor may play a physiological role in generating the intermittent mode of hypothalamic GnRH release.

Animals↗
PubMed1986

Characterization and androgen dependence of specific proteins in the epididymis of adult rhesus monkey (Macaca mulatta).

The androgen dependence and regional distribution of specific epididymal proteins have been investigated in the adult rhesus monkey (Macaca mulatta). The protein pattern of the epididymal cytosol was studied in intact, castrated, and testosterone-treated castrated monkeys by polyacrylamide gel electrophoresis (PAGE) and electrofocusing. At least five distinct protein components of the epididymal cytosol were androgen-sensitive. The PAGE of cytosol from various portions of the epididymis showed that whereas four protein components were uniformly distributed in the caput, corpus, and caudal segments, one of the androgen-dependent proteins was found to be associated with the caudal portion of the epididymis. Electrofocusing of epididymal cytosol also confirmed the presence of five androgen-dependent proteins in the adult monkey. The isoelectric points of these proteins were shown to range between 5.6 and 6.5, and the molecular weights were found to range between 15,000 and 61,000.

Androgens↗
PubMed1986

Changes in circulating levels of immunoreactive follicle stimulating hormone, luteinizing hormone, and testosterone during sexual development in the rhesus monkey, Macaca mulatta.

Basal serum levels of follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone (T) and the responsiveness of these hormones to a challenge dose of luteinizing hormone releasing hormone (LHRH), were determined in juvenile, pubertal, and adult rhesus monkeys. The monkey gonadotrophins were analyzed using RIA reagents supplied by the World Health Organization (WHO) Special Programme of Human Reproduction. The FSH levels which were near the assay sensitivity in immature monkeys (2.4 +/- 0.8 ng/ml) showed a discernible increase in pubertal animals (6.4 +/- 1.8 ng/ml). Compared to other two age groups, the serum FSH concentration was markedly higher (16.1 +/- 1.8 ng/ml) in adults. Serum LH levels were below the detectable limits of the assay in juvenile monkeys but rose to 16.2 +/- 3.1 ng/ml in pubertal animals. When compared to pubertal animals, a two-fold increase in LH levels paralleled changes in serum LH during the three developmental stages. Response of serum gonadotrophins and T levels to a challenge dose of LHRH (2.5 micrograms; i.v.) was variable in the different age groups. The present data suggest: an asynchronous rise of FSH and LH during the pubertal period and a temporal correlation between the testicular size and FSH concentrations; the challenge dose of LHRH, which induces a significant rise in serum LH and T levels, fails to elicit an FSH response in all the three age groups; and the pubertal as compared to adult monkeys release significantly larger quantities of LH in response to exogenous LHRH.

Animals↗
PubMed1984

Salivary testosterone levels in normal and testosterone treated monkeys.

Testosterone concentrations in saliva and matched serum samples were measured by radioimmunoassay, in normal and testosterone treated adult male cynomolgus monkeys (Macaca fascicularis) and in untreated rhesus monkeys (Macaca mulatta). Saliva and serum samples were collected under ketamine anaesthesia. In 4 cynomolgus monkeys, the mean basal testosterone levels were 195 +/- 22 pmol/l in saliva and 24 +/- 2 nmol/l in serum (n = 17). The salivary testosterone corresponded to 0.9 +/- 0.1% of the serum testosterone concentration. In 5 rhesus monkeys the mean testosterone concentrations were 147 +/- 10 pmol/l in saliva and 17 +/- 2 nmol/l in matched serum samples with a percent ratio of 1.6 +/- 0.3 (n = 15). Following a single i.m. injection of 50 mg testosterone propionate to 4 monkeys, both salivary and serum testosterone levels increased promptly and in parallel. The salivary testosterone levels correlated well with the serum testosterone values. The study suggests that, as in the human, determination of salivary testosterone can be used as an index of free testosterone in this animal. Moreover, the monkey can be used as a model for studies in the human involving monitoring of salivary testosterone.

Animals↗
PubMed1982

Effect of an LHRH analogue on testicular function in the immature monkey (Macaca mulatta).

Response of the immature monkey testis to an LHRH analogue, D-Ser-(TBu)6-EA10-LHRH, has been assessed by measuring testicular androgen production in the immature rhesus monkey. Administration of the analogue (2.5 micrograms X 2 daily) for 5 days induced a significant increase in testicular testosterone compared with untreated animals. The response of the control and the LHRH-agonist treated monkey testis to gonadotrophin (hCG) was assessed by in vitro androgen production. Whereas the testicular tissue from LHRH analogue primed monkeys responded to in vitro stimulation of hCG, no significant increase in androgen production was observed when testicular tissue from untreated animals was incubated with the gonadotrophin. The present data suggest a functional differentiation of the immature monkey testis following the LHRH analogue treatment.

Animals↗
PubMed1981

Effects of gonadotrophin treatment in vivo on testicular function in immature rhesus monkeys (Macaca mulatta).

Changes in testicular histology and concentrations of testosterone and oestradiol 17 beta in testicular tissue and plasma have been studied following administration of gonadotrophins (oFSH, oLH, hCG and PMSG) to immature male monkeys. Treatment with FSH (1 mg/day) or PMSG (100 IU/day) for five days, induced a marked enlargement of the seminiferous tubules and increase in the Sertoli cell cytoplasm. Injections of LH (1 mg/daily) or hCG (100 IU/daily) administered similarly, failed to produce hypertrophy of the Sertoli cell. In LH, hCG and PMSG stimulated testes morphologically differentiated interstitial cells could be recognized. FSH did not produce any detectable effect on the intertubular tissue. A significant increase in testicular and plasma testosterone levels was observed with LH, hCG and PMSG. FSH was shown to be much less effective in stimulating androgenesis. An increase in testicular oestradiol production over that of controls, was observed in FSH and PMSG treated monkeys but not in animals treated with LH or hCG.

Animals↗
PubMed1977

A new hypothesis on the plurifactorial etiology of Meniere's disease.

Meniere's disease is characterized by an extremely long trend: this fact, as in other diseases of very wide chronicity, permits one to formulate a special type of hypothesis regarding the aetiology and the pathogenesis of the disease; it is comprised of many individual factors, of differing chronology and which are connected to each other with successive causality. This hypothesis was founded on a large body of data concerning the multiple histopathological effects on the inner ear of an initially inflammatory disease of the middle ear.

Acute Disease↗