Search PubMed⌕ Search

Biomedical subjects

R F Walker

Publications and source records attributed to R F Walker.

At least 19 recordsLinked to original sources
PubMed2006

Wildfire effects on soil nutrients and leaching in a tahoe basin watershed.

A wildfire burned through a previously sampled research site, allowing pre- and post-burn measurements of the forest floor, soils, and soil leaching near Lake Tahoe, Nevada. Fire and post-fire erosion caused large and statistically significant (P < or = 0.05) losses of C, N, P, S, Ca, and Mg from the forest floor. There were no statistically significant effects on mineral soils aside from a decrease in total N in the surface (A11) horizon, an increase in pH in the A11 horizon, and increases in water-extractable SO4(2-) in the A11 and A12 horizons. Burning caused consistent but nonsignificant increases in exchangeable Ca2+ in most horizons, but no consistent or statistically significant effects on exchangeable K+ or Mg2+, or on Bray-, bicarbonate-, or water-extractable P concentrations. Before the burn, there were no significant differences in leaching, but during the first winter after the fire, soil solution concentrations of NH4+, NO3-, ortho-P, and (especially) SO4(2-) were elevated in the burned area, and resin lysimeters showed significant increases in the leaching of NH4+ and mineral N. The leaching losses of mineral N were much smaller than the losses from the forest floor and A11 horizons, however. We conclude that the major short-term effects of wildfire were on leaching whereas the major long-term effect was the loss of N from the forest floor and soil during the fire.

Calcium↗
PubMed2002

Is aging a disease? A review of the Serono Symposia Workshop held under the auspices of the 3rd World Congress on the Aging Male. February 9, 2002, Berlin, Germany.

On February 9, 2002, Serono Symposia sponsored a workshop at The 3rd World Congress on The Aging Male that was held in Berlin, Germany at the Hotel Inter-Continental. The title of the workshop 'Is aging a disease?', was intended to convey recent interest in the subject of aging as a clinically relevant entity and to discuss causes and approaches to its management. The Workshop was co-chaired by Drs Viktor Büber and Richard F. Walker. Speakers included Drs George R. Merriam, Heinrich M. Schulte, Felice Strollo and Richard F. Walker. Topics were arranged to proceed from a general overview of fundamental aspects of the aging process and their clinical consequences to specific aspects of the diagnosis and treatment of age-related disorders that could be associated with neuroendocrine dysfunction. F. Strollo initiated the series of lectures by reviewing some of the biological theories of aging and suggesting that maladaptive changes within the central nervous and endocrine systems play a major role in contributing to the cascade of events defined as senescence. R. Walker expanded upon this background by differentiating aging and disease. He suggested that while the process of aging is not a disease, it is directly responsible for the development of functional decrements causal of the intrinsic disease, frailty and general morbidity that occur in direct relation to advancing chronological age. From this generalized approach of linking age and disease, G. Merriam discussed a specific example in which age-related decrements in neuroendocrine dysfunction could contribute, at least in part, to senescent changes in body composition and physiological function. Specifically, he provided evidence that the gradual decline in growth hormone (GH) and testosterone secretion during aging is accompanied by anatomical and functional changes resembling pathogenic hormone deficiency. He went on to discuss possible interventions into this process, specifically showing data to support the view that a combination of GH secretagogues and sex hormones may be of value in sustaining health and vitality in the elderly. As an extension of this discussion, H. M. Schulte compared and contrasted age changes in sex hormone secretion between genders, and also stressed that the diagnosis and management of endocrine changes during life has become a serious challenge to those physicians intending to intervene in the aging process. Because the relationship of reduced hormone secretion to disease in the elderly is presently unclear, the Workshop concluded on a note of caution that guidelines for the replacement of endocrine substances as a prophylactic approach to aging have yet to be defined.

Aged↗
PubMed1997

Growth hormone secretagogues in children with altered growth.

A diagnostic test was devised to evaluate pituitary growth hormone (GH) secretory potential. GH secretory dynamics were assessed in children with and without GH deficiency. The GH response was measured to GH-releasing hormone (GHRH) and the GH-releasing peptide GHRP-2, administered sequentially. The mean (+/- SEM) peak GH response to GHRP-2 was 20.1 +/- 5.5, 63.6 +/- 24.9 and 42.2 +/- 4.3 micrograms/l for GH-deficient, slowly growing non-GH-deficient and control children, respectively (p < 0.02 and p < 0.05 for GH-deficient vs controls and slowly growing children, respectively). Corresponding values for area under the curve (AUC) were 995 +/- 371. 2460 +/- 953 and 1598 +/- 274 micrograms/l x minute. Peak GH (and AUC) responses to GHRH were 19.6 +/- 5.1 micrograms/l (924 +/- 232 micrograms/l x minute), 31.4 +/- 8.4 micrograms/l (1544 +/- 449 micrograms/l x minute) and 39.8 +/- 7.8 micrograms/l (2201 +/- 437 micrograms/l x minute) for the same three groups, respectively (p < 0.05 for peak GH in GH-deficient patients vs controls, and p < 0.02 and p < 0.01 for AUC in GH-deficient vs slowly growing children and controls, respectively). The ratio of the peak GH response to GHRP-2 and GHRH was similar in all three groups. As these secretagogues stimulate different aspects of hypothalamic function (i.e., they are functional complements), robust GH secretion in response to GHRH or GHRP could suggest adequate endogenous GHRP or GHRH, respectively. A poor response to either GH secretagogue administered individually could represent inadequacy of its endogenous complement. The integrity of functional pituitary elements could be differentiated from inadequate complements by administering both GH secretagogues simultaneously. Application of these principles should allow a better definition of the underlying disorder and provide the basis for therapeutic strategies for those patients with abnormal GH production and/or secretion.

Area Under Curve↗
PubMed1996

Evaluation of pituitary function in children using growth hormone secretagogues.

We have devised a diagnostic test to directly evaluate pituitary secretory potential, and also to identify the most appropriate therapy for slow growing children. The test compares responses to GH releasing hormone (GHRH) and GH releasing peptides or their non-peptidyl mimics (GHRP) administered sequentially and in combination. Since they are functional complements, robust GH secretion in response to GHRH or GHRP could be interpreted as representing adequate endogenous GHRP or GHRH, respectively. Alternatively, assuming that all pituitary cellular and molecular elements for GHRH- and GHRP-mediated GH secretion are functional, a poor response to either GH secretagogue administered individually could represent inadequacy of its endogenous complement. The integrity of functional pituitary elements could be differentiated from inadequate endogenous complement by administering both GH secretagogues simultaneously. Based upon this hypothesis, the proposed pituitary function diagnostic scheme could be used to test for endogenous GH secretagogue adequacy, as well as pituitary secretory capacity. The data resulting from application of these principles would allow appropriate selection of therapeutic entities, ranging from GHRH or GHRP administered separately or in combination, or alternatively, recombinant GH for those patients lacking a pituitary mechanism for GH production and/or secretion.

Adolescent↗
PubMed1994

Effects of stimulated growth hormone secretion on age-related changes in plasma cholesterol and hepatic low density lipoprotein messenger RNA concentrations.

Growth hormone (GH) secretion declines during aging. Since GH alters plasma cholesterol (PC) concentrations, it was of interest to determine how GH secretagogues affect age-related hypercholesterolemia. Fischer 344 rats (3 and 14 months old) were co-administered (s.c.) GH releasing hormone (3 micrograms/kg; GHRH) and GH releasing hexapeptide (100 micrograms/kg; GHRP) for 120 consecutive days. Aging was associated with a progressive increase in PC, which was reduced in rats administered GHRH and GHRP compared to those administered vehicle, i.e. changes in PC during the study were 26.5 +/- 1.2 mg/dl vs. 40.1 +/- 0.9 mg/dl (P < 0.05) in the younger rats and 17.6 +/- 2.3 mg/dl vs. 31.6 +/- 5.3 mg/dl (P < 0.05) in the older rats, respectively. The lower concentrations of PC in GH secretagogue-treated older rats were associated with higher mean concentrations of hepatic LDL receptor mRNA (1.27 +/- 0.4 vs. 0.4 +/- 0.1; P < 0.05) but not cholesterol 7-alpha hydroxylase mRNA. Although GH secretagogue treatment was also associated with lower plasma cholesterol in the younger rats, it was not accompanied by quantitative changes in mean group concentrations of hepatic LDL receptor mRNA. Instead, daily administration of GHRH and GHRP in the younger rats correlated with a significant reciprocal relationship (P < 0.05) between PC and hepatic LDL receptor mRNA for individual group members. The results of this study suggest that reduced GH secretion during aging contributes, at least in part, to a progressive increase in plasma cholesterol that can be partially prevented with GH secretagogues. Furthermore, the effects on PC may result from GH-mediated, qualitative and quantitative changes in hepatic LDL receptor mRNA that increase receptor-mediated cholesterol clearance.

Aging↗
PubMed1993

Saliva as a medium for chronobiological studies: its particular potential in steroid endocrinology.

This paper indicates the potential of saliva as a medium for chronobiological studies. It has principally focussed on the work of the Tenovus Institute for Cancer Research, at the University of Wales College of Medicine over the past decade or more, particularly for steroid hormones, so as to give an authoritative viewpoint based on practical experience. The article discusses issues ranging from technical to clinical aspects of hormone assay in saliva, showing disadvantages and limitations of use. Increasingly, many other investigators are developing and applying assays for salivary steroids and it is timely that such assays become tools in the hands of the chronobiologist. The clinical-biochemical importance of saliva resides also in the fact that in its context it is possible to assay enzymes, toxic substances and drugs.

Adult↗
PubMed1992

Role of selected endogenous peptides in growth hormone-releasing hexapeptide activity: analysis of growth hormone-releasing hormone, thyroid hormone-releasing hormone, and gonadotropin-releasing hormone.

The purpose of this study was to evaluate the contribution of endogenous GH-releasing hormone (GHRH) to exogenous GH-releasing hexapeptide (GHRP-6) activity, and to determine whether TRH or GnRH are endogenous analogs of GHRP-6. The activity of GHRP-6, a synthetic GH secretagogue, was significantly attenuated in rats administered GHRH antiserum or alpha-methyl-rho-tyrosine to reduce endogenous GHRH concentrations, and also in rats administered 5-50 micrograms/kg of [N-Ac-Tyr1,D-Arg2]-GRF 1-29 amide to block pituitary GHRH receptors. However, GHRP-6 activity was potentiated in rats administered 150 micrograms/kg [N-Ac-Tyr1,D-Arg2]-GRF 1-29 amide, presumably due to partial agonist activity of the GHRH receptor antagonist at the higher dose. These data show that endogenous GHRH contributes to full expression of exogenous GHRP-6 activity in vivo. Like TRH, a subthreshold dose of GHRP-6 was significantly more effective in hypothyroid rats than in euthyroid rats. However, suprathreshold doses of GHRP-6 were less effective in hypothyroid rats. Unlike TRH, GHRP-6 had no effect on GH and prolactin release from GH3 cells, and TRH and GnRH were poor competitors for 3H-GHRP-6 binding sites on pituitary membranes. A GnRH receptor antagonist did not block GHRP-6 activity in vivo, and GnRH administered alone or in combination with GHRP-6, did not stimulate GH release. The results of this study suggest that synergy between GHRH and GHRP-6 seen in pharmacological studies is physiologically relevant, and that TRH and GnRH are not endogenous analogs of GHRP-6.

Animals↗
PubMed1992

Effects of coadministered growth hormone (GH)-releasing hormone and GH-releasing hexapeptide on maladaptive aspects of obesity in Zucker rats.

The purpose of this study was to determine the effect of chronic pharmacological stimulation of the pituitary gland on GH hyposecretion and other maladaptive aspects of obesity. Obese Zucker rats were coadministered GH-releasing hormone (GHRH; 3 micrograms/kg) and GH-releasing hexapeptide (GHRP-6; 300 micrograms/kg), a potent combination of synergistic GH secretagogues, once daily for 60 consecutive days. Although pituitary weights and GH concentrations were higher in obese rats administered the peptides than in obese rats administered saline, stimulated GH secretion was lower in obese rats than in lean rats. However, compared to those in lean rats, plasma insulin-like growth factor-I and insulin concentrations were higher in the obese rats regardless of treatment. The GH secretagogues did not alter food intake or body weight gain in sexually mature obese rats, whereas body weight gain was significantly increased when they were administered to prepubertal obese rats. Although glucose tolerance was impaired in both groups of obese rats, it improved in obese rats administered GHRH and GHRP-6 compared to that in obese rats administered saline. On the other hand, plasma cholesterol concentrations were elevated in obese rats administered the GH secretagogues but not saline. In conclusion, the results of this study suggest that hyposensitivity to GHRH and GHRP-6 in obese Zucker rats results from high concentrations of plasma insulin-like growth factor-I that negatively feedback on stimulated GH secretion. Nonetheless, daily episodes of endogenous GH secretion resulting from chronic coadministration of GH secretagogues significantly influenced the pituitary gland as well as lipid and carbohydrate metabolism.

Animals↗
PubMed1992

Oral testosterone undecanoate in the management of delayed puberty in boys: pharmacokinetics and effects on sexual maturation and growth.

Therapeutic induction of puberty using oral testosterone (T) undecanoate (TU) 40 mg daily was performed in 4 pubertal boys aged 12.7-17.1 yr with constitutional delayed puberty and/or short stature. Single-dose pharmacokinetics study was performed on matched plasma and saliva samples obtained half-hourly for 10 h after the first dose and then repeated 3 and 6 months later. Treatment was continued for 15-21 months. Peak plasma total T concentration was achieved at 255 +/- 51 (SEM) min after the first 40 mg dose of TU, 300 +/- 76 min at 3 months, and 293 +/- 103 min at 6 months, the levels remaining elevated above baseline for at least 8 h after a single oral dose. Total T levels were initially high (mean 13.0 +/- 2.5; peak 38.7 +/- 4.2 nmol/L) but dropped significantly at 3 months (mean 8.3 +/- 1.8; peak 23.6 +/- 5.6 nmol/L) and at 6 months (mean 9.2 +/- 1.6; peak 24.8 +/- 3.5 nmol/L) paralleled by a dramatic fall in sex hormone binding globulin (73.9 +/- 18.0 to 35.1 +/- 9.7 at 3 month and 29.2 +/- 6.0 nmol/L at 6 month). Mean concentrations of unbound and free T (non-sex hormone binding globulin-bound T, free T, and salivary T) were below the normal adult range and remained unchanged over the same period. Plasma dihydrotestosterone concentrations were elevated after the first dose (mean 5.4 +/- 1.3; peak 11.0 +/- 2.5 nmol/L), the extent of this rise being less after 6 months (mean 4.1 +/- 0.8; peak 7.1 +/- 1.1 nmol/L) as was the case with mean estradiol (51.5 +/- 8.9 to 38.1 +/- 3.7 pmol/L). Signs of virilization progressed to Tanner stage G3 PH2-3 with testicular volumes increasing to 3-4 mL at 12 months, and G4 PH4-5 with further testicular growth to 6-10 mL at 24 months. Height velocity rose from 3.2 +/- 0.3 cm/yr (pretreatment) to 7.2 +/- 1.0 cm/yr in the first year and was maintained at 7.3 +/- 0.4 cm/yr despite cessation of therapy during the second year. Bone age advanced by 1.1 +/- 0.1 yr at 12 months and a further 0.8 +/- 0.3 yr at 24 months. Predicted adult height remained unchanged. No side effects were observed. Our preliminary data suggest that oral TU is a well accepted, effective, and safe treatment for the initiation of male puberty without disproportionate skeletal maturation. Continued pubertal advance was evident after cessation of treatment in all patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1991

Robust growth hormone (GH) secretion in aged female rats co-administered GH-releasing hexapeptide (GHRP-6) and GH-releasing hormone (GHRH).

Aging is associated with a blunted growth hormone (GH) secretory response to GH-releasing hormone (GHRH), in vivo. The objective of the present study was to assess the effects of aging on the GH secretory response to GH-releasing hexapeptide (GHRP-6), a synthetic GH secretagogue. GHRP-6 (30 micrograms/kg) was administered alone or in combination with GHRH (2 micrograms/kg) to anesthetized female Fischer 344 rats, 3 or 19 months of age. The peptides were co-administered to determine the effect of aging upon the potentiating effect of GHRP-6 on GHRH activity. The increase in plasma GH as a function of time following administration of GHRP-6 was lower (p less than 0.001) in old rats than in young rats; whereas the increase in plasma GH secretion as a function of time following co-administration of GHRP-6 and GHRH was higher (p less than 0.001) in old rats than in young rats (mean Cmax = 8539 +/- 790.6 micrograms/l vs. 2970 +/- 866 micrograms/l, respectively; p less than 0.01). Since pituitary GH concentrations in old rats were lower than in young rats (257.0 +/- 59.8 micrograms/mg wet wt. vs. 639.7 +/- 149.2 micrograms/mg wet wt., respectively; p less than 0.03), the results suggested that GH functional reserve in old female rats was not linked to pituitary GH concentration. The differential responses of old rats to individually administered and co-administered GHRP-6 are important because they demonstrate that robust and immediate GH secretion can occur in old rats that are appropriately stimulated. The data further suggest that the cellular processes subserving GH secretion are intact in old rats, and that age-related decrements in GH secretion result from inadequate stimulation, rather than to maladaptive changes in the mechanism of GH release.

Aging↗
PubMed1991

Intranasal activity of the growth hormone releasing peptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 in conscious dogs.

This series of experiments was conducted to evaluate the growth hormone (GH) releasing activity of intranasally administered His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6, SK&F 110679) in conscious dogs. Intranasal administration of GHRP-6 increased plasma growth hormone levels in the conscious dog in a dose-related manner. Doses of 0.25 and 0.5 mg/kg produced GH levels of 11.3 +/- 4.8 ng/ml and 28.6 +/- 8.0 ng/ml, respectively. Peak levels were observed 15 minutes after dosing and GH levels were elevated for up to 105 minutes after intranasal dosing. Intranasal administration of isotonic saline did not produce any change in basal (negligable) GH levels. When GHRP-6 was given by the intravenous route, a maximal dose of 0.5 mg/kg, produced a peak plasma GH concentration of 60.8 +/- 10.5 ng/ml. Saline had no effect on GH levels when given intravenously. Using the intravenous and intranasal GH response data (i.e., area under the time-response curves), the intranasal bioavailability of GHRP-6 was estimated to be 34.4 to 44.9%. The results of these studies suggest that significant activity and excellent bioavailability can be achieved when GHRP-6 is administered by the intranasal route to conscious dogs. Based on these results, the intranasal activity of GHRP-6 should be evaluated in man. The successful intranasal administration of this peptide in man should provide GH therapy with reduced patient discomfort and better patient compliance when compared to presently available parenterally administered remedies.

Administration, Intranasal↗
PubMed1991

Sex differences in growth hormone (GH) secretion by rats administered GH-releasing hexapeptide.

The purpose of this study was to compare GH secretion after the administration of GH-releasing hexapeptide (GHRP-6) in conscious male and female rats. Plasma GH was significantly elevated in female rats (six of six) compared to male rats (three of six) 15 min after administration of a single sc injection of GHRP-6 (0.5 mg/kg). In male rats, GHRP-6 administration was associated with suppression of episodic GH secretion and desensitization to a second injection administered 6 h later, whereas in female rats, GH secretion occurred after both GHRP-6 injections. After 14 consecutive days of administering GHRP-6 twice per day, mean plasma GH concentrations in males decreased from 110 +/- 91 to 2.8 +/- 0.6 ng/ml (P less than 0.05) and in females increased from 170 +/- 53 ng/ml to 361 +/- 81 ng/ml (P less than 0.05). Desensitization to GHRP-6 in conscious male rats was not observed in pentobarbital-anesthetized male rats, suggesting that GHRP-6 administration enhanced somatostatin release in the conscious state. After 14 consecutive days of GHRP-6 administration, the mean pituitary GH concentration in female rats was significantly lower than that in male rats (5.1 +/- 0.2 vs. 12.9 +/- 1.2 micrograms/mg, respectively). Lower pituitary GH concentrations in females correlated with higher GH secretion after GHRP-6 administration. Desensitization to GHRP-6 in male rats is attributed to neurohumoral factors producing their unusual pattern of episodic GH secretion, and the response is probably not typical of other species.

Animals↗
PubMed1990

Comparisons of plasma and salivary cortisol determinations for the diagnostic efficacy of the dexamethasone suppression test.

The current status of the saliva dexamethasone suppression test (DST) is discussed and results from the literature reviewed. Evidence is presented that demonstrates that the efficacy of the salivary-based test is equal to that of the plasma DST provided that specifically developed radioimmunoassays are used for determination of salivary cortisol. Such evidence relied on measurement of cortisol in 300 matched samples of plasma and saliva provided by patients admitted to a routine psychiatric ward over a 2-year period. The results according to diagnosis (DSM-III categories) were in line with those generally reported. The influence of anticholinergic medication was examined: this had no significant effects on the performance of the plasma or salivary-based DST.

Depressive Disorder↗
PubMed1990

Oral activity of the growth hormone releasing peptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 in rats, dogs and monkeys.

The purpose of this study was to evaluate the growth hormone (GH) releasing activity of orally administered His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 (GHRP-6, SK&F 110679) in rats, dogs and monkeys. Rats were administered GHRP-6 orally by gavage or parenterally through femoral artery catheters. Blood was collected before and after GHRP-6 administration for estimation of plasma GH and comparison of GH changes resulting from enteral and parenteral administration of the peptide. GHRP-6 was administered to dogs intravenously (i.v.) through cephalic vein catheters, intragastrically (i.g.) through esophagostomy tubes or intraduodenally (i.d.) through vascular access ports, and blood was collected before and after peptide administration for estimation of plasma GH. Cynomolgus monkeys were administered GHRP-6 i.g., and blood was collected from abdominal aorta for estimation of changes in plasma GH. Enteral activity of GHRP-6 was observed in all 3 species tested. In rats, ED50's for enteral and parenteral administration of GHRP-6 were 4 mg/kg and 28 micrograms/kg, respectively. Thus in rats, enterally administered GHRP-6 was 0.7% as bioactive as the parenterally administered peptide. In dogs GHRP-6 was slightly less potent than in rats, with ED50's for i.g. and i.v. administration approximately 15 mg/kg and 125 micrograms/kg, respectively. However, enteral potency of GHRP-6 in dogs was 0.8% of parenteral potency, and thus, comparable to that in rats. Additionally, comparison of plasma GH levels following i.g. vs i.d. administration in dogs suggested greater activity by the i.d. route. Monkeys were the species most sensitive to enterally administered GHRP-6, with plasma GH increased in those receiving i.g. doses as low as 0.3 mg/kg and an ED50 of 0.75 mg/kg compared to 4 and 15 mg/kg in rats and dogs, respectively. The results of this study demonstrate that GHRP-6 releases GH when administered directly into the gastrointestinal tract. Although enteral activity is approximately 1% of parenteral activity, GHRP-6 is potent, especially in primates which require relatively low doses to provoke GH release. These data suggest that orally active GHRP-6 may provide a practical therapeutic alternative to parenterally administered peptides such as GHRH, especially if enteral activity is enhanced with appropriate formulation.

Administration, Oral↗
PubMed1990

A non-opioid pattern characterizes inhibition of growth hormone releasing peptide binding by dynorphin-related peptides.

GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-LysNH2; SK&F 110679) is a hexapeptide that specifically releases growth hormone. Although derived from methionine enkephalin, 3H-SK&F 110679 binding profiles suggest that it retains little mu or delta opioid activity. In the present study, dynorphin A was a potent inhibitor of SK&F 110679 binding. However, detailed structure-activity studies using dynorphin-related compounds suggest that the interaction between SK&F 110679 and dynorphin was non-opioid in nature. The non-opioid peptide des-Tyr-dynorphin was virtually as potent an inhibitor of 3H-SK&F 110679 binding as the intact dynorphin peptide. Additionally, the non-peptide, kappa selective ligand U-50,488 was a very weak inhibitor of 3H-SK&F 110679 binding. Since dynorphin but not U-50,488 has been reported to release growth hormone, the present results suggest that a non-opioid dynorphin site participates in SK&F 110679's growth hormone releasing action.

Animals↗
PubMed1990

Dopamine in the cerebrospinal fluid of prepubertal and adult horses.

Catecholamine concentrations (pg/ml) in the cerebrospinal fluid (CSF) of prepubertal (n = 9) and adult (n = 18) horses were determined by radioenzymatic assay. Norepinephrine was low or non detectable in all CSF samples. In contrast, measurable CSF dopamine concentrations were effected by age, reproductive status and exogenous steroid treatments. The concentration of dopamine in the CSF of prepubertal females (733 +/- 92) was greater (p less than 0.05) than the concentration in the CSF of prepubertal males (117 +/- 67). Prepubertal male horses which were treated with testosterone for 5 days (50 mg/day) had elevated (p less than 0.05) dopamine concentrations (2,533 +/- 1,160) in the CSF compared to control males. In adult mares, dopamine was lower (p less than 0.05) in the ovulatory season (25 +/- 10) than during the anovulatory season (200 +/- 101). Daily intramuscular estradiol-17 beta (5 mg/day) injections had no effect (p less than 0.05) on dopamine concentrations in the CSF of seasonally anovulatory mares (250 +/- 35). Further, concentrations of dopamine in the CSF of long-term ovariectomized mares (80 +/- 21) were not influenced (p less than .05) by season. These results suggest that age, sex and gonadal steroids may effect dopamine, but not norepinephrine, concentrations in the brain ventricular system of the equine species. Further, seasonal effects on CSF dopamine concentrations are dependent upon the presence of the ovaries.

Animals↗