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Biomedical subjects

G A Mason

Publications and source records attributed to G A Mason.

At least 91 records · Page 5Linked to original sources
PubMed1983

Interactions of neurotensin with brain dopamine systems: biochemical and behavioral studies.

Intracisternal (i.c.) injection of neurotensin (NT) to rats or mice attenuated the locomotor hyperactivity induced by d-amphetamine, methylphenidate or cocaine, but not the increased activity induced by apomorphine or lergotrile. The reduction of methylphenidate-induced locomotor activity by i.c. NT was not due to an increased drug metabolism because i.c. NT did not change plasma methylphenidate concentrations. These actions of NT are distinct from those of the dopamine receptor antagonist haloperidol, which blocked the locomotor hyperactivity induced by all five stimulant drugs in rats. A further difference between NT and neuroleptics was demonstrated by the observation that i.c. NT did not block apomorphine-induced stereotypic behavior. In vitro, NT did not displace [3H]spiperone from its binding sites in homogenates of either the striatum or nucleus accumbens from rat brain. Moreover, i.c. injection of NT did not alter the subsequent in vitro binding of [3H]spiperone to membranes of the nucleus accumbens or striatum. In addition, NT did not alter basal or dopamine-stimulated adenylate cyclase activity in homogenates of the nucleus accumbens or striatum. However, i.c. injection of NT produced a significant increase in the concentrations of homovanillic acid, a major dopamine metabolite, in the nucleus accumbens, olfactory tubercles and striatum. In addition, the concentration of dihydroxyphenylacetic acid was increased in the nucleus accumbens and olfactory tubercles after i.c. NT. Peripheral injection of haloperidol produced qualitatively similar effects on dopamine metabolism, but the effects of haloperidol, unlike those of i.c. NT, were attenuated by apomorphine injection. Taken together, these data indicate that centrally administered NT affects certain brain dopamine systems without interacting directly with those dopamine receptors labeled by [3H]spiperone, coupled to adenylate cyclase or mediating the pharmacological effects of apomorphine.

Adenylyl Cyclases↗
PubMed1982

Interaction of neurotensin with prostaglandin E2 and prostaglandin synthesis inhibitors: effects on colonic temperature in mice.

Neurotensin (NT) administered intracisternally (i.c.) to adult mice produced a marked hypothermia while prostaglandin E2, administered by the same route, produced hyperthermia. When administered concurrently the effects of the two substances were neutralized. The prostaglandin synthesis inhibitors, indomethacin and acetylsalicylic acid, were injected subcutaneously 30 min prior to i.c. administered NT and/or thyrotropin-releasing hormone (TRH). Both inhibitors failed to potentiate the hypothermia induced by NT or alter its antagonism by TRH in mice kept at 26 degrees C. When mice were kept at 6 degrees C, pretreatment with indomethacin, but not acetylsalicylic acid, potentiated NT-induced hypothermia and prevented its antagonism by TRH. Because indomethacin inhibits synthesis of prostaglandins within the central nervous system (CNS) as well as in peripheral organs while acetylsalicylic acid acts only in the periphery, it appears that NT-induced hypothermia in a cold environment is enhanced by a reduction of prostaglandins in the CNS.

Animals↗
PubMed1982

The TRH test in normal subjects: methodological considerations.

Changes in serum TSH, PRL, GH, T3, T4 and FT4-Index after injection of TRH (500 micrograms i.v.) were measured in 13 normal women and 12 normal men. In both sexes, TSH and PRL concentrations rose significantly over baseline after TRH injection (p less than 0.01). The PRL response, but not the TSH response, was significantly lower in men than in women. Although most TSH and PRL peaks occurred about 30 min after TRH injection, a delayed PRL peak was seen in four men. Thyroid hormones also rose significantly after TRH, with T3 peaking earlier (60 min) than T4 and FT4-Index (greater than or equal to 180 min). The TSH area under the curve correlated well with the TSH peak value (p less than 0.001), with the TSH value at 30 min (p less than 0.001), with the delta max TSH (p less than 0.001), and with the delta TSH measured at 30 min (delta 30 TSH) (p less than 0.001). The PRL area under the curve correlated well with the PRL peak value (p less than 0.005) and with delta max PRL (p less than 0.05) in both sexes, but the PRL value at 30 min was significantly correlated with the area under the curve only in women (p less than 0.005). These data indicate that in both sexes a baseline sample and a 30-min sample provide an excellent index of the entire TSH secretory response to TRH; the PRL response to TRH is clearly related to sex; and the 30-min value of PRL in women, but not in men, is an adequate measure of the PRL secretory response to TRH.

Adult↗
PubMed1982

Subchronic dietary exposure of rats to chlordecone (Kepone) modifies levels of hypothalamic beta-endorphin.

Rats were exposed for extended times to low doses of chlordecone (1 and 6 ppm in the diet). After 105 days of exposure of female rats to this diet, levels of circulating prolactin and growth hormone were not significantly altered, but at the higher dose of chlordecone, hypothalamic beta-endorphin levels were selectively reduced. Since no changes were seen in pituitary levels of beta-endorphin of treated rats, chlordecone had some regional specificity. Levels of dopamine, serotonin, and their metabolites were unchanged in the caudate nucleus of female rats exposed to chlordecone. Thus, low levels of chlordecone appear to selectively affect hypothalamic beta-endorphin suggesting the hypothalamus may be especially sensitive to this neurotoxicant. The gestationally and lactationally-exposed female offspring of these rats showed a major increase in the levels of growth hormone at 100 days of age. However, other parameters assayed remained unaltered. These consisted of biogenic amines within the caudate nucleus, pituitary and hypothalamic met-enkephalin and circulating prolactin, growth hormone, and estrogen.

Animals↗
PubMed1981

Marked reduction in gonadal steroid hormone levels in rats treated neonatally with monosodium L-glutamate: further evidence for disruption of hypothalamic-pituitary-gonadal axis regulation.

Serum levels of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, estradiol-17 beta and testosterone were determined in adult rats that were treated in the neonatal period with monosodium L-glutamate (MSG) which has previously been shown to reliably produce destruction of arcuate nucleus perikarya. MSG-treated males had significantly smaller accessory sexual organs (seminal vesicles and ventral prostate) and tests and had significantly lower serum concentrations of FSH and testosterone than sex-matched controls. MSG-treated females had significantly lower serum concentrations of LH, FSH and estradiol-17 beta. Prolactin levels of MSG-treated rats were no different than sex-matched controls. This marked reduction in gonadal steroid levels (decreases 68%) and inappropriately low gonadotropin levels further characterizes the deficit of feedback regulation in the hypothalamic-pituitary-gonadal axis in MSG-treated rats.

Animals↗
PubMed1981

Osmotic fragility of erythrocytes of lemurs.

Erythrocytes of five species of lemurs were found to be significantly more susceptible to lysis by osmotic stress than erythrocytes of man. In one lemur species, Lemur macaco, the red cell osmotic fragility profile resembles that of human subjects with hereditary spherocytosis.

Animals↗
PubMed1981

Neurotensin-induced antinociception in mice: antagonism by thyrotropin-releasing hormone.

Neurotensin (NT), administered intracisternally to mice, produced significant dose-dependent antinociception in three analgesic tests: tail immersion, hot-plate and acetic acid writhing. Naloxone (1-5 mg/kg), an opiate antagonist administered i.p. 20 min before NT administration, did not significantly alter NT-induced antinociception in any of these tests; naloxone did significantly reverse beta-endorphin-induced antinociception. However, centrally and peripherally administered thyrotropin-releasing hormone antagonized NT-induced (but not beta-endorphin-induced) antinociception. Equimolar doses of another tripeptide (Pro-Leu-Gly-NH2; melanostatin) did not alter the effects of NT. The data obtained in this study confirm NT-induced antinociception, provide further evidence that NT does not activate naloxone-sensitive opiate receptors and demonstrate that this brain effect of NT is antagonized by thyrotropin-releasing hormone. These findings therefore support the hypothesis that NT and thyrotropin-releasing hormone are functional antagonists in the central nervous system.

Analgesics↗
PubMed1977

Codominant autosomal inheritance of polymorphic red cell acid phosphates of lemurs and some properties of the enzymes.

Red cell acid phosphatase phenotypes of 207 captive animals of the genera Lemur, Hapalemur, and Prophithecus were determined by starch gel electrophoresis and phosphatase-specific staining. In Lemur fulvus, three phenotypes, designated A, B, and AB, were observed. In each of the species L. catta, L. macaco, L. mongoz, and L. variegatus, a single phenotype was observed, In Hapalemur griseus, three phenotypes were found: A,B, and AB. In Propithecus verreauxi, a single phenotype was found. Examination of breeding records in conjunction with the results of the electrophoretic analyses supports the conclusion that the erythrocytic acid phosphatases in this group of nonhuman primates are the products of at least two codominant autosomal alleles. There is a wide range of specific activities of the acid phosphatases as determined by colorimetric assays. The values range from 60.6 micronmoles of p-nitrophenol released per gram of hemoglobin per 30 min in Lemur catta to 429.1 micronmoles in Propithecus verreauxi. The enzymes of L. fulvus and P. vereauxi were purified approximately 400-fold, and Michaelis-Menten constants were determined on the purified preparations. For L. fulvus phenotype A, Km = 0.8 mM; for L. fulvus phenotype B, Km = 0.8 mM; and for P. verreauxi, Km = 0.6 mM; the substrate in each case was p-nitrophenylphosphate.

Acid Phosphatase↗
PubMed1977

Automated fluorometric analysis of galactose in blood.

In galactosemia, prevention of mental retardation depends on early recognition of the disorder and institution of dietary restriction of galactose. We describe an automated fluorometric micromethod for galactose in whole blood spotted on filter paper. Galactose is oxidized by galactose oxidase to D-galacto-hexadialdose and H2O2 and measured as the highly fluorescent condensation product of homovanillic acid formed when H2O2 is acted upon by horseradish peroxidase. The procedure is 10-fold more sensitive than colorimetric procedures for galactose and is not hampered by the nonspecific fluorescence from endogenous NADPH that is encountered in methods in which galactose dehydrogenase is used. At a sampling rate of 40/h with a sample-to-wash ratio of 1/2, carryover is negligible, reproducibility is excellent, and 80% of steady state is achieved. Analytical recovery of added galactose was 95%. The method has the requisite sensitivity and accuracy for quantification of galactosemia and galactosuria in milkfed newborn infants and genetic evaluation of families of patients.

Autoanalysis↗