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Biomedical subjects

N Barden

Publications and source records attributed to N Barden.

At least 91 records · Page 5Linked to original sources
PubMed1982

Diurnal variations in rat posterior pituitary catecholamine levels.

Diurnal variations, ranging over a twofold difference in concentrations of dopamine, norepinephrine and epinephrine, occur in the rat posterior pituitary gland during a 24-hour period. Highest catecholamine concentrations were seen during daylight hours and low levels reached a nadir 5 h after the onset of darkness. Dopamine concentrations rapidly returned to high levels at the onset of the daylight period, whilst the increase in norepinephrine and epinephrine concentrations was delayed. These diurnal variations in catecholamine content may reflect their modulation of neural lobe peptide secretion.

Animals↗
PubMed1982

Effects of acute and chronic 17-beta-estradiol administration on rhombencephalic, pineal and pituitary catecholamine levels in ovariectomized rats.

In the intermediate-posterior lobe of the pituitary gland there was a 2-fold increase in both dopamine and norepinephrine concentrations 12 h following estradiol injection to ovariectomized rats. Similar, but smaller, increases in dopamine levels were noted 24 h after injection of estradiol and following chronic estradiol treatment, as well as in norepinephrine levels 24 h after estradiol. In contrast, the dopamine content of anterior pituitary decreased following estradiol treatment. Epinephrine levels were not changed in the pituitary gland. No changes in four discrete brain stem regions or pineal gland catecholamine concentrations, with the exception of a small increase in dopamine concentration in the A2 area, were observed following either acute or chronic estradiol administration. Our results suggest that estrogens can selectively modulate catecholamine metabolism in the anterior and intermediate-posterior lobes of the pituitary gland.

Animals↗
PubMed1981

Twenty-four hour rhythm in monoamine oxidase activity in specific areas of the rat brain stem.

Diurnal variations in activities of both type A and type B monoamine oxidase (MAO) in specific areas of the brain stem were investigated in male rats maintained on a 12 h light-12 h dark schedule (06.00 to 18.00 h light). A significant diurnal variation in the activity of both type A and type B MAO was observed in the areas A1, A2 and in the locus coeruleus, but not in the cerebellar cortex. For both type A and type B MAO lowest activities were found during the morning, while highest activities occurred in the late afternoon and the beginning of the night. These results may reflect a role of MAO in the circadian variation of the concentrations of catecholamines in the brain stem.

Animals↗
PubMed1981

Estradiol treatment decreases type A and increases type B monoamine oxidase in specific brain stem areas and cerebellum of ovariectomized rats.

Ovariectomized rats were given either acute (50 micrograms 12 h or 24 h before sacrifice) or chronic (2 micrograms/day for one month) subcutaneous administration of 17 beta-estradiol. The activities of both type A and type B monoamine oxidase (MAO) in the cerebellum and in the areas A1, A2, and locus coeruleus of the brain stem were determined. The activity of type B MAO was increased by acute and chronic estrogen treatment in the different areas studied, whereas that of type A MAO did not change in the areas A1 and A2 and was decreased in the locus coeruleus and the cerebellum. These results indicate a discriminative action of estrogens on different forms of monoamine oxidase.

Animals↗
PubMed1981

Effects of chronic estrogen treatment on dopamine concentrations and turnover in discrete brain nuclei of ovariectomized rats.

We investigated the effects of chronic estrogen treatment in ovariectomized rats on the concentration of dopamine in 33 discrete brain nuclei. In order to assess estrogen's influence on dopamine turnover, some of the rats were administered alpha-methyl-p-tyrosine. Estrogen treatment reduced the concentrations of dopamine in the nucleus accumbens septi, striatum, median eminence, nucleus anterior hypothalami, nucleus suprachiasmaticus, nucleus arcuate IV-V, area ventralis tegmenti, interpeduncular nucleus and nucleus interstitialis striae terminalis. Treatment was without effect on dopamine turnover in all areas studied.

Animals↗
PubMed1981

Changes in the beta-endorphin content of discrete hypothalamic nuclei during the estrous cycle of the rat.

Concentrations of beta-endorphin were measured in discrete brain nuclei of 4-day cycling rats on each day of the estrous cycle. On the afternoon of proestrus beta-endorphin levels were significantly higher in median eminence and suprachiasmatic nucleus, and lower in arcuate nucleus, when compared to levels found on other days of the cycle. These changes coincided with the peak of plasma prolactin, which was blocked by prior administration of naloxone.

Animals↗
PubMed1981

Regional distributions of somatostatin and cholecystokinin-like immunoreactivities in rat and bovine brain.

The distribution of somatostatin- and cholecystokinin octapeptide (CCK-8)-like immunoreactivities in the central nervous system of bovine and rat has been studied using a sensitive and specific radioimmunoassay. The most interesting information is the high concentration of CCK-8 in the various cortical areas in rat and bovine. The nuclei of amygdala contain the highest amount of octapeptide in rat while in bovine brain, this structure contains the second highest concentration after polus frontalis.

Animals↗
PubMed1981

Inhibition of anterior pituitary prostaglandin-stimulated adenylyl cyclase activity by somatostatin.

Rat anterior pituitary gland adenylyl cyclase activity is stimulated by prostaglandins with an order of potency of PGE1 congruent to PGE2 greater than PGA1 much greater than PGB1 congruent to PGF1 alpha congruent to PGF2 alpha which is the same for cAMP accumulation and growth hormone release. Somatostatin inhibited prostaglandin-stimulated adenylyl cyclase with an ID50 of 1.48 X 10(-8) +/- 0.27 X 10(-8) M. GTP also stimulated adenylyl cyclase activity at concentrations greater than 10(-6) M but did not prevent inhibition by somatostatin. These results indicate that at least one action of somatostatin is exerted directly on cAMP formation.

Adenylyl Cyclases↗
PubMed1981

Effect of neonatal thyroid deficiency on the catecholamine, substance P, and thyrotropin-releasing hormone contents of discrete rat brain nuclei.

The effects of neonatal thyroidectomy and thyroid hormone replacement therapy on the development of catecholamine-, TRH-, and substance P-containing neurons in discrete rat brain nuclei were studied. Newborn male rats were rendered hypothyroid by the injection of 125 muCi 131I and, after 45 days, were compared with normal littermate controls and 131I-injected animals subsequently maintained on T4 injections. The peptide or catecholamine content of discrete brain nuclei removed by punches of frozen brain slices was measured by RIA or radioenzymatic assay, respectively. The success of the thyroidectomy was verified by criteria of weight, length, plasma T4, and pituitary GH content. Animals receiving T4 replacement therapy were indistinguishable from normal littermates. Substance P was measured in 32 different brain nuclei and was significantly increased in 19 of these areas in hypothyroid animals. No changes in norepinephrine were detected, and the dopamine content of all but 3 brain nuclei was increased by thyroidectomy. The TRH concentration was drastically reduced in the median eminence of hypothyroid animals and also changed in 3 other extrahypothalamic areas. All of the changes seen in catecholamine, TRH, and substance P distribution in hypothyroid animals were completely reversed by T4 replacement therapy. These results demonstrate changes in brain peptide neurotransmitters during the hypothyroid state and open new vistas for comprehension of biochemical mechanisms underlying central nervous system malfunction.

Animals↗
PubMed1980

Adrenocortical responses to adrenocorticotrophin in the rat.

The time course of plasma adrenocorticotrophin (ACTH), adrenal cyclic AMP, adrenal corticosterone, and plasma corticosterone was measured in male Sprague-Dawley rats whose endogenous release of ACTH had been blocked (1) following rapid injections of 100 and 300 ng ACTH/100 g body weight, i.v., (2) during prolonged infusions at rates of 1, 2, and 4 ng ACTH/min per 100 g body weight, and (3) after termination of 30-min infusions at rates extending from 0.06 to 8 ng ACTH/min per 100 g body weight. Following injections, the time course of the variables is similar to the one simulated from our models of adrenal cortical secretion, including the simulation of an intermediate variable of our models of the adrenal cortex cell which was presumed to correspond to cyclic AMP. However, during prolonged infusions there is an unexpected overshoot of adrenal cyclic AMP content whereas adrenal and plasma corticosterone concentrations rise to a steady-state value without overshoot. The total amount of cyclic AMP gradually increases following the three increasing infusion rates of ACTH whereas similar levels of plasma corticosterone concentrations are reached at steady state; therefore the saturation of the adrenal cortical secretion is due to a step ulterior to cyclic AMP formation in the steroidogenesis. After 30-min infusions, plasma corticosterone concentration reaches its maximal value following a rate of ACTH input which evokes only a 4-fold increase in adrenal cyclic AMP content; however, there is a 250-fold increase of adrenal cyclic AMP with respect to control value following the higher rates of infusion of ACTH.

Adrenal Cortex↗
PubMed1980

beta-Endorphin and met-enkephalins: their distribution, modulation by estrogens and haloperidol, and role in neuroendocrine control.

A single dose of 0.5 micrograms beta-endorphin injected intraventricularly in unanesthetized male rats bearing chronic intraventricular and intrajugular cannulas led to a sevenfold stimulation of plasma prolactin (PRL) levels 10 to 20 min after injection of the peptide, while a dose of 2 micrograms of beta-endorphin led to a comparable stimulation of plasma growth hormone (GH) concentration. Met-Enkephalin was much less potent than beta-endorphin in stimulating PRL and GH release. Naloxone, a specific opiate antagonist, completely blocked the stimulation of GH and PRL release at the doses of 0.5 and 12.5 mg/kg, respectively. beta-Endorphin and Met-enkephalin from 41 discrete brain nuclei were measured by radioimmunoassay (RIA). beta-Endorphin was found in the hypothalamus medial preoptic nucleus, nucleus interstitialis striae terminalis (NIST), nucleus medialis thalami, and periaqueductal gray. Met-Enkephalin was found predominantly in the globus pallidus, NIST, medial preoptic nucleus, nucleus amygdaloideus centralis, and nucleus lateralis hypothalami. Treatment with both estrogens and haloperidol led to differential effects on Met-enkephalin content in various brain nuclei. Estrogen treatment increased Met-enkephalin levels in globus pallidus, NIST, medial and lateral preoptic nuclei, and periaqueductal gray, while a decrease of the Met-enkephalin content in the nucleus amygdaloideus centralis was found. Haloperidol treatment led to a stimulatory effect in striatum, medial and lateral preoptic nuclei, and interpeduncular nucleus.

Animals↗
PubMed1979

Sensitive radioimmunoassay for somatostatin using N-[125I]-Tyr-somatostatin as labelled antigen.

A sensitive radioimmunoassay for somatostatin using N-[125I]-Tyr-somatostatin is described and compared with that using [125I]-Tyr1-somatostatin. The minimum detectable amount of somatostatin using N-[125I]-Tyr-somatostatin as tracer was 0.1 to 0.5 pg, which is approximately 10-fold lower than the lower detection limit of the RIA using [125I]-Tyr1-somatostatin. Moreover, it was found that the shelf-life of N[125I]Tyr-somatostatin was prolonged in comparison with labelled Tyr1-somatostatin. Human pancreatic and gastric extracts displayed immunological similarity to synthetic somatostatin tetradecapeptide.

Animals↗