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Biomedical subjects

A Yuwiler

Publications and source records attributed to A Yuwiler.

At least 73 records · Page 4Linked to original sources
PubMed1983

Vasoactive intestinal peptide stimulation of pineal serotonin-N-acetyltransferase activity: general characteristics.

Vasoactive intestinal polypeptide (VIP) stimulates basal serotonin-N-acetyltransferase (NAT) activity in pineals in organ culture and enhances the effects of catecholamines in inducing the enzyme. VIP appears to act postsynaptically; its action is independent of the beta receptor and is dependent upon protein synthesis. Its effects may be mediated by a receptor. The magnitude of the pineal response to VIP varies with age, is greater in pineals maintained in 48-h organ culture than in those in acute culture, and can be detected in pineals from newborns after 48-h organ culture. Intravenous administration of VIP can increase pineal NAT activity in vivo.

Acetyltransferases↗
PubMed1982

Is there a probenecid sensitive transport system for monoamine catabolites at the level of the brain capillary plexus?

Probenecid inhibits the transport of the small monocarboxylic acids lactate and propionate from blood to brain but does not affect the transport of 5HIAA or HVA. Neither lactate, 5HIAA, HVA, nor probenecid itself inhibits probenecid uptake into brain from blood and neither lactate nor 5HIAA itself inhibits 5HIAA uptake. These results indicate first that probenecid inhibits the lactate carrier but is itself not transported by that carrier and second that 5HIAA and probenecid are independently transported from blood to brain by a low affinity system, probably by diffusion. Preloading animals with both tryptophan and probenecid increased the apparent transport of lactate, probenecid and 5HIAA but not the transport of glucose. This indicates that the transport of 5HIAA, lactate and probenecid from brain to blood involves a common, saturable carrier. These two sets of data indicate that either the brain capillary transport system is asymmetric or that probenecid-inhibited transport of monoamine catabolites from brain occurs at sites other than the capillary transport system of the blood-brain barrier.

Animals↗
PubMed1981

Neurotransmitter control of hypothalamic-pituitary-thyroid function in rats.

The possible roles of monoamine neurotransmitters in the regulation of the hypothalamic-pituitary-thyroid axis were examined in the rat. Rats were treated acutely and repeatedly with drugs which are presumed to alter neurotransmitter functional activity. These drugs include neurotransmitter precursors (tryptophan and L-DOPA), synthesis inhibitors (p-chlorophenylalanine and alpha-methyltyrosine), uptake inhibitors (desipramine and zimelidine) and lithium carbonate. The hormone levels measured were hypothalamic TRH and SLI content and serum TSH, T4 and T3. We conclude that augmented serotonergic or dopaminergic activity may inhibit TRH release, but that release from these inhibitions is not sufficient to stimulate TRH release. The release of TRH seems to be mediated by norepinephrine. Lithium treatment results in increased hypothalamic TRH.

Animals↗
PubMed1981

Short-term and repetitive administration of oral tryptophan in normal men. Effects on blood tryptophan, serotonin, and kynurenine concentrations.

Single and repetitive tryptophan loads were consumed by normal, adult male volunteers, and blood concentrations of tryptophan, serotonin, and kynurenine, their time courses, and their distributions within blood were measured. Repeated measures of basal and tryptophan-induced changes in tryptophan and serotonin blood concentrations were characteristic for individual subjects. Tryptophan dose-responsive increases in measured substances returned to basal levels within 24 hours after single tryptophan loads. However, cumulative increases in serotonin concentration in early-morning, predose blood samples were seen following repetitive daily tryptophan administration. Extra-platelet serotonin could be detected in blood samples taken after tryptophan loading and after repetitive daily tryptophan consumption but not in baseline samples taken before short-term loading. Neither platelet number nor size was altered by the loading procedures. Tryptophan loading produced lethargy and drowsiness within 30 minutes of ingestion under all loading conditions. Subjects with the slowest kynurenine response to tryptophan were most behaviorally affected.

Administration, Oral↗
PubMed1981

Peripheral correlates of serotonergically-influenced behaviors in vervet monkeys (Cercopithecus aethiops sabaeus).

The associations among twelve behaviors and three potential peripheral markers of central serotonergic activity were investigated in vervet monkeys (Cercopithecus aethiops sabaeus). The behaviors monitored included approach, heterogroom, rest, eat, avoid, be solitary, be vigilant, huddle, initiate aggress, receive aggress, and engage in sexual behavior. The biochemical parameters measured were whole blood serotonin, plasma free tryptophan, and plasma total tryptophan. Throughout the study period, intraindividual variability in both the behavioral and the biochemical measures was small, although there was substantial interindividual variability in both sets of measures. Free and total tryptophan correlated positively with approach, heterogroom, and eat, and inversely with avoid and be solitary. Whole blood serotonin correlated inversely with avoid and be solitary. These data are compatible with previously reported observations on the behavioral consequences of manipulating serotonergic systems in vervet monkeys and suggest that in normal, drug naive monkeys, free and total tryptophan are better correlates of the central serotonergic activity influencing behavior than is whole blood serotonin.

Animals↗
PubMed1981

Neonatal hormone treatment and maturation of the pineal noradrenergic system: hydrocortisone and thyroxine.

The circadian release of norepinephrine from nerve terminals in the pineal gland drives acetyl-CoA:serotonin N-acetyltransferase (NAT; EC 2.3.1.5) activity in the adult pineal from a daytime low to a nighttime high. In the newborn, enzyme activity is intermediate between the adult's daily extremes and has only a small circadian fluctuation. With age, these fluctuations increase in amplitude until the adult pattern is attained at about days 10-12. Treatment of neonates with thyroxine for the first 3 days of life accelerated, whereas administration of hydrocortisone acetate at birth retarded the developmental decline in daytime serotonin-N-acetyltransferase activity. Maximal differences in daytime enzyme activity of controls and thyroxine-treated animals were seen at day 4 and between controls and steroid-treated pups at day 8. Desipramine treatment increase NAT activity in 8-day-old animals; hydrocortisone-treated animals were least affected. Freshly cultured pineals from steroid-treated animals were more responsive to low, and less responsive to high, concentrations of norepinephrine than glands from thyroxine-treated or control animals. They were also less responsive to isoproterenol both in acute and 48-h organ culture. Pineals from hydrocortisone-treated animals in culture accumulated less exogeneous norepinephrine than glands from controls but released a greater fraction of their content on transfer to fresh medium. Normal and steroid-treated animals released the same fraction of their norepinephrine contents into the medium when reuptake was blocked by desipramine (DMI).

Acetyltransferases↗
PubMed1981

Modification of pituitary-adrenal feedback sensitivity in young rats by neonatal treatment with cortisol.

Neonatal exposure of rats to cortisol acetate was found to alter pituitary-adrenal feedback regulation at 20-25 days of age. Plasma levels of adrenocorticotrophin (ACTH) after ether stress were reduced in cortisol-treated rats pre-treated with 100 microgram corticosterone/100 g body weight, while rats given vehicle neonatally did not show suppression of the ACTH response below levels in animals given saline only or not injected as pre-treatments. Neonatal cortisol increased sensitivity to dexamethasone in inhibition of the stress response; cortisol-treated animals had a reduced plasma corticosterone response to stress 3 h after pre-treatment with 1.25, 2.5, 25, or 250 microgram dexamethasone/100 g body weight, while the stress response in animals given vehicle neonatally was not inhibited by the lowest dosage of dexamethasone. Neonatal cortisol treatment did not affect corticosteroid-binding globulin (CBG) binding capacity in plasma of 25-day-old animals. Thus, neonatal treatment with cortisol appears to increase feedback sensitivity to circulating corticosteroids at 20-25 days of age.

Adrenocorticotropic Hormone↗
PubMed1980

Serotonergic and catecholaminergic influence on thyroid function in the vervet monkey.

Vervet monkeys were pharmacologically treated acutely and with repeated dose loading to alter serotonergic systems to assess the role of serotonin in the regulation of the hypothalamus-pituitary-thyroid axis. Acute L-tryptophan administration failed to alter basal levels of thyroid hormones but did decrease the TRH-induced TSH response. Repeated dose loading of tryptophan or 5-hydroxytryptophan increased blood serotonin and plasma T3 and decreased plasma TSH. The tryptophan hydroxylase inhibitor p-chlorophenylalanine yielded decreased blood serotonin, but did not affect plasma TSH, T4 or T3. The monoamine oxidase inhibitor chlorgyline also resulted in increased blood serotonin, but increased plasma TSH and T4 and decreased T3. These data may be explained by a unitary hypothesis involving central catecholaminergic, rather than serotonergic, control of TRH release. Chlorgyline may produce its effects predominantly by facilitating catecholaminergic stimulation of TRH release resulting in increased TSH and a consequent increase in T4. It is suggested that the effects of tryptophan and 5-hydroxytryptophan result from increases in serotonin levels in the thyroid gland to produce an increase in T3 with a compensatory decrease in TSH via negative feedback. The differences observed between the acute and repeated dose loading studies stress the need for both types of studies before drawing conclusions about the effects of pharmacological manipulations on hormonal levels.

5-Hydroxytryptophan↗
PubMed1980

Amphetamine-induced hyperthyroxinemia.

Four patients had high serum thyroxine (T4) concentrations during periods of heavy amphetamine abuse. After amphetamine was withdrawn, serum T4 returned to normal. Administration of amphetamine to monkeys induced a rise in serum T4; in this model the high T4 level appeared to be caused by increased serum thyrotropin. The mechanism of this effect is unclear but is presumably mediated via the hypothalamus. Awareness of transient hyperthyroxinemia due to amphetamine may allow the physician to avoid confusion with true thyrotoxicosis.

Adult↗
PubMed1979

Hypothalamus-pituitary-thyroid axis interactions with pineal gland in the rat.

We examined in the rat several possible relationships between the pineal gland and the hypothalamus-pituitary-thyroid axis. The pineal gland, the retina, and the hypothalamus exhibited a diurnal rhythm in thyrotropin-releasing hormone (TRH) content with peak values occurring around 1200 h. This rhythm in the hypothalamus was abolished by constant light but was not affected by pinealectomy. Nor did pinealectomy affect hypothalamic TRH content, pituitary content of thyroid-stimulating hormone (TSH) or prolactin; serum levels of (TSH), triiodothyronine (T3), or thyroxine (T4), or serum free-thyroxine index; or free-triiodothyronine index. Melatonin did not affect TSH or prolactin release from the anterior pituitary or TRH release from the hypothalamus in vitro. Isoproterenol did not affect the TRH content of pineal glands in vitro; nor did TRH or T3 affect basal or stimulated activities of serotonin N-acetyltransferase, the presumed controlling enzyme in melatonin production. We found no evidence for significant interactions between the pineal gland and the hypothalamus-pituitary-thyroid axis.

Animals↗
PubMed1979

Effects of neonatal hydrocortisone treatment of pituitary and adrenocortical response to stress in young rats.

Administration of corticosteroids to rat pups within the first several days of life results in retardation of several behavioral, neurophysiological, and biochemical developmental patterns. At 25 days of age, animals treated neonatally with 1.0, 0.5, or 0.1 mg hydrocortisone acetate showed dose-dependent decreases in plasma ACTH following 2.5 min continuous exposure to ether. On day 20, plasma corticosterone values did not differ between these groups 15 min after ether stress, but lower values were seen 60 min after ether in animals treated at birth with 0.5 mg hydrocortisone. At 45--48 days of age, hydrocortisone-treated animals exposed to one of 2 different stressors showed decreased plasma corticosterone response to stress; females had lower corticosterone levels following both stressors, while males showed suppressed corticosterone levels following exposure to the mild (novelty) but not to the intense (ether) stress. These data demonstrate that neonatal exposure to hydrocortisone results in decreased CNS-pituitary responsivity to stress at 20--25 days of age, and that the adrenocortical response to stress in impaired at 45--48 days of age.

Adrenocorticotropic Hormone↗
PubMed1978

Effect of neonatal corticoid treatment on tryptophan and serotonin metabolism.

Glucocorticoid administration to newborn rats leads to the premature induction of hepatic tryptophan oxygenase. This is accompanied by a retardation of the developmental increase in brain serotinin both in regions of serotoninergic cell bodies and in terminal projection areas. The magnitude of the fall in serotonin is relatively small. This appears due, at early ages to the concomitant induction of brain tryptophan hydroxylase and at late periods to retarded development of the blood brain barrier against tryptophan.

Animals↗
PubMed1977

Adrenergic control of pineal N-acetyltransferase activity: developmental aspects.

The activity of pineal N-acetyltransferase in the neonatal rat does not exhibit the large daily rhythm seen in the adult and is intermediate between the low day and high night adult values. These intermediate values appear to result from adrenergic stimulation. Blockade of adrenergic receptors or of catecholamine synthesis results in a decrease in enzyme activity in vivo. In vitro studies provide additional evidence of a completely developed postsynaptic adrenergic control system for pineal N-acetyltransferase activity at birth. Our observations indicate that the appearance of a circadian rhythm in pineal N-acetyltransferase at the end of the first week of life reflects the development of presynaptic mechanisms and structures necessary for the control of catecholamine release and uptake. These events follow the developmental appearance of the postsynaptic mechanisms required to mediate the adrenergic-cycle AMP regulation of pineal N-acetyltransferase activity, which can be detected prior to birth.

Acetyltransferases↗
PubMed1976

Effect of lithium and other alkali metals on brain chemistry and behavior. II. Intracranial self-stimulation behavior.

Rats implanted with bipolar electrodes aimed at the medial forebrain bundle (MFB) were trained to self-stimulate. Six daily injections of 2 mEq/kg of the chloride salts of Li+, Rb+ or Cs+ were administered and the rate of intracranial self-stimulation (ICSS) was recorded. Lithium caused a reversible decrease in ICSS rate, beginning on the second day and returning to pretreatment rate on the fourth day of injections. The decrease was more pronounced in animals with high baseline rate (over 500 responses/10 min) than in low responders. Rubidium enhanced ICSS rate whereas cesium had no effect. These results agree with other accumulating data showing the opposite effects of Li+ and Rb+, but their relevance to effective disorders is not clear.

Affective Symptoms↗