Effect of immobilization stress on serotonin content and turnover in regions of the rat brain.

Sprague-Dawley rats were stressed by immobilization from 30 to 300 minutes and the effects on serotonin (5-HT) and 5-hydroxy-indoleacetic acid (5-HIAA) content were determined in the cerebral cortex, diencephalon, striatum, hippocampus and the brain stem. In a subsequent study 5-HT turnover rate in these brain areas was estimated by measuring 5-HIAA accumulation 0, 30, 60 and 90 minutes after probenecid. The content of 5-HIAA and the turnover rate of 5-HT were significantly increased in the cerebral cortex shortly after the onset of immobilization. The content of 5-HIAA in the brainstem was increased by immobilization although 5-HT turnover rate was not increased. Short term increases in 5-HIAA content were observed in the striatum and hippocampus. However, no significant changes in 5-HT turnover rate were observed in either of these 2 brain areas. Immobilization did not affect 5-HIAA content or 5-HT turnover in the diencephalon. The sensitivity of the serotonergic system in the cerebral cortex to immobilization stress suggests that this brain region could be used in future studies of the interrelationships between stress and the brain serotonergic system.     

Effect of West Nile Virus on serotonin concentration of mouse brain

Summary Following intracerebral inoculation of West Nile Virus into suckling mice, the serotonin content of the brain tissue decreased 15% after 48 h and by 78% after 72 h.

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Effet du virus du Nil de l'Ouest sur la concentration en serotonine du cerveau de souris

Résumé L'inoculation intracérébrale du virus du Nil de l'Ouest chez le souriceau allaité, entraîne une diminution du contenu en serotonine du tissus cérébral de 15% après 48 h et de 78% après 72 h.

     

Thermoregulatory responses of a hibernator to hypothalamic and ambient temperatures

Local cooling or heating of the hypothalamus of yellow bellied marmots elicited appropriate thermoregulatory responses to maintain body temperature. Increases in EMG, heart rate, and oxygen consumption were observed during hypothalamic cooling. Conversely, hypothalamic heating generally decreased thermogenic parameters toward minimal levels. Normothermic marmots retained thermoregulatory heat production throughout the year although loss of vasomotor regulation seemed to occur as they prepared for hibernation. The relationship between manipulated changes in hypothalamic temperature and induced changes in oxygen consumption was linear. This proportional relationship at one air temperature (15 °C) was parallel and displaced to the right of that relationship obtained at a lower air temperature (10 °C). These results are consistent with the hypothesis that hypothalamic regulation of body temperature in normothermic marmots is similar to that of nonhibernating mammals, although vasomotor regulation may differ.     

Tryptophan and serotonin turnover rate in the brain of genetically hyperammonemic mice

An investigation was made into the effects of hyperammonemia on the metabolism of brain serotonin (5-HT). The animal model used was the sparse fur (spf) mouse, which possesses an inborn error of the urea cycle, i.e. an abnormal form of ornithine transcarbamylase. Several indoles were measured in brain and plasma using liquid chromatography with electrochemical detection coupled to an u.v. detection (LCEC-u.v.). In the mutant mice, plasma total tryptophan (TRP) was higher when compared with the controls, while plasma free-TRP portion was unchanged. In these animals, brain TRP was increased whilst the 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels were significantly higher in the hypothalamus and midbrain. Experiments with NSD-1015 (100 mg/kg i.p.) indicated that the 5-hydroxytryptophan (5-HTP) synthesis rate was increased in the hyperammonemic mice. Pargyline experiments (100 mg/kg i.p.) confirmed the enhanced brain 5-HT turnover rate in the spf mice. In addition, these experiments led to the conclusion that hyperammonemia does not affect the various rate constants. After administration of NSD-1015, TRP level slightly increased in the spf mouse brains, while it was stationary in those of the controls. This result could indicate an increased activity of hepatic TRP-pyrrolase in the hyperammonemic mice. Valine (VAL) administration (200 mg/kg i.p.) reduced brain TRP content in the two kinds of mice, but its effect was of shorter duration in the spf when compared with the control. Comparison of brain tryptamine level indicated a slight but not significant increase in the mutant mice. The data reported here indicate that hyperammonemia may affect peripheral TRP metabolism with consequences upon brain 5-HT synthesis, which could promote certain neurologic disorders.     

Effect of etimizol on behavioral responses, brain serotonin concentration and plasma corticosteroid levels

The influence of ethymisol on behavioural reactions was studied on 100 albino rats in the "open field" and "passive avoidance" tests. It was shown that a 5 mg/kg dose of this neurotropic drug with synaptic effect, changes behavioural reactions, lowers the general emotional stress and emotional memory of the electro-cutaneous stimulation. Simultaneously the level of corticosteroids in the blood plasma significantly rises, while the serotonin content in the hypothalamus decreases. A direct correlation between the changes in the emotional stress and the content of corticosteroids in blood plasma is noted. The effects of ethymisol partially persists after adrenalectomy. Ethymisol in optimal doses may be used for regulation and lowering of emotional stress.     

Effect of L-tryptophan and restraint stress on hypothalmic and brain serotonin turnover, and pituitary TSH and prolactin release in rats.

The dose response and time course effects of L-tryptophan and restraint stress on the metabolism of serotonin and release of thyroid stimulating hormone (TSH) and prolactin (PRL) were tested in male rats. Both treatments increased serotonin turnover in the hypothalamus (H) and remaining brain tissue minus the cerebellum (brain) as determined by enhanced accumulation of serotonin following monoamine oxidase (MAO) inhibition. L-tryptophan but not restraint stress elevated levels of tryptophan in the cerebellum. Both L-tryptophan and restraint stress inhibited TSH release and stimulated PRL release. These findings indicate that enhanced rates of serotonin turnover produced by L-tryptophan and physical restraint are associated with inhibition of TSH and stimulation of PRL release from the anterior pituitary.     

Effect of different environmental factors on the brain during animal ontogenesis

The aim of the work was to follow in rats, mice and dogs effects of different environmental factors in certain postnatal periods on the weight indices of the brain. The following factors influenced the brain development: light deprivation, excess of nutrition during suckling period, excess of information. Changes in weight indices are more pronouned if the time of the effect coincides with that of intensive growth and maturation of the brain structure (N. I. Dmitrieva, 1966). Duration of the effects proportionally increases their influence.     

Effect of monensin on performance in growing ruminants reared under different environmental temperatures

To evaluate the effect of monensin on the performance of growing cattle under different environmental temperatures, 24 male calves (81.9 ± 7.7 kg mean weight and 100 days old) were distributed in a 2 × 2 factorial arrangement, contrasting 0 or 85 mg monensin/animal per day at 24.3 or 33.2 °C (environmental temperatures). Monensin supplementation increased weight gain (P=0.036), improved feed efficiency (P=0.040), increased ruminal concentrations of volatile fatty acids (VFA; P=0.003) and decreased the molar proportion of butyrate (P=0.034); all effects irrespective of environmental temperatures. A temperature-dependent monensin effect was detected on nitrogen retention (P=0.018) and N retained:N absorbed ratio (P=0.012). Animals fed monensin retained higher N amounts than those of the non-supplemented ones when the environmental temperature was 33.2 °C. Environmental temperature and monensin supplementation showed an interaction effect on urine N concentration (P=0.003). Temperature did not affect N excretion in monensin-fed animals, but increased N excretion in the non-supplemented ones. Monensin increased the crude protein (CP) digestibility (P=0.094) for animals at both temperatures. In conclusion, monensin changes the metabolism of the heat-stressed animals by increasing rumen VFA concentration, digestibility and protein retention, thus improving food use and weight gain.     

Gamma-hydroxybutyrate increases tryptophan availability and potentiates serotonin turnover in rat brain

Gamma-hydroxybutyrate (GHB) is both a therapeutic agent and a recreative drug. It has sedative, anxiolytic and euphoric effects. These effects are believed to be due to GHB-induced potentiation of cerebral GABAergic and dopaminergic activities, but the serotonergic system might also be involved. In this study, we examine the effects of pharmacological doses of GHB on the serotonergic activity in rat brain. Administration of 4.0 mmol/kg i.p. GHB to rats induces an accumulation of tryptophan and 5-HIAA (5-hydroxyindole acetic acid) in the frontal cortex, striatum and hippocampus without causing significant change in the tissue serotonin content. In the extracellular space, GHB induced a slight decrease in serotonin release. The tryptophan and 5-HIAA accumulation induced by GHB is mimicked by the GHB receptor agonist para-chlorophenyl-transhydroxycrotonate (NCS-356) and blocked by NCS-382 (6,7,8,9-tetrahydro-5-[H]-benzocycloheptene-5-ol-4-ylidene acetic acid) a selective GHB receptor antagonist. GHB induces the accumulation of either a derivative of or [3H]-tryptophan itself in the extracellular space, possibly by increasing tryptophan transport across the blood-brain barrier. The blood content of certain neutral amino-acids, including tryptophan, is also increased by peripheral GHB administration. Some of the effect of GHB could be reproduced by baclofen and reduced by the GABAB antagonist CGP 35348. Taken together, these results indicate that the GHB-induced stimulation of tissue serotonin turnover may be due to an increase in tryptophan transport to the brain and in its uptake by serotonergic cells. As the serotonergic system may be involved in the regulation of sleep, mood and anxiety, the stimulation of this system by high doses of GHB may be involved in certain neuropharmacological events induced by GHB administration.     

Effect of monensin on mineral balance in growing ruminants reared under different environmental temperatures

To test the effect of monensin on the mineral balance of growing cattle under different environmental temperatures, 24 male steers were assigned in a 2 × 2 factorial arrangement, contrasting 0 and 85 mg monensin/animal per day at 24.3 and 33.2 °C (environmental temperatures). Monensin effect was directly modulated by the environmental temperature: it increased apparent retentions of P (P=0.066), Na (P=0.005) and K (P=0.003), at the higher temperature and decreased these apparent retentions at the lower temperature, as compared with non-supplemented animals. Monensin increased fecal Ca (P=0.037), and urinary P (P=0.002), Na (P=0.003), K (P=0.014), Mg (P=0.051) and Zn (P=0.091), with higher concentrations of these minerals in animals held at 24.3 °C and lower concentrations in those at 33.2 °C, as compared with non-supplemented animals. Monensin decreased serum Mg (P=0.001) and increased serum Zn (P=0.071) in animals at 33.2 °C and increased serum Mg and decreased serum Zn at 24.3 °C. Irrespective of temperature, monensin increased both apparent absorption (P=0.058) and apparent retention (P=0.093) of P, and also urine Cu (P=0.085). Environmental temperature modulated monensin effects on mineral balance. Monensin increased apparent retention of several minerals in animals under heat stress.     

Effects of short- and long-term neuroleptic treatment on brain serotonin synthesis and turnover: focus on the serotonin hypothesis of schizophrenia

Short-term (90 min) administration of haloperidol (2 mg/kg), or chlorpromazine (10 mg/kg) increased the activity of tryptophan hydroxylase as well as the levels of 5-hydroxytryptamine (serotonin) and 5-hydroxyindoleacetic acid in mid-brain of rats. The chronic neuroleptic treatment (21 days) produced more pronounced changes in all parameters related to serotonin synthesis and turnover. The activity of tryptophan hydroxylase in mid-brain was further augmented; the levels of 5-hydroxytryptamine and 5-hydroxyindole-acetic acid were significantly elevated not only in mid-brain, but also in several other discrete regions examined. These data suggest that neuroleptics enhance the synthesis and utilization of brain serotonin. The role of brain serotonergic neurons in the pathophysiology of schizophrenia is further considered.     

Effects of nutritional stress on brain tyramine concentration and dopamine turnover

This is an investigation of the effect of nutritional stress at various ages on the levels of thep- andm-isomers of tyramine in the caudate nucleus of the rat. For comparison, the effects of nutritional stress on the concentration and turnover of dopamine were also studied. Nutritional stress induced in pre-weaning (3 weeks of age) or post-weaning (up to 9 weeks of age) rats resulted in a decrease in the concentration ofp-tyramine and an increase in the concentration ofm-tyramine in the caudate nucleus. Dopamine concentration or turnover in the caudate nucleus was not affected by pre-weaning undernutrition; in the olfactory tubercles, however, a significant decrease was observed in dopamine turnover, calculated from the decrease in homovanillic acid levels after monoamine oxidase inhibition. The results suggest the changes observed are dependent on the availability of the amino acid precursorsp- andm-tyrosine and their competition towards aromatic-l-amino acid decarboxylase.     

Differential effects of long-term hypoxia on norepinephrine turnover in brain stem cell groups.

The influence of long-term hypoxia on noradrenergic cell groups in the brain stem was assessed by estimating the changes in norepinephrine (NE) turnover in A1, A2 (subdivided into anterior and posterior parts), A5, and A6 groups in rats exposed to hypoxia (10% O2-90% N2) for 14 days. The NE turnover was decreased in A5 and A6 groups but failed to change significantly in A1. The NE turnover was increased in the posterior part of A2 and remained unaltered in the anterior part. In normoxic rats, the hypotensive drug dihydralazine induced a reverse effect, namely increased NE turnover in anterior A2 and no change in posterior A2. The neurochemical responses to hypoxia were abolished by transection of carotid sinus nerves. The results show that long-term hypoxia exerts differential effects on the noradrenergic cell groups located in the brain stem. Peripheral chemosensory inputs control the hypoxia-induced noradrenergic alterations. The A2 cell group displays a functional subdivision: the posterior part is influenced by peripheral chemosensory inputs, whereas the anterior part may be concerned with barosensitivity.     

Effect of ethanol on the concentration of serotonin in the brain of the rat and the excretion of 5-hydroxyindoleacetic acid

It is found that serotonin content in the brain areas and heart of rats with low alcohol motivation decreases after 5 months of chronic consumption of 48% ethanol solution in a dose of 4 g/kg; in animals with high alcohol motivation serotonin content decreases only in the hypothalamus. Under chronic alcoholization for 1 and 12 months no considerable changes were found in serotonin level of the studied tissues. 60 min after intraperitoneal administration of 20% ethanol solution in a dose of 3 g/kg in intact animals there occurs an increase of serotonin content in the brain hemispheres and heart and its decrease in the hypothalamus; in rat with low alcohol motivation after taking ethanol for 5 months this administration evokes a decrease of serotonin content in the hypothalamus and truncus cerebri; in rats with high alcohol motivation--its decrease in the hypothalamus. Excretion of 5-oxyindoleacetic acid with urine decreases 10 months after alcohol intoxication. When rats were not given ethanol after its chronic taking for 3 months serotonin oxidation was intensified for the first day, which was not observed after 7-month alcoholization of animals.