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Query: UNIPROT:Q86TM3 (cage)
29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of para-chlorophenylalanine (PCPA) on mouse killing behavior were examined in natural killer rats. Forty-eight hr after injection, this serotonin synthesis inhibitor, at relatively low doses of 75 and 150 mg/kg, facilitated mouse killing, as indicated by a decrease in latency to attack the mouse. This effect was revealed in a test of satiation, in which five successive mice were presented to the rat, and also in a novel cage situation. Other than the shorter latencies to attack and kill mice, the killing response was similar in topography to the natural kill. The increase in killing after PCPA injection was associated with a reliable reduction in brain serotonin and in 5-hydroxyindoleacetic acid, and the time courses of the behavioral and biochemical changes were generally similar. In contrast to PCPA, injection of the serotonin precursor 5-hydroxytryptophan (5-HTP, 100 mg/kg) reliably lengthened attack and kill latencies in killer rats. In rats pretreated with PCPA, 5-HTP not only reversed this drug's facilitation of killing, but completely blocked killing in 67% of the rats tested. These results strengthen the hypothesis that brain serotonergic neurons are involved in the inhibition of mouse killing.
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PMID:Effects of para-chlorophenylalanine and 5-hydroxytryptophan on mouse killing behavior in killer rats. 15 66

The effects of disturbing groups of 24 hr fasted rats on plasma unesterified fatty acid (UFA) and tryptophan concentrations and brain tryptophan concentrations were investigated. Removing rats from cages rapidly increased plasma UFA and corticosterone and decreased plasma and whole blood tryptophan of cage mates. The disturbance also appeared to influence biochemical values of rats in other cages within the same chamber. Effects specific to individual cages were also suggested. In subsequent experiments 24 fasting rats caged together were rapidly transferred to 24 separate cages and killed at intervals. Plasma UFA rose to a maximum by 12 min and then fell toward initial values. Plasma total tryptophan concurrently fell then rose. Its percentage in the free (ultrafilterable) state, and in some experiments the absolute values of free tryptophan rose then fell. When the latter rise was marked then brain tryptophan and the 5-HT metabolite 5-hydroxyindoleacetic acid rose. Tyrosine changes were negligible. Thus altered brain tryptophan level and 5-HT metabolism may be associated with plasma tryptophan changes caused by brief environmental disturbance.
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PMID:Fatty acid and tryptophan changes on disturbing groups of rats and caging them singly. 56 80

Rats with chronic experimental portocaval anastomosis were hypoactive as indicated by diminished activity in the home cage, during habituation in red light to an observation box and during exposure in white light to an open-field. Food intake and responsiveness to electric shock were also decreased. However, there was an abnormally high frequency of social activity when anastomosed rats were paired together after having been caged singly for 3 weeks. Also, sham-operated rats interacted more with anastomosed rats than they did with other sham-operated animals. Anastomosis also raised brain concentrations of tryptophan, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid. Administration of tryptophan to sham-operated rats increased shock threshold and decreased ambulation in an open-field. Thus, while anastomosed rats are not comatose they do have considerable behavioural abnormalities for which brain tryptophan changes may be in part responsible.
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PMID:Effects of chronic experimental liver dysfunction and L-tryptophan on behaviour in the rat. 71 68

The effects of repeated treatment of rats with 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), 1.0 mg/kg, subcutaneously, twice daily for 7 days, on the stimulation of post- and presynaptic 5-HT1A receptors were examined. The postsynaptic responses, hypothermia and inhibition of the cage-leaving response, evoked by 0.05 mg/kg 8-OH-DPAT, were measured 48 hr after the final injection. Another postsynaptic response, the 5-HT syndrome (flat body posture and forepaw treading) was observed after the third injection of 8-OH-DPAT (1.0 mg/kg s.c.). One presynaptic response examined was the 8-OH-DPAT-induced decrease in the concentration of 5-hydroxyindoleacetic acid (5-HIAA), that indicates a decrease in turnover of 5-HT, due to stimulation of 5-HT receptors on the cell bodies and measured as the ratio of 5-HIAA to 5-HT in the hippocampus, hypothalamus and medulla oblongata. Another presynaptic response was the 8-OH-DPAT-induced decrease in the accumulation of 5-hydroxytryptophan (5-HTP) in the hippocampus and hypothalamus, after inhibition of L-aromatic amino acid decarboxylase by 3-hydroxybenzylhydrazine (NSD 1015), that is due to stimulation of autoreceptors on the 5-HT cell bodies. The kinetic properties of 5-HT1A receptors in the cerebral cortex and hippocampus, hippocampus alone, hypothalamus and medulla oblongata were determined with [3H]8-OH-DPAT. It was found that the postsynaptic effects were markedly attenuated after the treatment, the hypothermic effect already after a single dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Different effects on the responses of functional pre- and postsynaptic 5-HT1A receptors by repeated treatment of rats with the 5-HT1A receptor agonist 8-OH-DPAT. 169 32

The effect of a novel calcium antagonist, KB-2796, on the central dopaminergic system was behaviorally and biochemically studied in mice and compared with that of flunarizine, nicardipine and chlorpromazine. Neither KB-2796 nor nicardipine had an inhibitory effect on apomorphine-induced cage climbing and turning behavior in mice with unilateral lesions in the striatum, even at a high dose of 100 mg/kg p.o. Both drugs slightly inhibited methamphetamine-induced increases in locomotor activity and turning behavior but only at a high dose (100 mg/kg p.o.). KB-2796 and nicardipine did not affect the content of dopamine (DA), norepinephrine, and serotonin, or the content of their metabolites homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC), and 5-hydroxyindoleacetic acid, or the DA turnover rate in the forebrain of mice. However, flunarizine and chlorpromazine inhibited behavioral changes induced by apomorphine or methamphetamine in a dose-dependent manner, increased the content of DOPAC and HVA and accelerated the DA turnover rate in mouse brain. These results suggest that KB-2796 has a negligible effect on the central dopaminergic system.
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PMID:Behavioral and biochemical effects of a novel calcium antagonist, KB-2796, on the central dopaminergic system. 178 92

The effect of short term administration of lithium on the hyperactivity induced by a mixture of d-amphetamine (DEX) and chlordiazepoxide (CDZP) have been examined in the rat and an attempt made to relate this action to changes in brain concentrations of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA). The DEX-CDZP mixture caused a large increase in Y-maze entries (P less than 0.001). Lithium (2 or 4 mEq/kg) attenuated the increase in entries (P less than 0.001) and activity cage locomotion (P less than 0.01) without significantly affecting these parameters in saline-treated rats. However, the increased 5-HT concentration (P less than 0.05) found in the midbrain after the DEX-CDZP mixture was not modified by prior administration of lithium. In control rats lithium had no effect on the level of 5-HT in the cerebellum, cerebral cortex, midbrain or striatum. Levels of 5-hydroxyindoleacetic acid (5-HIAA) in all four brain regions were unaffected by both the DEX-CDZP mixture or pretreatment with lithium. The possible action of the DEX-CDZP mixture on central 5-HT systems and the suitability of the hyperactivity induced by the drug mixture as a model for mania is discussed.
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PMID:Effect of lithium administration on rat brain 5-hydroxyindole levels in a possible animal model for mania. 243 49

Two groups of vervet monkeys were fed, on alternate days, either before or after a morning observation period. This enabled us to determine changes in behavior when the animals were fed a nutritionally balanced breakfast of monkey chow. Feeding did not alter the proportion of behaviors that were social or non-social, but had a marked effect on individual behaviors. Feeding increased active behaviors among the adult animals except for the vervets who were lowest in the social hierarchy in each cage. For some of the individual behaviors that were altered by feeding, the changes were most marked early on in the observation period, when the animals were still feeding. Other behavioral changes were seen only later in the observation period, a time course consistent with a food-mediated change in brain biochemistry. A parallel biochemical experiment showed that feeding decreased the levels of tryptophan and 5-hydroxyindoleacetic acid in the CSF. Our data indicate that feeding can influence both brain biochemistry and behavior. The behavioral changes may be influenced by social and psychological factors as well as changes in brain biochemistry.
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PMID:The effect of breakfast on social behavior and brain amine metabolism in vervet monkeys. 335 16

Brains from Cebus Apella monkeys have been mapped biochemically using a cryo-section technique which enables exact micro-dissectioning of tissue. Two neurotransmitters; noradrenaline (NA) and gamma-amino-butyric acid (GABA) were measured by gas chromatography-masspectrometry technique. In addition biochemical markers reflecting metabolic activity in the dopamine (homovanillic acid, HVA, 3, 4-dihydroxyphenylacetic acid, DOPAC), serotonin (5-hydroxyindoleacetic acid, 5-HIAA), noradrenaline (4-hydroxy-3-methoxy-phenylglycol, HMPG), acetylcholine (choline acetyltransferase, CAT) and GABA (glutamic acid decarboxylase, GAD) transmitter systems were assayed. The distribution of these transmitter markers roughly corresponded to earlier studies in other non-human primates, whereas similar studies on the human brain generally show lower concentrations and enzyme activities. One monkey exposed to severe stress immediately before death deviated from the normal animals with regard to HVA, 5-HIAA, GAD and GABA. For the study of neuroleptic drugs, and notably their neurological side-effects, Cebus Apella monkeys have turned out to be particularly useful. In our laboratory we have employed this species of monkey to develop a model for acute dystonia and tardive dyskinesia (Gunne and Barany 1976, 1979, Barany et al. 1979). As a first step in the topological mapping of brain neuro-chemistry in these animals we here present data from normal monkeys, not treated with neuroleptics. During the ongoing project there was an unplanned "stress experiment" in one monkey, which had a nightly fight with a cage partner and had to be sacrificed the morning after due to severe wounds. The present communication describes a method for obtaining well-defined samples from monkey brains and presents the data on homovanillic acid (HVA), 3.4-dihydroxyphenylacetic acid (DOPAC), 5-hydroxyindoleacetic acid (5-HIAA), noradrenaline (NA), 4-hydroxy-3-methoxy-phenyl glycol (HMPG), choline acetyltransferase (ChAT), glutamic acid decarboxylase (GAD), and gamma-amino-butyric acid (GABA) in discrete regions from 7 drug-naive control monkeys. Also data from the stressed animal are presented.
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PMID:Discrete regional distribution of biochemical markers for the dopamine, noradrenaline, serotonin, GABA and acetylcholine systems in the monkey brain (Cebus Apella). Effects of stress. 615 Jun 1

To study serotonergic involvement in the development of gastric lesions following activity wheel stress, three groups of rats (gastric lesions, no gastric lesions, and home--cage controls) were killed following exposure to the experimental procedures. The brains were dissected into eight specific areas and subjected to analyses for serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) using high performance liquid chromatography with EC detection. Lower levels of 5-HT were found in the midbrain, cortex, and hippocampus of rats with gastric lesions compared to either the no lesion group, subjected to shorter periods of activity--stress, or the home--cage control group. Levels of 5-HT and 5-HIAA were elevated in the pons/medulla oblongata of both the lesion and the no lesion groups compared to the home--cage controls. Corticosterone levels in blood were also significantly elevated in the lesion group. These data on serotonin changes in the CNS suggest a possible role for this neurotransmitter in stress-induced gastric pathology.
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PMID:Serotonergic changes in specific areas of rat brain associated with activity--stress gastric lesions. 619 50

Several theories have linked sleep with change in monoamine activity. However, the use of sleep deprivation to show that changes in sleep generate changes in monoamines (directly or through feedback) has produced inconsistent results. To explore whether longer sleep deprivation, better documented sleep loss, more complete controls or regional brain analyses would produce clear sleep loss-induced change, eight rats were subjected to total sleep deprivation (TSD) by the disk-over-water method for 11-20 days and were guillotined along with yoked control (TSC) and home-cage control (HCC) rats. Brains were removed and dissected to obtain the caudate, frontal cortex, hippocampus, hypothalamus, midbrain and hindbrain (pons-medulla). Tissue sections were analyzed for concentrations of serotonin (5HT), its metabolite 5-hydroxyindoleacetic acid (5HIAA), dopamine (DA), its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), and either norepinephrine or, in the caudate section, the DA metabolite homovanillic acid. The ratios DOPAC/DA and 5HIAA/5HT, which under some conditions are indicators of turnover, were also calculated. Because sleep deprivation time varied across sets of TSD, TSC and HCC rats and not all eight sets were analyzed simultaneously, a repeated-measures ANOVA was performed within sets with HCC, TSC and TSD considered as successive levels of sleep deprivation treatment. In no case did TSD rats have significantly higher or lower values of amines, metabolites or ratios than both HCC and TSC rats. The most common outlying values were for TSC rats. Thus, these results failed to demonstrate sleep loss-induced regional changes in levels of major brain monoamines or their metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sleep deprivation in the rat: XVIII. Regional brain levels of monoamines and their metabolites. 753 62


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