Gene/Protein Disease Symptom Drug Enzyme Compound
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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 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

1 Changes of plasma unesterified fatty acid (UFA) and tryptophan concentration in group-housed rats following removal of their cage-mates and the effects of antilipolytic drugs on these changes were investigated. 2 Removal of group-housed 24 h fasted rats but not fed rats from cages resulted in increased plasma UFA concentration in the remaining rats which was associated with significant increases of the proportion of free tryptophan but significant falls of total tryptophan concentration. These rapid changes were not associated with brain tryptophan changes. Plasma tyrosine concentration was unaffected. 3 The fall of plasma tryptophan did not appear to be due to passage into red cells as erythrocyte tryptophan concentration remained unchanged. 4 Plasma UFA concentrations correlated positively and significantly with corticosterone concentrations which were also increased following removal of cage-mates. 5 Plasma UFA increases and tryptophan changes in the fasting rats were both prevented by nicotinic acid or propranolol. Corticosterone concentration was increased by nicotinic acid but unaffected by propranolol. 6 The possible importance of these rapid changes of plasma tryptophan and of their prevention by antilipolytic drugs is discussed.
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PMID:Rapid effects of environmental disturbance on rat plasma unesterified fatty acid and tryptophan concentrations and their prevention by antilopolytic drugs. 116 95

In a series of 3 experiments the effects of 2, 4, 8, or 16 mg/kg d-amphetamine and 4, 8, 16, or 32 mg/kg l-amphetamine on acoustic startle amplitude in the rat were investigated. d-Amphetamine was 4--5 times as potent as l-amphetamine in augmenting startle amplitude. Startle potentiation was associated with vigorous stereotypies but the resultant cage movement could not account for the change in startle. Pretreatment with alpha-methyl-p-tyrosine (100 mg/kg, 1 hr before) had only a slight depressant effect on startle but essentially eliminated augmentation of startle by either d-amphetamine (8 mg/kg) or l-amphetamine (32 mg/kg). d-Amphetamine did not have a direct effect on startle but instead enhanced sensitization produced by the startle stimuli without altering sensitization produced by background white noise or habituation. The results suggest that startle sensitization is enhanced by increased availability of catecholamines and, by virtue of the different potencies of the d- and l-isomers, that dopamine and norepinephrine may affect startle differently.
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PMID:Effects of d- and l-amphetamine on habituation and sensitization of the acoustic startle response in rats. 117 55

Influence of tyramine (Ty) on behavioural changes in mice was studied and the following results obtained: 1) 30 min after Ty (160 mug, i.c.), brain noradrenaline and serotonin levels decreased while dopamine levels increased. 2) When Ty was injected i.c. into isocarboxazide (Iso) pretreated mice, spontaneous motor activity (SMA) measured by photo-cell counters method increased markedly but SMA by wheel cage method decreased. 3) When Ty was injected i.c. into Iso and p-chlorophenylalanine (p-CPA) (400 mg/kg, i.p., daily X 2) pretended mice, SMA measured by photo-cell counters method increased. While, SMA increased from 30 to 90 min after Ty, SMA measured by wheel cage method decreased till 30 min after Ty. 4) When Ty was injected i.c. into Iso and alpha-methyl-p-tyrosine (alpha-MPT) (125 mg/kg, i.p., daily X 2), SMA measured by photo-cell counters method decreased markedly when compared with Iso+saline treated group. When SMA was measured by wheel cage method, a difference between alpha-MPT+Iso-Ty treated group and Iso-saline group was not obtained. 5) When Ty was injected i.c. into p-CPA+alpha-MPT+Iso pretreated mice, SMA measured by photo-cell counters method did not show any increase compared with control group. 6) SMA produced by Iso-Ty in mice pretreated with haloperidol was significantly inhibited. A 50% dose of inhibition was seen with 0.3 mg/kg. From our results, it appears that an increase of SMA induced by Iso+Ty as revealed by the photo-cell counters method may be related to brain catecholamines and serotonin while a decrease of SMA in wheel cage method may be related to brain serotonin.
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PMID:[Effects of beta-phenylethylamine derivatives on the central nervous system. (5) Changes in the volume of spontaneous movement in mice with intracerebral administration of tyramine]. 124 Aug 29

The tetradecapeptide Ac-D-F-L-A-E-G-G-G-V-R-G-P-R-V-OMe, which mimics residues 7f-20f of the A alpha-chain of human fibrinogen, has been co-crystallized with bovine thrombin from ammonium sulfate solutions in space group P2(1) with unit cell dimensions of a = 83.0 A, b = 89.4 A, c = 99.3 A, and beta = 106.6 degrees. Three crystallographically independent complexes were located in the asymmetric unit by molecular replacement using the native bovine thrombin structure as a model. The standard crystallographic R-factor is 0.167 at 2.3-A resolution. Excellent electron density could be traced for the decapeptide, beginning with Asp-7f and ending with Arg-16f in the active site of thrombin; the remaining 4 residues, which have been cleaved from the tetradecapeptide at the Arg-16f/Gly-17f bond, are not seen. Residues 7f-11f at the NH2 terminus of the peptide form a single turn of alpha-helix that is connected by Gly-12f, which has a positive phi angle, to an extended chain containing residues 13f-16f. The major specific interactions between the peptide and thrombin are 1) a hydrophobic cage formed by residues Tyr-60A, Trp-60D, Leu-99, Ile-174, Trp-215, Leu-9f, Gly-13f, and Val-15f that surrounds Phe-8f; 2) a hydrogen bond linking Phe-8f NH to Lys-97 O;3) a salt link between Glu-11f and Arg-173; 4) two antiparallel beta-sheet hydrogen bonds between Gly-14f and Gly-216; and 5) the insertion of Arg-16f into the specificity pocket. Binding of the peptide is accompanied by a considerable shift in two of the loops near the active site relative to human D-phenyl-L-prolyl-L-arginyl chloromethyl ketone (PPACK)-thrombin.
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PMID:The structure of residues 7-16 of the A alpha-chain of human fibrinogen bound to bovine thrombin at 2.3-A resolution. 156 20

The application of 1.2 and 12.0 micrograms/side of the GABAA receptor agonist 3-aminopropane sulphonic acid bilaterally into the nucleus accumbens (Acb) of rats nonsignificantly depressed locomotor activity as assessed in automated Animex activity cages, while the highest dose (60 micrograms/side) significantly stimulated activity. The GABAA receptor antagonists picrotoxinin (0.0625 and 0.125 micrograms/saide) and bicuculline (0.895 micrograms/side) produced forward locomotion around the cage accompanied by a number of other behaviours. The GABAB agonist baclofen (0.023 and 0.092 micrograms/side) induced a short-lasting (18 min) locomotor depression. None of the GABAB antagonists tested (2-hydroxysaclofen 2.6 micrograms/side, two novel beta-(benzo[b]furan) analogues of baclofen 9G or 9H each 6.8 micrograms/side, 4-aminobutylphosphonic acid 1.32 micrograms/side and phaclofen 0.535 and 2 micrograms/side) significantly affected locomotor activity. In rats pretreated with reserpine and alpha-methyl-p-tyrosine, picrotoxinin (0.0625 and 0.125 micrograms/side) did not significantly alter locomotor activity. Furthermore, when picrotoxinin (0.0625 micrograms/side) was combined with either the selective dopamine (DA) D1 agonist SKF38393 or the selective D2 agonist quinpirole, no significant alteration in locomotor function occurred. When SKF38393 and quinpirole were coadministered, significant stimulation occurred which was further enhanced by the addition of picrotoxinin. It is concluded that GABAA receptors, together with D1 and D2 receptors, play a major role in modulating the control of motor function by the Acb of rats.
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PMID:Role of dopamine and GABA in the control of motor activity elicited from the rat nucleus accumbens. 165 18

The effects of heterosexual interactions on the in vivo rate of regional brain monoamine synthesis were examined in the male rat. To this end, the animals were administered an inhibitor of cerebral aromatic L-amino acid decarboxylase, NSD-1015 (100 mg.kg-1 i.p.), and regional brain DOPA and 5-HTP accumulation, over a 15-35 min period of sexual interaction, was compared with the DOPA or 5-HTP accumulation in time-matched home cage controls. Using the DOPA and 5-HTP accumulation as an estimate for the rate of tyrosine and tryptophan hydroxylase activity, respectively, the present results demonstrate: (1) an increased demand on catecholamine synthesis in the neocortex, the amygdala and in the septal area; and (2) an increased dopamine and serotonin synthesis in the ventral striatum (excluding the olfactory tubercle), and in the dorsal striatum.
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PMID:Effects of sexual interactions on the in vivo rate of monoamine synthesis in forebrain regions of the male rat. 178 20

Microinjection of arginine-vasopressin (AVP) into the medial preoptic area of the hypothalamus of the hamster stimulates flank marking, a complex stereotypic motor behavior involved in olfactory communication. Microinjection of an antagonist of AVP, [1-deaminopenicillamine-2-(O-methyl)-tyrosine]arginine-vasopressin, into the same site blocks both the effect of microinjected AVP as well as the natural flank-marking behavior normally elicited by placing a hamster into the recently vacated home cage of another hamster. This finding supports the notion that AVP is a transmitter in the expression of flank marking.
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PMID:Inhibition of flank-marking behavior in golden hamsters by microinjection of a vasopressin antagonist into the hypothalamus. 403 6

The effects of sulfated (CCK-8-SE) and non-sulfated (CCK-8-NS) cholecystokinin octapeptide on striatal dopamine (DA) metabolism have been investigated on mice. CCK-8-NS facilitated the disappearance of striatal DA, measured after synthesis inhibition with 350 mg/kg of alpha-methyl-p-tyrosine. CCK-8-SE did not affect DA disappearance. In vitro uptake of [3H]DA by striatal slices was affected by neither CCK-8-SE, nor CCK-8-NS (10(-5) M). Potassium-induced in vitro release of [3H]DA from striatal slices was significantly increased by 10(-5) M CCK-8-NS: however, CCK-8-SE likewise increased DA release in this model system. Apomorphine-induced (1.0 mg/kg) stereotyped cage-climbing behavior was not affected by CCK-8-SE but was enhanced by CCK-8-NS. This effect could be antagonized by haloperidol, but not by naloxone. The data suggest that CCK-8-NS affects striatal DA release, disappearance and receptor sensitivity in the mouse. Dopaminergic mechanisms should therefore be regarded as a possible mode of action of CCK-8-NS on brain functions.
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PMID:Effects of cholecystokinin octapeptide on striatal dopamine metabolism and on apomorphine-induced stereotyped cage-climbing in mice. 626 May 12

Harmine, a hallucinogen with potent monoamine oxidase inhibitory properties, induced abnormal behavior, including tremor, scratching, head twitch and cage biting, in the mouse. A dose-dependent tremor was produced by all routes of administration of harmine. Although oxotremorine tremor was markedly suppressed by atropine, harmine tremor was unaffected by cholinergic drugs, remarkably inhibited by dopaminergic drugs, antidepressants and diazepam, mildly diminished by p-chlorophenylalanine, markedly augmented by 5-hydroxytryptophan and mildly increased by alpha-methyl-p-tyrosine. These findings suggest that a catecholaminergic (particularly dopaminergic) and serotonergic system imbalance plays an important role in the manifestation of harmine tremor. In view of these characteristics, harmine tremor may be useful as an effective experimental model for the evaluation of antiparkinsonism drugs, along with oxotremorine tremor because of the different mechanism of occurrence. In addition, harmine tremor appears to be useful in characterizing the properties of antidepressant drugs.
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PMID:Pharmacological characteristics of abnormal behavior induced by harmine with special reference to tremor in mice. 697 66


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