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)

Effect alterations of methamphetamine by pretreatment of amino acids or their salts on ambulatory activity in mice were investigated to confirm a fact that certain amino acids, particularly monosodium L-glutamate, are added to methamphetamine by the street users, and that the amino acids augment the effect of methamphetamine. The ambulatory activity of mouse was measured by a tilting-type round activity cage of 25 cm in diameter. The amino acids or their salts tested were monosodium L-glutamate, monosodium L-aspartate, gamma-amino-butyric acid, L-alanine, L-lysine hydrochloride and L-arginine hydrochloride. A single administration of each chemical at doses of 1 and 2 g/kg i.p. did not induce a marked change in the ambulatory activity in mice. Methamphetamine 2 mg/kg s.c. induced an increase in the ambulatory activity with a peak at 40 min after the administration, and the increased ambulatory activity persisted for 3 hr. The ambulation-increasing effect of methamphetamine was augmented by the pretreatment of monosodium L-glutamate and monosodium L-aspartate at 30 min before the methamphetamine administration, while attenuated by the pretreatment of L-lysine hydrochloride and L-arginine hydrochloride in a dose-dependent manner. Gamma-aminobutyric acid and L-alanine did not affect the effect of methamphetamine. Similar augmentation and attenuation in the ambulation-increasing effect of methamphetamine were induced by the pretreatment of sodium bicarbonate 0.9 g/kg i.p. (urinary alkalizer) and ammonium chloride 0.07 g/kg i.p. (urinary acidifier), respectively. The urinary pH level was elevated by the administration of monosodium L-glutamate, monosodium L-aspartate and sodium bicarbonate, and decreased by L-lysine hydrochloride, L-arginine hydrochloride and ammonium chloride. Gamma-aminobutyric acid and L-alanine did not elicit a marked change in the urinary pH level. The present experiment confirms the fact in human that monosodium L-glutamate augments the effect of methamphetamine. Moreover, the present results suggest that monosodium salts of acidic amino acids augment, and conversely monohydrochloric salts of basic amino acids attenuate the effect of methamphetamine. The alterations of the ambulation-increasing effect of methamphetamine may be due to the urinary excretion rates of the drug through changes in the urinary pH level after the administration of amino acids or their salts.
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PMID:Effect alteration of methamphetamine by amino acids or their salts on ambulatory activity in mice. 687 1

Effect of GABA on the motor activity of rats of the first month of life was studied in conditions of free behaviour in the maternal cage. It has been found that at the age of 1-10 days the injection of GABA increases, and at the age of 11-30 days decreases both the general motor activity and the grooming activity. It is suggested that a possible mechanism of the observed effect of GABA consists in the deepening of presynaptic inhibition, which results, during the earlier stages of postnatal ontogeny, in intensifying the autorhythmical activity of spinal motor centres, whereas during the later stages, when the autorhythmical activity of the spinal cord is replaced by reflex excitatory mechanisms, in depressing the latter.
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PMID:[Effect of GABA on motor activity in the rat during the early postnatal period]. 706 53

Although isolated rat pups emit ultrasonic vocalizations (USVs), those kept warm and undisturbed in the home cage with their littermates seldom do. Drugs were administered to 10-day-old pups in the home cage to determine whether pharmacological agents can elicit USV in this familiar environment. Ten-day-old Wistar rats were injected with U50,488, a highly selective kappa opioid agonist; pentylenetetrazol (PTZ), an anxiogenic drug that binds at the GABA-benzodiazepine receptor complex; or naltrexone (NLX), an opiate receptor blocker, and then were returned to their littermates in the home cage. U50,488 increased USV and activity levels, lowered body temperature, and disrupted contact with littermates. PTZ raised activity levels but had a smaller effect on vocalization rates and did not alter temperature or contact with littermates. Behavioral measures and body temperature were unchanged by NLX.
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PMID:Ultrasonic vocalizations are elicited from rat pups in the home cage by pentylenetetrazol and U50,488, but not naltrexone. 828 Mar 94

Attacks of sustained dystonia of the limbs and trunk can be initiated by handling or mild environmental stimuli (e.g. new cage) in mutant (gene symbol dtsz) Syrian golden hamsters. The severity of the dystonic syndrome in these mutant hamsters is age-dependent, with a peak at weaning (21 days of age) and a second peak at about 30-40 days of age. Spontaneous remission occurs at an age of about 70 days. The syndrome in hamsters is thus similar to transient paroxysmal dystonia in children. In the present experiments, it was examined whether dystonic hamsters exhibit age-dependent differences in susceptibility to drugs which affect GABA (gamma-aminobutyrate)ergic, glutamatergic or dopaminergic functions. After acute administration, the GABA-elevating drug aminooxyacetic acid was significantly less potent in attenuating the severity of dystonic attacks at 21 days than at 31 days of age. Similar but less marked age-dependent differences in antidystonic activity were found for phenobarbital and diazepam. In contrast to these GABAmimetic drugs, the NMDA receptor antagonist CGP 37849 (DL-[E]-2-amino-4-methyl-5-phosphono-3-pentenoic acid) or the dopamine receptor antagonist haloperidol had about the same antidystonic potency at both 21 and 31 days of age. Chronic treatment of dystonic hamsters with aminooxyacetic acid, starting at 21 days of age, did not alter the time course or the severity of dystonia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alterations in pharmacological sensitivity of GABAergic but not dopaminergic and glutamatergic systems during ontogenesis in dystonic mutant hamsters. 838 61

Changes in release and uptake of [3H]5-HT and [14C]GABA were compared in slices taken from the hippocampus and frontal cortex of rats, left undisturbed in their home-cages, or exposed for 5 min to the elevated plus-maze or social interaction tests of anxiety. Exposure to the plus-maze decreased cortical GABA function (shown by decreased release) and increased hippocampal 5-HT function (shown by increased K(+)-evoked release but more markedly by decreased uptake). Compared with undisturbed home cage controls, only the high light, familiar condition of the social interaction test resulted in a significant increase in K(+)-evoked release of both [3H]5-HT and [14C]GABA from the hippocampus. All four social interaction test conditions resulted in increases in cortical uptake of [3H]5-HT and all but the high light, unfamiliar condition increased cortical uptake of [14C]GABA. Analysing the two factors manipulated in the social interaction test, unfamiliarity with the test arena resulted in increased uptake of hippocampal [3H]5-HT and decreased cortical [14C]GABA, whereas an increase in the level of light decreased the cortical uptake of [14C]GABA. The results show that changes in presynaptic function occur rapidly in response to a brief exposure to animal tests of anxiety. However, only the increased hippocampal release of 5-HT is likely to be causally linked to anxiety and the results show that this cannot be the sole explanation.
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PMID:Social interaction and elevated plus-maze tests: changes in release and uptake of 5-HT and GABA. 847 17

Rats were pretreated for 11 months with vehicle or with chronic haloperidol (HAL), administered either continuously (in the drinking water) or intermittently (via weekly injections). During this time the animals were habituated to an enclosed tube and periodically monitored by a computerized video device which measured their oral movements. The rats were then withdrawn from chronic HAL and bilateral cannulae were implanted in the ventrolateral striatum (VLS) and substantia nigra (SN). One week later oral movements were observed in an open cage and then measured by the computerized video device following bilateral infusions into VLS of the muscarinic agonist pilocarpine or the dopamine D1 agonist SKF38393, or following infusions of the GABA antagonist bicuculline into SN. Agonist infusions into VLS had different effects depending upon the prior regimen of chronic HAL. Infusions of pilocarpine into VLS led to an exaggeration of the distinctive oral movement form which follows continuous HAL but an attenuation of the different oral syndrome in the intermittent chronic HAL animals. Infusions of SKF38393 into VLS had similar, but considerably smaller effects. Infusions of bicuculline into SN did not induce either effect. These results indicate differences exist in either striatum or its output circuitry in the neurochemical mechanisms which mediate the different oral movement forms induced by different chronic neuroleptic regimens.
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PMID:Oral movement patterns induced in rats by local infusions into striatum depend upon the regimen of prior neuroleptic exposure. 854 32

In vivo microdialysis combined with HPLC-EC analysis was used to monitor extracellular glutamate and GABA in the medial nucleus accumbens of Lister hooded rats during acquisition and expression of a conditioned emotional response. Footshock paired with tone (acquisition of conditioned emotional response) causes a significant decrease in extracellular glutamate during the period of footshock followed by a marked, but short lasting increase when the rats return to their home cage. Expression of the conditioned emotional response on exposure to the contextual cue produces no change in glutamate during exposure to the contextual cue, but a short lasting increase after. Thus, both the conditioned emotional response and footshock are associated with marked, but short lasting, increases in extracellular glutamate in the nucleus accumbens which, in both cases, occurred after the aversive stimuli, i.e., when the rats are returned to their home cage. In contrast, when control rats are exposed to the testing box without giving footshock there is an increase in extracellular glutamate during the exposure period and this is accompanied by exploratory behaviour. The conditioned emotional response (contextual cue), footshock and exposure of the control rats to the test box all resulted in increased extracellular GABA during exposure to the test situation. These results suggest that increases in extracellular glutamate in the medial nucleus accumbens caused by the conditioned emotional response or footshock are probably associated with relief from, rather than response to danger.
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PMID:Extracellular glutamate in the nucleus accumbens during a conditioned emotional response in the rat. 858 69

Neural connections from the hippocampus and nucleus accumbens to the subpallidal area have been implicated by behavioral observation. The locomotor activity recorded in an automated activity cage increased substantially after the bilateral injection of carbachol, a cholinergic agonist, into the dentate gyrus of the hippocampus, and this increase of activity was reduced significantly after the injection of glutamate antagonist into the nucleus accumbens. On the other hand, this hyperactivity elicited by the injection of carbachol was also reduced by the injection of GABA into the subpallidal area. In another observation, increased locomotor activity was recorded following the injection of dopamine into the nucleus accumbens. However, the increase of locomotor activity induced by dopamine was attenuated by the injection of GABA into the subpallidal area. These observations suggest that neural connections from hippocampus and nucleus accumbens to the subpallidal region may contribute to locomotor activity.
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PMID:Neural connection from hippocampus to nucleus accumbens and the subpallidal area and their contribution to locomotor activity. 869 95

In step-down test, diazepam (1 mg.kg-1 po, 1 h before training) was shown to significantly impair memory acquisition in mice. But piracetam (200 mg.kg-1 ip, 1 h before training) was found to improve the diazepam-induced impairments of learning. By photocell cage method, piracetam showed no significant inhibitory effect on the diazepam-induced spontaneous motor activity in mice. In Y-maze test, Glutamic acid (0.1 microgram, icv, 3 min before training) significantly improved learning in normal mice and the amnesic effect of GABA and diazepam were completely antagonized by Glutamic acid and piracetam (200 mg.kg-1 ip, 1 h before training). These results suggest that increasing GABA-ergic neuronal transmission is unfavorable to learning and memory, but increasing Glu-ergic transmission is contrary to the former. It seemed that the presence of Glu/GABA system in the brain could regulate learning and memory.
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PMID:[Antagonism of piracetam on the amnestic effect of diazepam in mice]. 876 67

The time- and temperature-dependencies of binding are overviewed for the benzodiazepine, GABA and convulsant binding sites of the GABAA receptor-ionophore complex. Kinetic separation of the dissociation phases of a beta-carboline inverse agonist demonstrated the heterogeneity of its binding sites. The kinetics and thermodynamics of benzodiazepine binding alone do not correlate with ionophore function. The majority of the data suggest that agonist- and antagonist-preferring conformations exist for GABAA receptors. The high affinity binding of GABAA antagonists (SR 95531 and bicuculline) corresponds to the (super) low affinity binding of GABA. The correlation between the thermodynamic parameters of binding and efficacies common for GABAA and glycine receptor agonists and antagonists supports the functional similarities of these anionophore complexes. Binding kinetics of the bicyclic cage convulsants show several correlations with ionophore function because the convulsant sites are most intimately coupled to the ion channels. Kinetic interactions of the convulsant sites with the binding sites of benzodiazepines, GABA and central depressants have revealed several pharmacologically relevant allosteric GABAergic modulatory effects. Arrhenius analysis, Hammond's postulate and transition state theory were applied for the dissociation of convulsants. A kinetic model of interconvertible multiaffinity states of the convulsant sites shows correlations with the functional states of the GABAA ionophore.
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PMID:From kinetics and thermodynamics of GABAA receptor binding to ionophore function. 893 44


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