Solubilization of gamma-aminobutyric acid receptor from rat brain.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Asano.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The activity of pergolide, an N-propylergoline derivative, has been tested for stimulation of central dopaminergic receptors. Binding to dopamine receptors shows that pergolide acts as an agonist with respect to these receptors. GTP decreases the potencies of dopamine agonists and of pergolide, but not of bromocriptine, to displace [3H]spiroperidol ([3H]Spi) from striatal membrane sites. The GTP-sensitive site labeled by [3H]Spi seems to be localized on intrastriatal dopamine receptors. The potency of dopamine agonists and of pergolide to displace [3H]Spi from striatal receptor sites is reduced in membranes exposed to higher temperatures. Pergolide, but not hitherto-tested dopaminergic ergots, stimulates dopamine-sensitive adenylate cyclase in striatal homogenates. Thus, pergolide, unlike other dopaminergic ergots, acts as an agonist on GTP-sensitive components of [3H]Spi binding and stimulates dopamine receptors linked to dopamine-sensitive adenylate cyclase. The drug also induces turning behavior in rats with 6-OH-dopamine lesions and relieves tremor in monkeys with ventromedial tegmental lesions for a longer time at a lower dose than other tested dopaminergic ergots. Other studies have shown that it is effective in the treatment of patients with advanced parkinsonism.
1. Dry matter and crude protein (nitrogen x 6.25) digestibility of four poultry diets determined by an in vitro method using the intestinal fluid of pigs was significantly correlated with corresponding in vivo digestibility values obtained with hens. 2. The intestinal fluid could be lyophilized and stored for at least 35 d without losing its activity on digestion.
In the present study, the vasocontractile activities of purified oxyhemoglobin, methemoglobin, peroxides of linoleic and arachidonic acid, and hydrogen peroxide were examined in vitro, using the canine basilar artery. It was shown that all of them possess a vasocontractile capacity in a dose-dependent fashion. Fresh canine arterial blood was incubated at 37 degree C for 2 weeks, and the daily change of its vasocontractile capacity and the amount of TBA-reactive substance was studied. This study revealed a gradual and parallel increase in both of them. In a clinical study with 32 SAH patients, the amount of TBA-reactive substance in the CSF was more elevated when angiographically confirmed vasospasm was present. The angiographical and histological responses of the basilar artery to the cisternal injection of 15-HPAA were studied in dogs. The cisternal injection of 15-HPAA (0.2 and 2.0 mg dissolved in bovine serum) caused a mild initial contraction of the basilar artery that lasted about 7 hours. On the third day, a stronger contraction occurred, persisting thereafter until sacrifice. Electronmicroscopy of those arterial samples revealed the disappearance of myofibrils, pyknotic changes of nuclei, and the appearance of vacuoles as well as electron-dense granules in the tunica media. The prolonged arterial contraction was always associated with remarkable destruction of the endothelial cells. These changes were essentially the same as those in experimental and clinical vasospasm. These data strongly indicate that free radical reactions initiated by clot lysis, represented by lipid peroxidation, plays an important role in the genesis of chronic vasospasm in subarachnoid hemorrhage.
Electrophysiological effects of a new antiarrhythmic agent, lorcainide, were studied in the isolated guinea pig ventricular myocardium and were compared with those of disopyramide; some of the experiments were also made by using the canine ventricular myocardium. Both lorcainide and disopyramide selectively depressed the maximum rate of rise of the action potential with little effect on the resting and overshooting potential. The action potential duration tended to be shortened slightly, and the prolongation of the refractory period produced by these agents was only slight. Both agents did not produce the substantial modification of the slow response produced by isoproterenol in the depolarized muscle at the concentrations enough to depress the maximum rate of rise of the action potential. Both agents also produced the marked depression of the rate of the action potential of the canine ventricular muscle, and the conduction velocity measured in the canine false tendon was markedly decreased by both agents. It was concluded that both lorcainide and disopyramide are typical Class I agents according to the classification proposed by Vaughan Williams and that lorcainide is about 10 times (at least 3 times) more potent than disopyramide in this respect.
To elucidate the physiological role of benzodiazepine receptors in convulsion, these receptors were studied in the brain of the Mongolian gerbil (Meriones unguiculatus), an animal model used for the study of epilepsy. Benzodiazepine binding sites in the gerbil brain were demonstrated using [3H]diazepam. The binding was saturable and stereospecific. Benzodiazepines inhibited [3H]diazepam binding to the membranes and their ability to inhibit the binding closely correlated with their potency as anticonvulsants. These results showed that the characteristics of the benzodiazepine receptors in the Mongolian gerbil were similar to those obtained from rat and human brain. Seizures increase the specific binding of [3H]diazepam to the membranes of all regions of the gerbil brain, the most remarkable increase seen in the striatum. Time course studies showed that the increase reached a maximum 10 min after the seizure and the binding returned to the control level within 20 min. The increase in specific [3H]diazepam binding was due almost entirely to shifts in the affinity of [3H]diazepam for its receptors. Thus, the seizures may not be due to changes in the benzodiazepine receptors, and seizures produce an increase in receptor binding, which may be related to a physiological modification of excessive excitation.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The effect of transient bilateral carotid occulsion on levels of free fatty acids, phospholipids, and lipid peroxides in the brain was studied in gerbils. During occulsion, both saturated and polyunsaturated free fatty acids increased strikingly to approximately 11-fold in total by 30 minutes. During recirculation, however, a selectively rapid decrement occurred in arachidonic acid, while saturated fatty acids gradually decreased to their basal levels in 180 minutes. The peroxide level, estimated by a thiobarbituric acid test, did not change during occlusion, but was elevated on reperfusion. Phosphatidylethanolamine content decreased throughout the periods examined. These results do not support a hypothesis that lipid peroxidation is initated during ischemia by the lack of oxygen at the terminus of the mitochondrial respiratory chain. Instead, it is suggested that severe cerebral ischemia disintegrates membrane phospholipids, probably through activation of hydrolytic enzymes, and that overt peroxidative processes take place during reflow by means of restoration of oxygen supply. The peroxidative reactions may indeed, cause additional damage during the postischemic phase.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.