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Biomedical subjects

N Iwata

Publications and source records attributed to N Iwata.

At least 217 records · Page 12Linked to original sources
PubMed1981

Hormonal properties of avidin-biotinylinsulin and avidin-biotinylcorticotropin complexes.

In connection with the development of affinity columns (based on the avidin-biotin interaction) for retrieval of peptide and protein hormone receptors, the hormonal properties of a number of avidin-biotinylinsulin and avidin-bioinylcorticotropin complexes were examined. Of particular interest was an evaluation of streptavidin as a ligand for the attachment of biotinylated hormones to solid supports and its possible advantage over SpHPP-avidin (S = succinoylated; pHPP = 3-(p-hydroxyphenyl)propionyl). As concerns binding kinetics using rat liver plasma membranes, streptavidin was found superior to avidin since it does not display apparently nonsaturable binding. Scatchard analyses of the binding of 125I-streptavidin, 125I-S-streptavidin and 125I-SpHPP-avidin to rat liver plasma membranes gave KD value of 6.7, 13.2, and 10.6 nM respectively. The binding was saturable and the unlabeled proteins competed with their labeled counterparts for the membrane binding sites. Biotinylinsulin, attached to either streptavidin or SpHPP-avidin was able to compete for 125I-insulin-binding sites on rat liver plasma membranes though somewhat larger concentrations of the complexes than of insulin were required to achieve comparable inhibition. The ID50 values for insulin and the biotinylinsulin complexes were 5 and 80 nM respectively. Biotinylcorticotropin was found to be a more effective activator of particulate rat adrenal adenylate cyclase when complexed with unmodified avidin than with streptavidin, S-streptavidin or SpHPP-avidin.

Adenylyl Cyclases↗
PubMed1980

EEG change in the conscious rat during immobility induced by psychological stress.

EEG changes in the conscious rat under conditions of stress were quantitatively analyzed. After conditioning the rat to expect an electroshock when placed in the test box, the rat assumed a catatonia-like immobility when placed in the box even though the electroshock was not applied. While in this state relative brain-wave activity over the range 7.5--13.0 Hz significantly increased in the cortex and the hippocampus, but not in the amygdaloid and the caudate nuclei. The immobility accompanied by changes in the EEG disappeared when the animal was returned to the home cage and immediately reappeared after the rat was retransferred to the test box. Diazepam (10 mg/kg, PO), CS-386 (5 mg/kg, PO), nicotinamide (1 mg/kg, IP), and chlorpromazine (10 mg/kg, PO) significantly suppressed the augmented activity under the same stress condition. The difference between drug-induced catatonia or catalepsy and the catatonia-like immobility under the stress condition was discussed.

Animals↗
PubMed1980

Effects of CS-386 and diazepam upon the gastric contraction and excitation of lumbar gamma-motoneurons following stimulation of the hypothalamus in the cat.

Effects of a new minor tranquilizer, CS-386 and diazepam were studied upon the gastric contraction and excitation of lumbar gamma-motoneurons following stimulation of some of the brain structures as well as upon the spontaneous gastric motility in the cat. CS-386 inhibited the hypothalamus-induced gastric contraction with little changes in spontaneous motility at doses of 5 and 10 mg/kg (i.d.). Diazepam inhibited both the hypothalamus-induced contraction and spontaneous motility at these doses. The vagal nerve-induced gastric contraction was suppressed by diazepam (5 mg/kg, i.d.) but not by the same dose of CS-386. Bemegride (5 mg/kg, i.v.) antagonized almost completely the depression caused by 5 mg/kg of CS-386, but not that by a dose of 10 mg/kg or 5 as well as 10 mg/kg of diazepam. Excitation of the lumbar gamma-motoneuron following stimulation of the posterior hypothalamus or the mesencephalic reticular formation was depressed by CS-386 or diazepam (10 mg/kg, p.o.), but not by lower doses. Based on the these evidences, it was suggested that CS-386 could be effective in stress-induced gastric lesions with lower side effects in digestive organs than diazepam.

Animals↗
PubMed1979

[Effects of vitamin B complex in functional changes of the peripheral nerves of alloxan-induced diabetic rats (author's transl)].

Neurophysiological properties of the peripheral nerves of alloxan-induced diabetic rats and effects of vitamin B complex (V) were studied. Alloxan monohydrate was administered to Wistar (38 mg/kg, i.v.) and Sprague-Dawley (SD, 45 mg/kg, i.v.) rats. In Wistar diabetic rats (blood sugar level: more than 400 mg/dl for 6--8 weeks), nerve potentials with 2 peaks were recorded from the tibial and peroneal nerves. The late component had a higher threshold, longer time of recovery from excitation and slower conduction velocities. Large doses of V (B1: 100, B6: 100 and B12: 1 mg/kg, i.p.) administered daily until the experiment inhibited the appearance of the late component. In SD diabetic rats(the same blood sugar content for 6 approximately 8 months), the ventral root potentials had a longer duration, higher threshold and longer time of recovery from excitation. In V administered rats, particularly along with insulin, these changes were prevented. Most efferent fibers of non-treated rats had a refractory period of less than 3.0 msec. The number of fibers with this refractory period was greatly reduced in the diabetic rats. Although rats administered each component of V 100 and V 50 had efferent fibers with similar refractory periods to that of rats in A-S group, those administered V 100 had efferent fibers with significantly shorter refractory periods. Thus, efferent fibers seem to be more sensitive than the afferent ones at the early stages of the long term diabetic state and a large dose of V, particularly along with insulin, depressed these changes.

Action Potentials↗
PubMed1978

Effects of an anabolic steroid and vitamin B complex upon myopathy induced by corticosteroids.

In rats repeatedly treated with dexamethasone, body weight decreased severely, creatine content in urine increased, tetanic contraction of the gastrocnemius muscle decayed easily and twitch tension of the muscle had a slow rise time. In a group of rats given large doses of vitamin B complex along with the anabolic steroid, nandrolone phenylproprionate, all syndromes described above for the dexamethasone-treated rats were prevented, dose dependently by vitamin B complex. The individual components of the vitamin B preparation combined with the nandrolone phenylpropionate partially suppressed the changes induced by dexamethasone. Diphenylhydantoin depressed the slow rise time of twitch tension as effectively as did vitamin B complex with nandrolone phenylpropionate. From the results presented here and facts previously reported it was concluded that the condition of the animals could be well controlled by repeated administration of vitamin B complex with nandrolone phenylpropionate, even though dexamethasone was repeatedly injected.

Animals↗
PubMed1978

[Effects of a new psychotropic agent, CS-430, on the central nervous system of experimental animals (author's transl)].

In rats and rabbits with chronically implanted electrodes CS-430(10-bromo-2, 3, 7, 11b-tetrahydro--11b-(2-fluorophenyl)-oxazolo(3, 2d) [1, 4]benzodiazepine-6(5H)-one) (3 mg/kg, .o.) decreased the slightly awake period and increased the slow-wave sleep period. The onset time of sleep was significantly shortened. In the rat pre-treated with p-chlorophenylalaine (500 mg/kg, p.o.), the awake period was remarkable increased and the slow wave sleep period was considerably decreased at 48 hours after the pre-treatment. In these rats CS-430 given in the same dose decreased significantly the awake peiod and the onset time of sleep and increased the slow wave sleep period. CS-430 raised the threshold of the arousal response with stimulation of the posterior hypothalamus, but not of the mesencephalic reticular formation. These effects of CS-430 were almost as potent as those of nitrazepam (NZP). CS-430 reduced duration of after-discharges following stimulation of the hippocampus, depressed the decerebrate rigidity and inhibited activity of lumbar gamma-motoneurons in anesthetized cats. CS-430 (10 mg/kg, p.o.) inhibited the evoked responses recorded from the proreus gyrus following stimulation of either the baso-magnocellularis of the amygdaloid nuclear or the ventral hippocampus, although such did not inhibit the responses between the olfactory bulb and the pyriform cortex, the thalamus and the sensory-motor cortex. Thus CS-430 has a sleep-inducing effect in animals of almost the same potency as is seen with NZP, and site(s) of the action in the limbic system appear to be specific.

Amygdala↗
PubMed1978

Brainstem acetylcholine sensitive neurons activated by cutaneous impulses in cats.

In order to determine the cholinoceptive mechanism associated with cutaneous inhibition of jaw-closing and lumbar motoneurons, the area related to the inhibition produced by stimulation of the superficial radial nerve was identified by a lesion within the pontomedullary reticular formation and effects of drugs upon neurons were studied within this area. The cutaneous inhibition, as tested by the inhibition of monosynaptic reflex activity of jaw-closing and that of hindlimb spinal motoneurons was completely abolished by lesion of the medial portion of the pontomedullary reticular formation, but was little affected by lesions of the lateral portion. Intravenously administered physostigmine (0.15--0.30 mg/kg) excited 11 of 21 neurons whereas electrophoretic ACh (90 nA) excited 26 and inhibited 4 of 96 brainstem neurons located in this area. Eight of 11 physostigmine, and 4 of 26 ACh excited neurons were reticulospinal neurons with axonal conduction velocities of 20--40 m/sec. From results presented here together with those reported previously, these physostigmine sensitive and ACh excited brainstem neurons, reticulospinal and non-reticulospinal neurons, could be cholinoceptive interneurons of the polysnaptic inhibitory pathway, from the superficial radial nerve to jaw-closing and hindlimb spinal motoneurons.

Acetylcholine↗