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Biomedical subjects

E Itoga

Publications and source records attributed to E Itoga.

At least 19 recordsLinked to original sources
PubMed1985

Immunohistochemical localization of neurotensin and beta-endorphin in the rat anterior pituitary gland.

Nakane's enzyme-labeled antibody technique revealed that cells containing neurotensin-like immunoreactivity were widely distributed in the anterior lobe of the pituitary body. Immunohistochemical studies on serial sections showed that a part of neurotensin positive anterior lobe cells contained beta-endorphin-like peptide simultaneously. The results show that beta-endorphin and neurotensin occur together in certain pituitary cells and this is an evidence of coexistence of more than one peptide within one anterior pituitary cell.

Animals↗
PubMed1984

Ontogenetic development of the specific [3H]nitrendipine binding sites in the rat whole brain.

[3H]Nitrendipine binding sites are localized much more in the synaptosomal membrane than in the mitochondrial and microsomal membranes. To use a whole homogenate (crude membrane fraction) for the purpose of observing nitrendipine binding sites in the synaptosomal membrane instead of P2-B fraction has its reason. The Bmax of specific nitrendipine binding in the rat brain increases linearly until it reaches to the adult level after birth. High affinity binding at early developmental stages shifts to low affinity after the 7 day postnatal stage. Autoradiographically, nitrendipine binding sites are rich in the interpeduncular nucleus, olfactory bulb, hippocampus and superior colliculus in an adult rat. In autoradiography, the density in the hippocampus increases gradually until it reaches the adult level at the 28 day postnatal stage.

Animals↗
PubMed1983

Studies on biological actions of dimethyl sulfoxide in familial amyloidosis.

DMSO was therapeutically administered to patients with FAP and in about half of the patients there was some clinical improvement. Urinary proteins were analyzed biochemically and immunochemically before and after DMSO administration in seven cases of amyloidosis. As the results, increased excretion of various proteins of different molecular weights in the urine was observed depending on cases and examined organs. The in vitro effects of DMSO on amyloid proteins were examined. DMSO-degraded amyloid proteins showed void-volume materials and lower molecular weight components on Sephadex G column elution profiles as did guanidine-degraded amyloid protein. Among various denaturating or reducing agents, DMSO is the least potent in dissolving amyloid fibrils into prealbumin-related proteins.

Adult↗
PubMed1983

Morphological study of neurotransmitter receptors in the rat brain.

1. We performed light and electron microscopic autoradiography of GABA and opiate receptors using 3H-muscimol and 3H-DAMA. 2. Selection of development method is important for electron microscopic autoradiography. The authors obtained silver grains in a pattern precisely localized to the cytoplasmic membrane, i.e., the receptor site by means of EAA development. 3. We observed 3H-muscimol binding site in the neuropiles of the cerebellar molecular layer and the substantia nigra ultrastructurally. Receptor sites labeled with silver grains are located not only on the synaptic regions but also on the plasma membranes of the dendrites and axons not corresponding to synaptic sites. 3H-DAMA binding sites in the caudate nucleus and the amygdaloid nucleus are noticed on the plasma membranes of the axons, dendrites, and nerve cell somas, some corresponding to synapses, others not. There are still problems to be solved in the autoradiographical observation of neurotransmitter receptors. Nevertheless, this technique is very important in observing the morphological relationship between transmitters and their receptor sites.

Animals↗
PubMed1982

The binding of [3H]nitrendipine to receptors for calcium channel antagonists in the heart, cerebral cortex, and ileum of rats.

The binding properties of the calcium channel antagonist, [3H]nitrendipine, were investigated in homogenates of the rat cerebral cortex, heart and ileum. The specific component of [3H]nitrendipine binding was consistent with mass-action behavior and was characterized by a high affinity dissociation constant in the range of 0.1-0.3 nM. A variety of other calcium channel antagonists inhibited the binding of [3H]nitrendipine with Ki's that agree generally with the ability of these drugs to block contractions of cardiac and smooth muscle. The inhibition of [3H]nitrendipine binding by other dihydropyridines was consistent with competitive antagonism whereas the inhibition caused by verapamil and D600 resembled negative heterotropic cooperativity. Consistent with this latter postulate was the observation that the kinetics of [3H]nitrendipine binding are altered by verapamil, with both the association rate and the dissociation rate being increased. La+3 and several divalent cations caused an inhibition of [3H]nitrendipine with the rank order of potency being Cd+2 greater than La+3 greater than Ni+2 greater than Co+2 = Mn+2 greater than Mg+2 = Ba+2 greater than Ca+2.

Animals↗
PubMed1982

Binding experiments of muscarinic acetylcholine and dopamine receptors in human brains with emphasis on a case of striatonigral degeneration.

In the regional distribution of I-3H-quinuclindinyl benzilate (3H-QNB) binding in human brains of neurologically unaffected cases, it was highest in the caudate nucleus which was followed by the putamen, amygdala, cerebral corteces and olfactory bulb and lowest in the substantia nigra. As to the regional distribution of 3H-spiroperidol binding in human control brains, it was highest in the caudate nucleus and was followed by the cerebral corteces, amygdala and lowest in the cerebellar cortex. In a case of striatonigral degeneration (SND), 3H-QNB binding in the putamen and thalamus was lowered and 3H-spiroperidol binding was decreased in the putamen, frontal and parietal corteces, Ammon's horn, amygdala and substantia nigra as compared to human brains of control cases. These results were noteworthy since no pathological changes were observed in the thalamus, cerebral corteces, amygdala and Ammon's horn in this case. The 3H-spiroperidol binding was increased by injection of 6-hydroxydopamine (6-OHDA) into the substantia nigra of rat brains by 17% as compared to the contralateral intact side. Conversely, 3H-spiroperidol binding was decreased by injection of kainic acid (KA) into the striatum of rat brains by 43% as compared to the contralateral intact side. This meant that dopamine receptors labelled by 3H-spiroperidol were at least partially localized at the postsynaptic site of the nigrostriatal dopamine neuron.

Animals↗
PubMed1981

Discrete regional distributions of thyrotropin releasing hormone (TRH) receptor binding in monkey central nervous system.

Thyrotropin releasing hormone (TRH) directly influences central nervous system (CNS) function, independent of its pituitary action. Although these CNS effects have been behaviorally characterized, information is not yet available on the precise regional distribution of its receptor. TRH receptor binding was examined in the monkey CNS by the radioreceptor assay for clarifying the site of TRH action. TRH was bound to brain tissue membranes via high-affinity (Kd = 5.9 x 10(-9) M) and low-affinity (Kd = 11.2 x 10(-8) M) components. TRH receptor binding varied dramatically throughout the monkey brain, with more than 40-fold variation. The limbic system contained the greatest amount of binding. The next highest areas were the cerebral cortex, hypothalamus, interpeduncular nucleus and periaqueductal gray matter of the midbrain. Receptor binding was very low or not detectable in the medial thalamus, cerebellum, brain stem, spinal cord and white matter. These data suggest that TRH has an effect on the CNS via limbic system, cerebral cortex and midbrain.

Animals↗
PubMed1980

A pedigree of amyotrophic chorea with acanthocytosis.

Several pedigrees of which some members showed a clinical syndrome consisting of mental changes, choreatic involuntary movements, limb muscles atrophy, and acanthocytosis have been reported in the United States and the United Kingdom. Such a case and some of the family members who had such abnormalities as acanthocytosis, hypo-beta-lipoproteinemia, convulsions, and confusion was observed. Results of biochemical analysis of catecholamines and their metabolites in CSF and urine showed an elevated value of norepinephrine in CSF and increased urinary secretion of DOPAC. The authors propose to designate this syndrome an amyotrophic chorea with acanthocytosis.

Athetosis↗