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E Aoki

Publications and source records attributed to E Aoki.

At least 55 records · Page 3Linked to original sources
PubMed1991

[Analysis of muscarinic receptors on rat pancreatic acini by using 125I-quinuclidinyl benzilate and N-[3H]-methylscopolamine].

To analyze muscarinic receptors on rat pancreatic acini, we studied the binding of 125I-quinuclidinyl benzilate (125I-QNB) and N-[3H]-methylscopolamine ([3H]-NMS) to these acini. Binding of 125I-QNB and [3H]-NMS to acini was specific and reversible. 125I-QNB bound to low affinity site, which was not recognised by [3H]-NMS. However, nonspecific binding of 125I-QNB to acini was very high (46%), so 125I-QNB may be inadequate to analyze muscarinic receptor on pancreatic acini. Muscarinic receptors are classified in two groups, M1 and M2, according to affinity of pirenzepine which binds to M1 receptor selectively. Pirenzepine was 530 times less potent than atropine in inhibiting the binding of 125I-QNB, and 250 times less potent than atropine in inhibiting the binding of [3H]-NMS. These results suggest that muscarinic receptors on pancreatic acini are mainly M2 receptors.

Animals↗
PubMed1991

[Broncholithiasis: clinical experience of three operated cases].

Three patients with broncholithiasis had an operation in our hospital. Patient 1 had no history of tuberculosis. She had the pulmonary stones removed bronchoscopically twice. The stones were composed of inflammatory granulomas. Patient 2 had a history of pulmonary tuberculosis. Endoscopical removal of the pulmonary stone was not successful. After 6 days, she coughed up a large amount of blood, and the operation was performed. Patient 3 coughed up blood for 10 years. The amount of blood gradually increased and the operation was performed. All three cases had calcification of the hilar lymph nodes. Broncholithiasis appears to be related not only to pulmonary tuberculosis but also to other chronic inflammatory diseases of the lung.

Adult↗
PubMed1990

Parvalbumin immunoreactivity in the central auditory system of the gerbil: a developmental study.

Changes in parvalbumin-like immunoreactivity were studied during ontogenetic development of the central auditory system of the Mongolian gerbil (Meriones unguiculatus). The nucleus of the trapezoid body contained cells that could be stained on the day of birth while in the superior olivary complex, prominent staining of cell somata was only found at P15 (postnatal day 15). Neurons located in the ventral nucleus, in the dorsal nucleus of the lateral lemniscus and in the inferior colliculus developed parvalbumin immunoreactivity mostly between P11-P15 (ventral nucleus), P15-P19 (dorsal nucleus) and P15-P19 (inferior colliculus), respectively. The accumulation of PV correlates reasonably well with the functional maturation of the neurons in these areas.

Animals↗
PubMed1990

Coexistence of parvalbumin and glycine in the rat brainstem.

The coexistence of glycine- and PV-immunoreactivities was studied immunocytochemically in the nuclei of the superior olive, trapezoid body, cochlea and lateral lemniscus. All of the PV-immunoreactive neurons in the nuclei of the superior olive and trapezoid body were immunoreactive to glycine but not to GABA. In the dorsal cochlear nucleus, PV-positive neurons were sometimes immunoreactive to glycine. In the ventral nucleus of the lateral lemniscus, PV-positive cells were immunoreactive neither to glycine nor to GABA. Consequently, it was concluded that PV-immunoreactivity was distributed not only in the GABAergic neurons, but also in the glycinergic neurons and possibly in wider neuronal populations.

Animals↗
PubMed1990

Appearance of parvalbumin-specific immunoreactivity in the cerebral cortex and hippocampus of the developing rat and gerbil brain.

Developmental changes in the distribution of parvalbumin-specific immunoreactivity in the brain, in particular in the cerebral cortex and hippocampus, were followed immunohistochemically in two different species, the rat and the Mongolian gerbil (Meriones unguiculatus) using an antibody raised against for rat parvalbumin. The gerbil is known to develop its auditory and visual capacity later than rat. In both the rat and gerbil, parvalbumin-specific immunoreactivity appeared after birth in both the cerebral cortex and hippocampus. The timing of the development of expression of parvalbumin varied among different parts of the cerebral cortex. The parietal cortex showed evidence of the earliest expression of parvalbumin whilst the occipital and temporal cortices expressed parvalbumin at a later stage of a development. This feature was common to both the rat and gerbil but occurred at a relatively later stage in the gerbil. The profile of the distribution of parvalbumin in the brain of the developing and adult gerbil was similar to that of the rat, but there were some differences. The frequency of bead-like structures on the dendrites of the parvalbumin-positive cells in the CA1 region of the hippocampus was markedly lower in the gerbil; instead, straight non-beaded fibers which ran vertically into the pyramidal layer were stained. Parvalbumin-positive fibers were also found in the cerebral cortex of the gerbil.

Animals↗
PubMed1990

Cholecystokinin-induced regulation of muscarinic receptor on dispersed pancreatic acini.

We have examined the effect of cholecystokinin octapeptide (CCK-8) on the ability of carbamylcholine (carbachol) to inhibit binding of 3H-N-methylscopolamine (3H-NMS) to muscarinic receptors on dispersed acini from rat pancreas. Carbachol bound to muscarinic receptors on rat dispersed pancreatic acini with two different Kd values. EC50 value for the stimulation of amylase secretion by carbachol was well compatible to the calculated Kd value of high affinity binding site of carbachol, suggesting that high affinity binding sites were mainly involved in the secretory response. Simultaneous addition of CCK-8 decreased the ability of carbachol to inhibit binding of 3H-NMS to acini due to an apparent disappearance of high affinity binding site of carbachol. The effective range of concentrations of CCK-8 for such a receptor regulation, as well as the time course of CCK-8 effect, were in good agreement with those for the restriction of carbachol-induced amylase secretion by CCK-8. These findings suggest that the restriction of carbachol-stimulated amylase secretion by CCK-8 is mainly a result of the disappearance of high affinity binding site of muscarinic receptor as a result of CCK-8 administration.

Amylases↗
PubMed1990

Cholecystokinin downregulates receptors for vasoactive intestinal peptide and secretin in rat pancreatic acini.

We examined the effect of cholecystokinin (CCK) on the receptors for vasoactive intestinal peptide (VIP) and secretin in rat pancreatic acini. CCK decreased the specific binding of 125I-VIP and 125I-secretin by 42 and 51%, respectively. This CCK-induced inhibition was caused by an apparent decrease in the capacity of high-affinity binding sites of VIP and secretin receptors. CR 1409, a specific antagonist of CCK, abolished CCK-induced binding inhibition, whereas 12-O-tetradecanoylphorbol-13-acetate, A23187, and cycloheximide did not affect the binding of the radioligands. Both N2,O2-dibutyryl guanosine 3',5'-cyclic monophosphate (Bt2cGMP) and nitroprusside inhibited the specific binding of 125I-VIP. This inhibition, however, was because of an apparent decrease in the capacity of low-affinity binding sites on VIP receptors. CCK-induced downregulation of VIP and secretin receptors was associated with the diminished acinar response to VIP or secretin-induced adenosine 3',5'-cyclic monophosphate accumulation and amylase secretion, whereas neither Bt2cGMP nor nitroprusside affected VIP-induced amylase secretion. Data suggest that CCK-induced downregulation is mediated by the initial interaction of CCK with CCK receptors followed by some postreceptor process, which appears unrelated to protein kinase C, calcium mobilization, decrease in protein synthesis, or cellular cGMP increases. This downregulation, at least in part, accounts for CCK-induced restricted stimulation of amylase secretion by VIP and secretin.

Animals↗
PubMed1990

Human pancreas scintigraphy using iodine-123-labeled HIPDM and SPECT.

The pancreatic affinity of iodine-123-labeled HIPDM (N,N,N'-trimethyl-N'-(2-hydroxy-3-methyl-5-iodobenzyl)-1,3-propane diamine) ([123I]HIPDM) was studied in 18 cases (5 normal volunteers, 7 cases with pancreas cancer, and 6 with chronic pancreatitis). In the normal cases, the pancreas was visualized in the planar images as early as 3 hr, and again at 20 hr postinjection. Single-photon emission computed tomography (SPECT) performed following 3-hr planar scintigraphy, provided excellent pancreas images without an overlap of activity in the liver or spleen. The mean pancreas-to-liver (P/L) ratio was 1.26 +/- 0.22 in normal controls. With the exception of one case of massive calcification in the pancreas, the entire pancreas could be observed in the cases with chronic pancreatitis, but the P/L ratio was 0.74 +/- 0.15, significantly lower than that of normal cases. Defective areas of the distal portion of the pancreas were clearly seen in those with cancer of the pancreas. The results of our study indicate that [123I] HIPDM may have clinical potential as a human pancreas imaging agent.

Adult↗
PubMed1989

When does GABA-like immunoreactivity appear in the rat cerebellar GABAergic neurons?

The time of appearance of gamma-aminobutyric acid (GABA), a well-known neurotransmitter, during the development of cerebellar GABAergic neurons in rats was investigated immunocytochemically using purified anti-GABA antibody. Sprague-Dawley rats were used at embryonic days 15, 16, 18, 19 and 21, and postnatal days 0, 1, 5, 10, 15, 20 and 30. Golgi cells showed processes and GABA-like immunoreactivity at embryonic day 16 during migration. Purkinje cells were found immunoreactive at embryonic day 18, when they arrived at their destination. The reactivity of the basket cell was already apparent at postnatal day 5, and was thought to appear just after the end of migration. In all of the GABAergic neurons, GABA-like immunoreactivity was visible much earlier than the time of synapse formation and the emergence of their electrophysiological activity described in the literature. In addition, GABA-like immunoreactivity tended to shift from the soma and dendrite into the axon with development.

Aging↗
PubMed1989

[Analysis with immunoreactive CCKs and bioactive CCKs in rat duodenum and brain].

We extracted immunoreactive CCKs from rat duodenum and brain. We fractionated these samples by gel-filtration and analyzed with immunoreactivity and bioactivity of each fraction. 1) Elution profile of CCKs in duodenum and brain was well corresponding to that of bioactive CCKs. 2) Contents of CCKs determined by both RIA and Bioassay in each fraction were well correlated with each other. 3) Apparent molecular weights of CCKs of duodenum calibrated in column chromatography were approximately 2200, 1000 and 800. 4) Apparent molecular weight of CCK of brain seemed to be 1000.

Animals↗
PubMed1988

Glycine-like immunoreactivity in the rat auditory pathway.

From neurophysiological and biochemical studies it has been suggested that glycine can function as a major inhibitory neurotransmitter in the central nervous system of mammals. In the present study, anti-glycine antiserum was obtained from rabbits immunized with glycine conjugated to rabbit serum albumin via glutaraldehyde and purified by affinity chromatography. The antibody thus obtained was found specific for glycine as determined by an enzyme immunoassay system. The immunocytochemical distribution of glycine in the auditory tract and internal ear was investigated with the antibody. In the central auditory pathway, glycine-like immunoreactivity was mainly located in the ventral and dorsal cochlear nuclei, trapezoid body, lateral lemniscus and inferior colliculus. In the labyrinth, immunoreactivity was detected in the vestibular ganglion and the supporting cells of the crista ampullaris and the organ of Corti, but not in the spiral ganglion. These findings suggest an important role of glycine in the auditory and vestibular pathways.

Animals↗
PubMed1988

Effect of AA861, a 5-lipoxygenase inhibitor, on amylase secretion from rat pancreatic acini.

We have examined the effects of 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861), a selective inhibitor of 5-lipoxygenase, on the action of cholecystokinin (CCK) and other secretagogues in the stimulation of amylase secretion from dispersed rat pancreatic acini. AA861 inhibited amylase secretion caused by CCK, carbamylcholine (carbachol), bombesin or calcium ionophore A23187 but failed to affect amylase secretion by vasoactive intestinal peptide or 12-O-tetradecanoyl-phorbol 13-acetate. Inhibition by AA861 of CCK or carbachol-induced amylase secretion was confined to the relatively lower concentrations of these secretagogues. AA861 did not inhibit receptor binding of CCK or alter the cellular calcium mobilization induced by CCK. In kinetic studies, AA861 was effective only on amylase secretion from pancreatic acini incubated with CCK for more than 5 min. Indomethacin, a known inhibitor of cyclooxygenase, did not affect the amylase secretion caused by all secretagogues used. These results indicate that the 5-lipoxygenase pathway of arachidonate metabolism may be involved in the actions of calcium-dependent secretagogues of amylase secretion in rat dispersed pancreatic acini, especially for sustaining stimulation of amylase secretion by CCK.

Amylases↗
PubMed1987

Purification of specific antibody against aspartate and immunocytochemical localization of aspartergic neurons in the rat brain.

The distribution of L-aspartate known as a putative excitatory neurotransmitter in the central nervous system was investigated immunocytochemically in the rat brain. Anti-aspartate antiserum was raised in rabbits using L-aspartate covalently conjugated to rabbit serum albumin with glutaraldehyde as the immunogen and was found to be cross-reactive with an L-glutamate conjugate. Monospecific anti-L-aspartate antibody was successfully purified using affinity gels coupled with several amino acids including L-aspartate and L-glutamate and with the L-glutamate conjugate. Putative aspartergic neurons were generally immunoreactive to the purified antibody, but epithelia of the choroid plexus were also stained. These results show that the antibody is a useful tool for the immunocytochemical demonstration of possible aspartergic neurons in the central nervous system, although the immunochemical expression of L-aspartate not used as a neurotransmitter must be taken into consideration.

Animals↗
PubMed1987

Carbachol regulates cholecystokinin receptor on pancreatic acinar cells.

We have examined the effect of carbamylcholine on the binding of cholecystokinin (CCK) to dispersed acini from rat pancreas. The CCK receptor on pancreatic acini possesses two classes of binding sites. Simultaneous addition of carbamylcholine inhibited binding of CCK to acini due to an apparent loss of high affinity CCK binding sites. Atropine prevented the inhibitory effect of carbamylcholine, whereas calcium ionophore A23187 did not alter binding of CCK. 12-O-tetradecanoylphorbol-13-acetate (TPA) inhibited binding of CCK in the same manner as carbamylcholine. Inhibition by carbamylcholine was reversible and the recovery was time dependent. By contrast, inhibition of binding of CCK by TPA did not reverse after a 60-min incubation without the agent. These findings, at least in part, account for the inhibition of the CCK-induced stimulation of amylase secretion by carbamylcholine. The action of TPA on binding of CCK suggests the possible involvement of the activation of protein kinase C in the inhibition of binding.

Animals↗
PubMed1987

Cholecystokinin-stimulated pepsinogen secretion and cholecystokinin receptors on gastric chief cells in guinea pigs.

We investigated cholecystokinin (CCK) receptors on isolated gastric chief cells from guinea pig. CCK stimulated pepsinogen secretion from chief cells at the same efficacy as that induced by carbamylcholine. Binding of 125I-labeled CCK-33 (125I-CCK) to chief cells was temperature-dependent, and was saturable and reversible at 37 degrees C. Hofstee plots of the ability of CCK-8 to inhibit binding of 125I-CCK showed a linear regression line, suggesting that CCK receptors possessed one binding site. The dissociation constant of the binding site was calculated to be 3.8 x 10(-10) M. The dose-response curve of CCK for pepsinogen secretion was superimposed on that for the binding to its receptors. These results indicated that gastric chief cells from the guinea pig possess CCK receptors that relate closely to the action of CCK involved in pepsinogen secretion.

Animals↗
PubMed1987

Autoantibody against diiodinated tyrosine-gastrin in a patient with Graves' disease.

We describe autoantibodies against iodinated gastrin in a patient with Graves' disease. Values for serum gastrin differed in this case, depending on which of two different radioimmunoassay (RIA) kits was used. RIA with the dextran-coated charcoal method for separation of free tracer gastrin gave a value less than 9.5 pmol/L, whereas the value by a RIA kit by the double-antibody method was 318 pmol/L. The patient's serum contained a binding protein for 125I-labeled gastrin, as detected by Sephadex G-200 column chromatography. The IgG fraction was responsible for the ability of serum to bind 125I-labeled gastrin. Interestingly, of the two possible forms of iodinated gastrins, monoiodinated (MIT) and diiodinated (DIT) tyrosine-125I-labeled gastrin, only the latter bound to patient's IgG. Furthermore, DIT-gastrin, but not gastrin or MIT-gastrin, inhibited the binding of DIT-125I-labeled gastrin. The patient's serum evidently contains autoantibodies against DIT-gastrin that interfere with RIA of gastrin.

Adult↗