Biomedical subjects

H Ishimaru

Publications and source records attributed to H Ishimaru.

At least 73 records · Page 4Linked to original sources

PubMed1994

Aspects of hypothalamic neuronal systems in VMH lesion-induced obese rats.

To clarify neuronal disturbance in the hypothalamus reflecting the development of obesity in ventromedial hypothalamic nucleus (VMH)-lesioned rats, we investigated the contents of neurotransmitters in the hypothalamus after pretreatment by microwave irradiation, contents of neurotransmitter metabolites in third ventricle fluid and catecholamine contents in the adrenal gland. The hypothalamic contents of norepinephrine (NE) and dopamine (DA) were selectively decreased, but acetylcholine (ACh) and serotonin (5-HT) levels were not changed from those in controls. In the lateral part of the hypothalamus, also, a significant decrease of NE content was detected. On the other hand, NE and DA metabolites, MHPG, DOPAC and HVA were increased in the third ventricle fluid in VMH lesion-induced obese rats. Wet weight and content of epinephrine in the adrenal gland were decreased, though the content of NE was preserved. These results indicate that a disturbance of NE and DA neurons in the hypothalamus is involved in the development of VMH lesion-induced obesity. In addition, an increment of the activities of NE and DA systems in the central nervous system as a whole and some irregularity in the sympatho-adrenal system might contribute to VMH obesity.

Adrenal Glands↗

PubMed1994

Striatal extracellular choline and acetylcholine in choline-free plasma rats.

Choline (Ch)-free plasma rats were induced successfully by intravenous (IV) injection of choline oxidase (ChO) (16). However, brain acetylcholine (ACh) levels were not affected by ChO treatment, maintaining the same levels as those in controls, although brain Ch levels were significantly decreased. To clarify the reasons for this, in vivo microdialysis was carried out in the treated rats' striata. The ChO treatment induced not only a 70% decrease of extracellular Ch levels but also a 40% decrease of extracellular ACh levels, reflecting the amount of ACh released from cholinergic terminals. In addition, plasma-bound Ch levels and choline acetyltransferase (CAT) and acetylcholinesterase (AChE) activities in the brain were examined in the rats receiving ChO treatment. No significant differences from controls were observed in these levels. The results suggest that: approximately 70% of striatal extracellular Ch is physiologically supplied from circulating plasma-free Ch; the inhibition of ACh release is related to the maintenance of tissue (intraneuronal) ACh levels under the condition of halting of the supply of free Ch from blood to the brain; if there is a compensative supply of free Ch from de novo synthesis, autocannibalism, or plasma-bound Ch, this may be supplied within neuronal cells, because the level of extracellular-free Ch maintained its depressed level even 11-14 h after ChO treatment.

Acetylcholine↗

PubMed1994

Hypothalamic cholinergic systems in mercuric chloride-induced hyperglycemia.

The roles of hypothalamic neuron mechanisms in regulation of blood glucose were studied in rats. Microinjection of HgCl2 and neostigmine into the third ventricle under anesthesia caused marked hyperglycemia. To characterize the effective neurons in the hypothalamus, tissue contents of neurotransmitters and extracellular levels of metabolites in the ventromedial part of the hypothalamus were measured by microwave irradiation and in vivo brain microdialysis. HgCl2 increased both the content and the extracellular levels of choline. Neostigmine increased the acetylcholine content. In both instances, norepinephrine (NE) and dopamine (DA) content were decreased. Extracellular levels of DA metabolites were increased. On the other hand, serotonin content and extracellular serotonin metabolite level remained constant. In medulloadrenalectomized and atropine-coadministered rats, no marked hyperglycemia was induced by HgCl2 or neostigmine. These results show that the muscarinic cholinergic system participates in the HgCl2-induced central hyperglycemic effect through the function of the adrenal medulla. NE neurons may also be related to hypothalamic glycoregulation, and DA neurons might modulate the regulatory mechanisms.

Animals↗

PubMed1994

Cloning, sequencing, and expression of bacteriophage BF23 late genes 24 and 25 encoding tail proteins.

Two bacteriophage BF23 late genes, genes 24 and 25, were isolated on a 7.4-kb PstI fragment from the phage DNA, and their nucleotide sequences were determined. Gene 24 encodes a minor tail protein with the expected M(r) of 34,309, and gene 25 located 4 bp upstream of gene 24 encodes a major tail protein with the expected M(r) of 50,329. When total cellular RNA isolated from either phage-infected cells or cells bearing the cloned genes was analyzed by the primer extension method using the primers specific to either gene 25 or gene 24, we identified a possible late gene promoter, designated P25, in the 5'-flanking region of gene 25. This promoter was similar in structure to Escherichia coli promoters for sigma 70. Studies of the translational gene 25- and gene 24-lacZ fusions in the cloned gene system revealed that the promoter P25 was responsible for the expression of both genes 25 and 24 even in the absence of the regulatory genes which were absolutely required for late gene expression in the normal phage-infected cells. These results indicate that the two genes constitute an operon under the control of P25 and that the regulatory gene products of BF23 do not participate directly in specifying the late gene promoter.

Amino Acid Sequence↗

PubMed1994

[Consecutive evaluation of vesico-urethral function in patients undergoing radical retropubic prostatectomy].

We evaluated vesico-urethral function after radical retropubic prostatectomy in 18 male patients by consecutive urodynamic studies. At the time of the operation average age was 68 years with a range between 56 to 78 years old. The follow-up period after the operation was over 12 months in all patients. Pathological stage was T1 in 2, T2 in 6, T3 in 8 and T4 in 2 patients. Urodynamic evaluation including uroflowmetry, cystometry, urethral pressure profilometry (UPP) and external anal or urethral sphincter electromyography was performed before and 1, 3, 6 and 12 months after the operation. The status of postoperative urinary incontinence was reported by the patients. Sixty-five per cent of the patients revealed the low compliance bladder less than 10 ml/cm water at one month after the operation, however, most patients had normal vesical compliance and normal cystometrogram at 12 months. Both functional profile length (FPL) and maximum urethral closure pressure (UCPmax) in UPP were markedly lowered immediately after the operation and both indexes were significantly lower even at one year after the operation than preoperative ones. Both the incidence and the degree of incontinence improved during postoperative 12 months; complete urinary control was achieved in 11 patients (61%), stress urinary incontinence was present in 6 patients (33%) and one patient (6%) was still totally incontinent. Shortening FPL was considered to be the risk factor on postoperative urinary incontinence. Resection of bilateral neurovascular bundles and lower UCPmax seemed to have the possibility of the influence on it. Low compliance bladder is also likely to be one of the factors to cause early postoperative incontinence.

Aged↗

PubMed1993

Intraventricular injection of neostigmine increases dopaminergic and noradrenergic nerve activities: hyperglycemic effects and neurotransmitters in the hypothalamus.

The contents of hypothalamic neurotransmitters were examined under inducement of hyperglycemia by intraventricular administration of neostigmine, after pretreatment with microwave irradiation. Extracellular levels of the metabolites of these neurotransmitters were also measured using in vivo microdialysis. Our data suggest that neostigmine affects not only the cholinergic system but also the noradrenergic and dopaminergic systems in the hypothalamus. In order to clarify the relationship between excitement or regulation of physiological events and activities of central specific neurons, we therefore suggest that studies by chemical stimulation are insufficient on their own; it is also necessary to measure fluctuations both in neurotransmitter content and in extracellular levels of their metabolites.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1993

Use of high-performance liquid chromatography continuous-flow fast atom bombardment mass spectrometry for simultaneous determination of choline and acetylcholine in rodent brain regions.

This report describes a method for assay of choline (Ch) and acetylcholine (ACh) levels in rodent brain regions by high-performance liquid chromatography combined with continuous-flow fast atom bombardment mass spectrometry. Following an investigation of various extraction procedures and chromatographic conditions, we found that homogenization in acetonitrile in the presence of magnesium sulphate followed by heptane extraction and then a flow rate programme for chromatographic separation yielded the best results of the protocols tested. Under these conditions, the recoveries of Ch and ACh were 75% and 80%, respectively, with detection limits of 5 pmol for Ch and 2 pmol for ACh. Using this method, Ch and ACh levels in rat and mouse brain regions were similar to those reported by other researchers.

Acetylcholine↗

PubMed1993

Compensation between sympathetic nerves and adrenal medullary activity:effects of adrenodemedullation and chemical sympathectomy on catecholamine turnover.

To clarify functional compensation between the sympathetic nerves and the adrenal medulla, the effects of adrenodemedullation and chemical sympathectomy on norepinephrine (NE) turnover in some sympathetically innervated tissues and on NE and epinephrine (E) turnover in the adrenal gland were studied in rats. The rate of NE turnover was significantly accelerated by bilateral adrenodemedullation in the pancreas and in interscapular brown adipose tissue (IBAT). Chemical sympathectomy accelerated E turnover in the adrenal gland. These data indicate that some adrenergic nerves show functional compensation under conditions of depression of the adrenal medulla, and that compensatory acceleration of the adrenal medullary function occurs under conditions of adrenergic dysfunction.

Adipose Tissue, Brown↗

PubMed1993

Dopamine output upon death reflects intraneuronal aspects while alive: accumulation of releasable dopamine during tetrodotoxin perfusion.

Intraneuronal and extracellular dopamine (DA) metabolism in rat striatum during inhibition of neurotransmission processes by tetrodotoxin (TTX) perfusion was examined by analysis of the striatal DA content and the amount of initial post-mortem DA output. In spite of there being an excess amount of DA already present in the striatum, the contents of DA and its metabolites were increased time-dependently by TTX perfusion through a microdialysis membrane. A massive increase in extracellular level of DA occurred immediately after death. The amount of the post-mortem DA output was further increased in proportion to the preceding TTX perfusion time. The ratio of the amount of post-mortem DA output to the striatal DA content was also increased by previous perfusion with TTX. Verapamil, a Ca2+ channel blocker, delayed the appearance of the peak of the DA output. These results suggest that releasable DA accumulates in neurons during TTX perfusion, and that the early part of the DA output upon death reflects intraneuronal aspects of DA metabolism while the animal is alive.

Animals↗

PubMed1993

Effects of choline-free plasma induced by choline oxidase on regional levels of choline and acetylcholine in rat brain.

Choline-free plasma (CFP) was induced in rats by intravenous (IV) injection of 56.0 x 10(2) units kg-1 of choline oxidase (ChO) which completely metabolized the free Ch circulating in the plasma for at least 15.0 h and caused subsequent significant decrease in the concentration of free Ch in the three brain regions examined, the striatum, hippocampus, and cortex. However, the treatment did not affect concentrations of acetylcholine (ACh) in these regions. By contrast, intraperitoneal (IP) injection of 1.0 mmol kg-1 Ch chloride resulted in a maximum concentration of free Ch in plasma in 5 min, after which tissue Ch in all regions examined increased (p < 0.001). Concomitant increases were observed in cortical and hippocampal ACh (p < 0.05) 20 min after the injection. It is thus suggested that the brain may possess compensative mechanisms to prevent the supply of free Ch from circulating to the brain during synthesis of ACh in the brain. It is also suggested that the CFP rat would be a useful and readily available animal model for future study.

Acetylcholine↗

PubMed1993

Acute neurochemical changes in mouse brain following cerebral ischemia.

Acute changes in neurochemical levels induced by ischemia were studied in the mouse brain. Contents of neurochemicals in the frontal, parietal and occipital cortices and hippocampus were determined immediately after 15 min of ischemia (0), and then at 15, 30, 90 and 180 min after recirculation following ischemia. These data were compared with those for sham-operated control mice. Choline (Ch) contents in ischemic animals increased by 530-630% from control levels immediately after ischemia, and returned to control levels by 90 min. Decreases in levels of norepinephrine (NE) and serotonin (5-HT) were observed during 30 min after recirculation. There were no significant changes in levels of acetylcholine (ACh) or dopamine (DA), throughout recirculation. On the other hand, DA and 5-HT metabolites (3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid) significantly increased. Thus, comprehensively investigating the various neurotransmitters will provide meaningful information regarding the disturbance of central nervous system induced by cerebrovascular disease.

Acetylcholine↗

PubMed1992

Histopathological studies of a case of cytomegalovirus retinochoroiditis.

A case of cytomegalovirus (CMV) retinochoroiditis initially misdiagnosed as fungal endophthalmitis is reported. An 83-year-old man who was suspected of having cholangiocarcinoma presented uveitis in both eyes. Candida endophthalmitis was suspected on the basis of ophthalmic findings and past history, which included systemic corticosteroid administration and intravenous hyperalimentation. Intravenous treatment with miconazole was not effective. At autopsy, 3 months after the initial ophthalmological examination, the right eye was enucleated and examined histologically and histochemically. Light microscopic examination showed extensive retinal necrosis and numerous cytomegalic cells, so-called owl's eye cells, with intranuclear and intracytoplasmic inclusion bodies. CMV particles were seen by electron microscopy, and CMV-infected cells were observed by immunohistochemical staining by the direct method with fluorescein-labeled antibodies. These findings indicate that in suspected cases of fungal endophthalmitis various tests should also be carried out for CMV.

Aged↗

PubMed1992

Effects of N-methyl-D-aspartate receptor antagonists on carbon monoxide-induced brain damage in mice.

The mechanism of neurodegeneration and the possible therapeutic amelioration were investigated in a model induced by successive carbon monoxide (CO) exposures. Successive CO exposures resulted in a consistent pattern of degeneration of hippocampal CA1 pyramidal cells, which was quantified using an image analyzer. Competitive and noncompetitive antagonists of N-methyl-D-aspartate (NMDA) receptors, cyclopentenophenanthrene, (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten,5,10-imine maleate and an antagonist of glycine binding sites, 7-chlorokynurenic acid, significantly reduced the CO-induced neurodegeneration. Ifenprodil (a antagonist of polyamine binding sites) and glycine had no effect. From these results, it is clear that NMDA receptor/ion channel complex is involved in the mechanism of CO-induced neurodegeneration, and that glycine binding site antagonist as well as NMDA competitive and noncompetitive antagonists may have neuroprotective properties in neurological disorders associated with overactivation of NMDA receptors.

Animals↗

PubMed1992

[The perineal implantation of a bladder tumor through urethro-vasal reflux].

Perineal implantation of urinary bladder cancer in a 57-year-old male is reported. The patient had been suffering from incomplete paraplegia and neurogenic bladder for these 29 years because of accidental injury of lumbar spinal cord with episodes of bladder stones two times and right epididymitis three times, and presented urinary leakage from a perineal fistula. The fistula orifice was surrounded by a hard mass lesion. Bilateral swelling of inguinal lymph nodes was present. Fistulogram and voiding cysto-urethrography revealed reflux from posterior urethra to the fistula through right vas and epididymis. Histological diagnosis of resected perineal mass and biopsied left inguinal lymph node was transitional cell carcinoma with predominant metaplasia of squamous cell carcinoma. Tissues obtained by TUR-biopsy of a mass lesion at bladder wall was also histologically diagnosed transitional cell carcinoma with metaplasia of squamous cell carcinoma. The present case indicates implantation of a bladder tumor to perineum by urethero-vasal reflux and metastases to inguinal lymphnodes from the perineal lesion.

Carcinoma, Squamous Cell↗

PubMed1991

Effects of successive carbon monoxide exposures on delayed neuronal death in mice under the maintenance of normal body temperature.

The 3 time carbon monoxide (CO) exposures potentiated the delayed neuronal death (DND) in comparison with that induced by single CO exposure. Deterioration of DND induced by CO exposures was observed when normal body temperature was maintained during the exposures, since CO exposure fell the body temperature to about 34 degrees C. Pretreatment with noncompetitive NMDA receptor antagonist, MK-801 (30 nmol/mouse), ameliorated DND induced by successive CO exposures under the maintenance of normal body temperature. These results suggest that the mice exposed successively to CO under the maintenance of normal body temperature is a useful hypoxic model.

Animals↗

PubMed1991

Memory impairment and morphological changes in rats induced by active fragment of anti-nerve growth factor-antibody.

Treatment of rats with a specific Fab' fragment of anti-nerve growth factor (NGF)-antibody (anti-NGF, 12, 120 and 400 micrograms/4 weeks, i.c.v.) impaired their learning ability. The distance of swimming of anti-NGF-treated rats in a water maze was shortened more slowly by training than that of control rats. Anti-NGF treatment altered the staining of nuclei of cells in the hippocampus, parietal cortex and dentate gyrus with hematoxylin. It is suggested that the anti-NGF-induced amnesia could be due to change in nuclear morphology.

Animals↗

PubMed1991

Aged-related changes in learning and memory, choline acetyltransferase activity and number of neuronal cells in rats.

In a water maze task, the goal latency and distance of swimming onto the platform of aged rats (24 months old) were slowly shortened by repeated training compared with those of young rats (8 weeks old). A significant decrease in choline acetyltransferase activity in the frontal cortex, parietal cortex and striatum was observed in aged rats. Moreover, the number of neuronal cells in the hippocampal CA1 subfield and dentate gyrus of aged rats was smaller than that of young rats. The atrophy of striatal cells was observed. These results suggest that age-related delay of acquisition is due to the above-mentioned biochemical and histological changes, and that rates of aging in biochemical and morphological parameters are different in the discrete brain areas.

Aging↗

PubMed1991

Carbon monoxide-induced delayed amnesia, delayed neuronal death and change in acetylcholine concentration in mice.

We investigated the interrelationship of delayed amnesia, delayed neuronal death and changes in acetylcholine concentration induced by carbon monoxide (CO)-exposure in mice. In the test for retention of the passive avoidance task, amnesia was observed 5 and 7 days after CO-exposure when the mice were exposed to CO 1 day after training; in the case when the mice were exposed to CO 5 and 7 days before training, amnesia was also observed in a retention test given 1 day after training. The number of pyramidal cells in the hippocampal CA1 subfield was lower than that of the control 3, 5 and 7 days after CO-exposure. But the neurodegeneration in the parietal cortex, area 1, was not observed until 7 days after CO-exposure. The findings indicated that the amnesia and the neuronal death were produced after a delay when the mice were exposed to CO. In addition, the delayed amnesia was closely related to the delayed neuronal death in the hippocampal CA1 subfield. Moreover, [3H]glutamate and [3H]glycine binding sites did not change after CO-exposure but, 7 days after CO-exposure, the concentration of acetylcholine and the binding of [3H]quinuclidinyl benzilate in the frontal cortex and the striatum were found to have significantly changed, but those in the hippocampus did not show significant change. Therefore, we suggest that delayed amnesia induced by CO-exposure may result from delayed neuronal death in the hippocampal CA1 subfield and dysfunction in the acetylcholinergic neurons, in the frontal cortex, the striatum and/or the hippocampus.

Acetylcholine↗