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Biomedical subjects

Y Kohno

Publications and source records attributed to Y Kohno.

At least 307 records · Page 17Linked to original sources
PubMed1983

Regional rat brain noradrenaline turnover in response to restraint stress.

Male Wistar rats were starved for 12 hr and then subjected to either 2 hr of wire mesh "envelope" restraint at room temperature; 2 hr of supine restraint in a specially constructed harness at room temperature or were not restrained. Eight brain regions were examined for NA level and the level of its major metabolite, MHPG-SO4. Plasma corticosterone and gastric ulcer incidence were also measured. All restrained rats displayed marked elevations in MHPG-SO4 levels in most brain regions. In addition, several brain regions in restrained animals showed a reduction in NA level. All restrained rats showed elevated plasma corticosterone levels and evidence of gastric lesions. In general, supine restraint produced greater alterations in regional brain NA turnover, greater evidence of ulcer disease, and higher plasma corticosterone levels than did wire mesh restraint. These data suggest that acute but intense stress in the form of restraint causes markedly altered brain NA activity--a possible neurochemical mechanism underlying the phenomenon of stress-induced disease.

Animals↗
PubMed1983

Daily increase in noradrenaline turnover in brain regions of activity-stressed rats.

Changes in contents of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in brain regions (the hypothalamus, amygdala, thalamus, hippocampus, midbrain, cerebral cortex, pons plus medulla oblongata and basal ganglia) of male Wistar rats were evaluated after 1, 3 or 5 days of exposure to the activity-stress paradigm, wherein rats were housed in a cage with a running-wheel and restricted to 1-hr of feeding per day. When compared to the non-stressed control rats, contents of MHPG-SO4 in all the brain regions except of the basal ganglia in the stressed rats increased as rapidly as 1 day and continued to increase throughout the 5-day activity-stress period. Contents of NA did not change significantly in most of these brain regions. The daily increase in regional NA turnover by continuous exposure to the activity-stress paradigm was related to the large increases in running activity and gastric ulcers, and to body weight loss at the 3-day and 5-day testing periods. These data suggest that pathological states produced by a 5-day activity-stress paradigm may reflect concomitant disturbances of noradrenergic function in various brain regions. The activity-stress paradigm is regarded as an intense and progressive stress, because it induces an increase in NA response in extended brain regions.

Animals↗
PubMed1983

Regional characteristics of stress-induced increases in brain noradrenaline release in rats.

Male Wistar rats were exposed to immobilization stress for various periods (1 to 5 hr) with or without an IP injection of probenecid at 400 mg/kg. The regional characteristics of stress-induced increases in noradrenaline (NA) release in the rat brain related to the time-course of stress were demonstrated by measuring levels of the major metabolite of NA, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4). Increases in MHPG-SO4 levels occurred mainly within the first hr of stress in the hypothalamus, amygdala and thalamus, while the peak elevations of the metabolite levels were delayed in the hippocampus, cerebral cortex, pons + medulla oblongata and basal ganglia. According to the accumulation of MHPG-SO4 during each 1-hr period of stress, regional characteristics of NA release were classified into the following four types based upon regions where the most marked increase in MHPG-SO4 levels occurs mainly: (1) within the first hr of stress (the hypothalamus, amygdala and thalamus), (2) during the first and second hr (the hippocampus and cerebral cortex), (3) during the third hr (the basal ganglia) and (4) to the same extent from the first to the fourth hr of stress (the pons + medulla oblongata). These results suggest that noradrenergic neurons in different brain regions respond differentially to stress and reflect their own characteristic patterns depending upon nature and time-course of the stressor.

Animals↗
PubMed1983

Tuberous sclerosis: proline and hydroxyproline contents in serum.

The serum levels of proline and hydroxyproline were determined by high-performance liquid chromatography using the post-labeled method with o-phthalaldehyde and sodium hypochlorite in 30 patients of tuberous sclerosis (TS) and compared with those in 32 pathological control subjects of similar age. No significant difference in the levels of serum free hydroxyproline was observed between TS and controls in any age group. In the age group of 9 to 18 years, TS showed significantly higher mean free proline levels in serum than controls with a difference of about 50 mumol/L. In both groups of TS and controls, total and free levels of hydroxyproline from ethanol-extractable serum showed similar age-dependent curves with peak values at age 12 years, and there was also no difference in the 2 levels between the 2 groups. It is suggested that this higher free proline level in TS with the autosomal dominant trait may be explained as the abnormal regulation of proline metabolism.

Adolescent↗
PubMed1983

Left ventricular size and performance during graded supine exercise in normal subjects.

To investigate left ventricular size and performance during graded submaximal exercise, 14 normal subjects with a mean age of 21 years exercised in a supine position to achieve the target heart rate. Using two-dimensional echocardiography, we recorded and analysed the left ventricular (LV) cross-sectional area and internal dimension at the level of the tips of the mitral valve at rest and during mild, moderate and severe exercise. The heart rate and systolic blood pressure increased substantially from rest to peak exercise (71 +/- 11 to 162 +/- 10 beats/min, 122 +/- 10 to 204 +/- 22 mmHg). The end-diastolic cross-sectional area and internal dimension (EDA & EDD) increased by 1.1-2.2 cm2 (7-13%) and 0.2-0.3 cm (4-7%), respectively, from mild to moderate exercise, (p less than 0.05-0.001). At peak exercise, however, these decreased and showed no statistically significant difference from the values at rest. The end-systolic cross-sectional area and internal dimension (ESA & ESD) decreased by 1.1 to 1.6 cm2 (14-20%) and 0.2-0.3 cm (7-10%), respectively, from moderate to severe exercise (p less than 0.01-0.001). However, the end-systolic values during mild exercise were not significantly different from those at rest. The stroke area (EDA-ESA) and dimension (EDD-ESD) increased by 1.6-2.6 cm2 (19-31%) and 0.2-0.6 cm (25-38%), respectively, during all levels of graded exercise (p less than 0.05-0.001). The percent change of LV cross-sectional area and internal dimension during systole increased gradually from rest to moderate exercise (51.0 +/- 7.1 to 61.9 +/- 4.4%, 35.4 +/- 3.9 to 45.0 +/- 3.7%), respectively, and showed no further increase during peak exercise. The mean circumferential fiber shortening velocity increased sharply from rest to peak exercise (1.27 +/- 0.14 to 2.25 +/- 0.21 circ/sec). These results suggest that the Frank-Starling mechanism operates during mild to moderate exercise, and contractility increases markedly at moderate to severe exercise levels as cardiac performance is augmented during graded submaximal exercise.

Adolescent↗
PubMed1983

[Regional characteristics of noradrenaline turnover as reflected in the brain levels of MHPG-SO4].

This paper reviewed the metabolism of noradrenaline (NA) in the brains of experimental animals and human beings, as well as the relationships between NA turnover and levels of 3,4-dihydroxyphenylethyleneglycol sulfate and 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in the rat brain. The procedure for simultaneous assay of NA and MHPG-SO4 in the rat brain was described. The fluorometric method is sensitive, accurate and rapid enough to determine both NA and MHPG-SO4 in a small amount of brain sample, and it is useful in the study of NA metabolism and turnover in discrete brain regions of the rat. The regional levels of NA and MHPG-SO4, their diurnal variations, and developmental changes from birth to 15 months were measured. Changes in regional NA turnover caused by a variety of acute and chronic stressful stimuli were related to behavioral and physiological changes in the stressed animals. In addition, examination of the interaction of opiate agents and the NA system in immobilization-stressed, methamphetamine-treated and untreated animals showed that the effect of opiate agents on NA turnover in stressed animals might be linked to some functional changes.

Animals↗
PubMed1982

Genetic control of immune response to myoglobin. Ir gene function in genetic restriction between T and B lymphocytes.

We studied the genetic restrictions on the interaction between T cells, B cells, and antigen-presenting cells (APC) involved in the H-2-linked Ir gene control of the in vitro secondary antibody response to sperm whale myoglobin (Mb) in mice. The B cells in this study were specific for Mb itself, rather than for a hapten unrelated to the Ir gene control, as in many previous studies. Low responder mice immunized in vivo with Mb bound to an immunogenic carrier, fowl gamma globulin (F gamma G), produced B cells competent to secrete anti-Mb antibodies in vitro if they received F gamma G-specific T cell help. However, (high-responder X low responder) F1 T cells from Mb-immune mice did not help these primed low responder (H-2k or H-2b) B cells in vitro, even in the presence of various numbers of F1 APC that were demonstrated to be component to reconstitute the response of spleen cells depleted by APC. Similar results were obtained with B6 leads to B6D2F1 radiation bone marrow chimeras. Genotypic low responder (H-2b) T cells from these mice helped Mb-primed B6D2F1B cells plus APC, but did not help syngeneic chimeric H-2b B cells, even in the presence of F1 APC. In contrast, we could not detect any Ir restriction on APC function during these in vitro secondary responses. Moreover, in the preceding paper, we found that low responder mice neonatally tolerized to higher responder H-2 had competent Mb-specific helper T cells capable of helping high responder but not low responder B cells and APC. Therefore, although function Mb-specific T cells and B cells both exist in low responder mice, the Ir gene defect is a manifestation of the failure of syngeneic collaboration between these two cell types. This genetic restriction on the interaction between T cells and B cells is consistent with the additional new finding that Lyb-5-negative B cells are a major participant in ths vitro secondary response because it is this Lyb-5-negative subpopulation of B cells that have recently been shown to require genetically restricted help. The Ir gene defect behaves operationally as a failure of low responder B cells to receive help from any source of Mb-specific T cells either high responder, low responder, or F1. The possible additional role of T cell-APC interactions, either during primary immunization in vivo or in the secondary culture is discussed.

Animals↗
PubMed1982

Genetic control of the immune response to myoglobins. Both low and high responder T cells tolerant to the other major histocompatibility complex help high but not low responder B cells.

We sought to examine the role of immune response (Ir) genes in helper T cells. To eliminate allogeneic effects, we used neonatally tolerized mice. The results bear not only on the mechanism of Ir genes, but also on the development of the T cell repertoire. B 10.BR (H-2(k)) or C57BL/10 (H-2(b)) mice, which were low responders to myoglobin (Mb), were neonatally tolerized to high responder H-2(d) alloantigens, and B10.D2 mice, which were high responders to Mb, were neonatally tolerized to low responder H-2(k) or H-2(b) alloantigens. Spleen cells from these tolerized mice did not show any reactivity in mixed-lymphocyte reaction or cell-mediated lympholysis against alloantigens used in tolerization. Mb-immune F(1) B cells were helped comparably by Mb-immune tolerized low or high responder T cells. Thus, low responder T cells functioned equivalently to high responder T cells. The failure of nonimmune T cells from tolerized low responder mice to help F(1) B cells and antigen-presenting cells (APC) indicated that collaboration between B10.BR or C57BL/10 T cells and F(1) B cells was not caused by a positive allogeneic effect. Spleen cells from tolerized mice were contaminated with 2-4 percent chimeric F(1) cells, as judged by fluorescence-activated cell sorter analysis, and no F(1) alloantigens were detectable in the thymus. However, removal of chimeric F(1) T cells from the tolerized cell population by treatment with anti-H-2 and complement did not change the helper activity of tolerized low responder T cells. These data indicated that helper activity in the T cell population from low responder mice was not due to F(1) cells. Also, the level of contamination was not sufficient to quantitatively account for the help. In examining the genetic restriction of these tolerized T cells, we found that T cells from tolerized low responder B10.BR or C57BL/10 mice helped F(1) or high responder B10.D2 B cells and APC but not syngeneic B10.BR or C57BL/10 B cells and APC, which were immunized with Mb-coupled fowl gamma globulin instead of Mb to prime low responder B cells with Mb. On the other hand, high responder B 10.D2 tolerized T cells helped syngeneic B 10.D2 B cells but not allogeneic low responder B10.BR B cells. These data indicated that clones of helper T cells specific for Mb exist in low responder mice, and these are not phenotypically different from those in high responder mice, in that both help high responder and F(1) but not low responder B cells and APC. These data are discussed in terms of the mechanism for Ir gene control, and the mechanism of T cell repertoire development- whether intra- or extrathymically-in neonatally tolerized mice.

Animals↗
PubMed1982

Naloxone enhances stress-induced increases in noradrenaline turnover in specific brain regions in rats.

Male Wistar rats were injected subcutaneously with either saline or naloxone, 1 mg/kg or 5 mg/kg, 10 min before exposure to 1-hour immobilization-stress. Control animals were sacrificed 70 min after respective injections. Levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-S04) in seven discrete brain regions and plasma corticosterone levels were fluorometrically determined. Immobilization stress caused significant elevations of plasma corticosterone which were not affected by pretreatment with naloxone. In the hypothalamus, amygdala and thalamus, immobilization-stress caused significant elevations of MHPG-S04 levels, and naloxone at 5 mg/kg significantly enhanced these stress-induced elevations virtually without affecting the basal level of the metabolite. In contrast, in the hippocampus, cerebral cortex and pons plus medulla oblongata, MHPG-S04 levels were elevated by stress, but were not affected by naloxone pretreatment. The effect of naloxone on stress-induced reductions of NA levels was unclear, since naloxone by itself (5 mg/kg) significantly decreased the amine levels in 5 of 7 brain regions examined. These results indirectly suggest that endogenous opioid peptides in the hypothalamus, amygdala and thalamus are partly involved in the stress process and attenuate increases in NA turnover induced by stress.

Amygdala↗
PubMed1982

Marked enhancement of noradrenaline turnover in extensive brain regions after activity-stress in rats.

Male Wistar rats were exposed to a 5-day activity-stress procedure wherein animals were housed in running-wheel activity cages and fed for only 1 hr each day (wheel-housed/food-restricted rats). This activity-stress procedure produced marked elevation in levels of the major metabolite of noradrenaline (NA), 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in eight brain regions, while a reduction of NA level occurred in several of these brain regions. These rats also exhibited excessive running activity and developed severe gastric glandular ulcers. Rats fed ad lib and housed in activity cages (wheel-housed/ad lib-fed) and rats housed in standard-individual cages and which received either 1-hr daily feeding (control cage-housed/food-restricted) or ad lib feeding (control cage-housed/ad lib-fed) showed neither significant changes in brain NA metabolism nor gastric ulcers. These results suggest that the interaction of a restricted feeding regimen and an increase running wheel activity caused marked enhancement of NA turnover in several brain regions, which is one of the neurochemical mechanisms underlying the physiological and behavioral changes produced by the activity-stress paradigm.

Animals↗
PubMed1982

Influence of feeding situation on stomach ulcers and organ weights in rats in the activity-stress ulcer paradigm.

Rats housed in running wheel activity cages except for 1 hr each day, during which time they were fed in their home cages, revealed more stomach ulceration, a higher level of brain MHPG-SO4, and larger weight changes in the thymus, spleen and adrenal gland, compared to rats housed in running-wheel activity cages and fed 1 hr daily in those same cages. Rats in the latter group showed more stress pathology than did control rats which were housed in standard home cages but which received the same restricted (1 hr per day) feeding schedule. These results did not support the idea that excessive running might occur in response to certain motivational states (e.g., frustration due to restricted feeding). The data suggested that feeding activity-stress rats in their home cages might aggravate the development of stomach ulcers coincident with the organ weight changes and the enhancement of noradrenaline turnover in the brain.

Adrenal Glands↗
PubMed1982

Priming effects of activity-stress ulcer in rats.

The activity-stress ulcer procedure consists of housing rats in running-wheel activity cages while at the same time, restricting their food intake to 1 hr per day. Male Wistar rats which had been habituated with ad lib feeding to the running-wheel cage environment for 3 days prior to the restricted feeding phase, developed significantly more gastric glandular ulcers and exhibited greater levels of running activity when compared to rats which had been given no habituation experience. Control rats housed in standard laboratory cages but which received the same restricted feeding regimen, developed significantly less stress pathology. Since allowing to rats access to the running-wheel during habituation resulted in enhanced stress pathology, this manipulation is referred to as a "priming effect." A possible explanation for such a "priming effect" is discussed in terms of procedures which may increase running wheel activity and decreases survival time during the restricted feeding phase of the activity-stress ulcer procedure.

Animals↗
PubMed1982

Time-related differences in noradrenaline turnover in rat brain regions by stress.

Male Wistar rats were stressed by immobilization from 15 to 180 min and the effect on noradrenaline (NA) and 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) contents in eight discrete brain regions were determined. NA levels significantly decreased and MHPG-SO4 levels increased in the hypothalamus, amygdala, thalamus, hippocampus, pons+ med.obl. and cerebral cortex. By contrast, the basal ganglia exhibited increases in NA levels and transient decreases in MHPG-SO4 levels. The midbrain failed to show significant alterations. The most rapid and marked increase in MHPG-SO4 level was found in the hypothalamus. When rats were exposed to stress after treatment with probenecid 400 mg/kg, the hypothalamus and amygdala showed greater accumulations of MHPG-SO4 in the early phase of stress, while the pons+ med.obl. and basal ganglia in the later phase. The other regions showed virtually the same accumulations. These results suggest that NA release is enhanced by immobilization in the six regions mentioned above and that response of NA neurons occurs rapidly in the hypothalamus and amygdala but is delayed in other regions.

Adrenal Cortex Hormones↗