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Y Ida

Publications and source records attributed to Y Ida.

At least 91 records · Page 5Linked to original sources

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↗

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↗

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↗

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↗

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↗

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↗

Psychological stress enhances noradrenaline turnover in specific brain regions in rats.

Concentrations of noradrenaline (NA) and 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in the hypothalamus, amygdala, cerebral cortex and pons + medulla oblongata were examined in male Wistar rats exposed to foot-shock or to psychological stress for 1 hour. Animals in the psychological stress group were prevented from receiving foot shock, but were exposed to responses of shocked rats. Foot shocked rats exhibited a significant reduction in NA content and a significant elevation in MHPG-SO4 level in all brain regions when compared to control rats which were neither shocked nor exposed to shocked rats. Rats exposed to the psychological stress displayed a significant reduction of NA level in the amygdala, significant elevation of MHPG-SO4 content in the hypothalamus and amygdala, and a moderate elevation of plasma corticosterone level. These results suggest that psychological stress produces mild enhancement of NA release preferentially in the hypothalamus and amygdala; while foot shock stress elicits a more intense response of noradrenergic neurons in more extended brain regions.

Amygdala↗

Effects of age and stress on regional noradrenaline metabolism in the rat brain.

Levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), were determined in eight brain regions of non-stressed rats at 2, 10 and 15 months of age, and of rats at 2 and 15 months of age stressed by immobilization for 3 hours. The NA levels in older rats were significantly lower in the hypothalamus, pons + med.obl. and midbrain, and higher in the amygdala, thalamus, hippocampus and cerebral cortex as compared to those of 2 month old rats. The MHPG-SO4 levels in the older rats were significantly lower in the hypothalamus, amygdala, pons + med.obl. and midbrain, and higher only in the cerebral cortex than those in 2 month old rats. Immobilization stress caused significant increases in NA turnover in all brain regions of both 2 and 15 month old rats. Age-related difference in the degree of stress-induced change in NA metabolism was found only in the hypothalamus; the increase of MHPG-SO4 by stress was greater in 2 month old rats than in 15 month old rats, although both age groups of rats showed the same degree of NA reduction by stress. These data suggest that brain NA metabolism changes in an age-related fashion, and that apparent regional differences exist in the pattern of these changes. Specifically, it appears that there is an age-related difference in the response of noradrenergic neurons to stress in the hypothalamus.

Aging↗

Postnatal development of noradrenaline and 3-methoxy-4-hydroxyphenylethyleneglycol sulphate levels in rat brain regions.

Developmental changes in brain levels of noradrenaline (NA) and 3-methoxy-4-hydroxyphenylethyleneglycol sulphate (MHPG-SO4) were studied in rats. In most brain regions, MHPG-SO4 level rapidly increased to approach or exceed adult levels at the time of weaning, while NA levels increased more gradually and reached adult levels following weaning. Pharmacological studies showed that the MHPG-SO4 level in the neonatal brain reflects the degradation of released NA. The developmental characteristics of noradrenergic neurons in eight discrete brain regions are discussed.

Aging↗