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Biomedical subjects

Y Ida

Publications and source records attributed to Y Ida.

At least 73 records · Page 4Linked to original sources
PubMed1988

The modified forced-swim test in rats: influence of rope- or straw-suspension on climbing behavior.

We modified Porsolt's forced-swim test by suspending ropes or straws above the water in order to investigate a possible relationship between immobility and perceived escape responses from water. In this modified test, it was demonstrated clearly that rats reduced their duration of immobility and attempted to climb up the suspended ropes or straws. Most rats which had remained immobile during a 5-min test period in the forced-swim test, exhibited such climbing responses within 5-10 min of rope-suspension. Despite the suspension of ropes, however, some rats showed immobile postures and did not respond to the rope. On the other hand, straws were used in order to produce sliding and prevent climbing when the animals attempted to climb. There were no differences in immobility during either rope- or straw-suspension. It seems that the climbing behavior displayed by forced-swimming rats is due to a "pseudo-escape" effect produced by the suspension of an object above the water. The present findings were interpreted as further evidence for the notion that immobility in forced-swimming rats does not necessarily imply "behavioral despair," but rather an emotional reaction to an inescapable stressor.

Animals↗
PubMed1988

Is immobility of rats in the forced swim test "behavioral despair"?

Rats were forced to swim in a cistern until sinking in order to examine the possible relationship between sinking and immobility which has been reported to reflect "behavioral despair" in the forced swim test. Rats were classified into sinking and non-sinking groups, according to the appearance of sinking behavior over a 2 hr test. The sinking rats showed significantly shorter immobility times during the first 15 min as compared to the non-sinking rats. Therefore, sinking behavior seems to be a sign of emotional behavior such as fear and/or anxiety accompanied by defecation. Discriminant analysis showed that the immobility time during the first 15 min was a prediction of sinking. These findings suggest that the rapidly induced immobility in this forced swim test reflects the possibility of floating behavior in connection with the emotional reaction.

Animals↗
PubMed1988

Naloxone, given before but not after stress exposure, enhances stress-induced increases in regional brain noradrenaline release.

Male Wistar rats were injected with either saline or naloxone at a dose of 5 mg/kg either 10 min before exposure to a 1-hour period of immobilization stress or after exposure to the same stress for 2 hours which was then followed by a further 1-hour stress exposure (a total of 3 hours of immobilization stress). Levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in six discrete brain regions were determined fluorometrically. Both one hour and three hours of immobilization stress significantly increased MHPG-SO4 levels in all brain regions examined. This effect was accompanied by significant reductions of NA levels excluding the cerebral cortex after 1 hour of stress. Naloxone, injected prior to stress exposure, significantly enhanced MHPG-SO4 increases in the hypothalamus, amygdala and thalamus, but did not do so when injected 2 hours after stress exposure. Naloxone administration at either time did not affect stress-induced increases in MHPG-SO4 levels in the hippocampus, cerebral cortex or pons plus medulla oblongata. These results suggest that naloxone enhances stress-induced increases in NA release in the hypothalamus, amygdala and thalamus only during the early period of immobilization stress. Furthermore, these findings suggest that endogenous opioid peptides might be preferentially released during the initial exposure to stress.

Animals↗
PubMed1988

Effect of acute ethanol administration on noradrenaline metabolism in brain regions of stressed and nonstressed rats.

The effects of ethanol on noradrenaline (NA) metabolism of brain regions in stressed and nonstressed rats were investigated. Male Wistar rats were injected IP with either saline, or ethanol at 0.5 g/kg or 2 g/kg, 5 min before exposure to 1-hr immobilization stress. Levels of NA and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4) in various brain regions and plasma corticosterone levels were fluorometrically determined. Immobilization stress caused significant increases in MHPG-SO4 levels in all brain regions examined, i.e., the hypothalamus, amygdala, hippocampus, cerebral cortex and locus coeruleus (LC) region. In nonstressed rats, ethanol significantly increased MHPG-SO4 levels in the hypothalamus, hippocampus and cerebral cortex, but not in the amygdala or in the LC region. In stressed rats, ethanol attenuated stress-induced increases in MHPG-SO4 levels preferentially in the amygdala and LC region, but not in the remaining three regions. Although ethanol per se dose-dependently elevated plasma corticosterone levels in nonstressed rats, ethanol at 2 g/kg attenuated the stress-induced elevation of corticosterone. These results suggest that the attenuating effect of ethanol on stress-induced increases in NA turnover in the amygdala and LC region might be related to the stress-relieving properties of this drug.

Animals↗
PubMed1987

The activation of mesoprefrontal dopamine neurons by FG 7142 is absent in rats treated chronically with diazepam.

Administration of methyl-beta-carboline-3-carboxamide (FG 7142, 15 mg/kg i.p.) to rats has previously been shown to cause a selective increase in the levels of 3,4-dihydroxy-phenylacetic acid (DOPAC) in the prefrontal cortex and ventral tegmental area (VTA) via an interaction with benzodiazepine receptors. On withdrawal 3 days following chronic treatment with diazepam for 21 days, FG 7142 no longer increased DOPAC levels in either the prefrontal cortex or the VTA. Chronic diazepam treatment alone was ineffective in altering dopamine metabolism in the eight brain regions examined. The present findings indicate that chronic diazepam treatment may cause changes at the level of GABA/benzodiazepine receptor macromolecular complex, which is normally functionally integrated with the mesoprefrontal dopaminergic neurons, so that FG 7142 can no longer exert its intrinsic actions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

[Stressor controllability and brain noradrenaline turnover in rats].

A series of experiments examined the effects of a purely psychological factor in a stressful situation (i.e., the ability to manage a stressor or inability to do so) on noradrenergic metabolism in regional rat brains. In Experiment 1, uncontrollable rats which could not escape and avoid electric shock developed more gastric ulceration than did controllable rats which had exactly the same shock but could exert control over the shock. In Experiment 2, the uncontrollable rats displayed sustained increases in noradrenaline (NA) turnover in various brain regions regardless of stress durations. After the controllable rats had firmly mastered the coping response, excess NA utilization at the earlier stage of stress was reduced in many brain regions. These findings suggested that noradrenergic neuronal activity in some specific brain regions, such as the hypothalamus and limbic areas, might be involved in the coping processes under a stressful situation. This hypothesis was supported by the results of Experiment 3 showing that the effects of stressor controllability on regional brain NA turnover were covaried with the complexity of coping task required. Taken together, it is concluded that the degree of behavioral control (the ability to alter the termination or duration) that an organism has over a stressor modulates the physiological and neurochemical impact of that stressor, and that brain NA is implicated in the learning process where an organism copes with a stressor.

Animals↗
PubMed1987

[Familial cardiomyopathy with different clinical features in individual members].

The mother and three children of a family whose parents were consanguineous, each had cardiomyopathy with various patterns of hypertrophy and dilatation. All members had asymmetrical septal hypertrophy (ASH), and three of them were characterized as hypertrophic cardiomyopathy (HCM). Another one had ventricular dilatation mimicking dilated cardiomyopathy (DCM). Case 1: The 57-year-old mother had a typical ASH pattern; her septal/posterior wall thickness ratio (IVST/LVPWT) was 2.5. Case 2: The 37-year-old daughter had basal septal hypertrophy. Case 3: The 32-year-old elder son had typical concentric hypertrophy. Case 4: The 30-year-old younger son had an episode of congestive heart failure, and showed DCM-like features with considerable dilatation and impaired wall motion of the left ventricle. The hypertrophic pattern in cardiomyopathies is thought to depend partially on the ages of the onset, or its evolution with aging.

Adult↗
PubMed1986

Effects of preshock experience on enhancement of rat brain noradrenaline turnover induced by psychological stress.

The present study examined alterations of brain noradrenaline (NA) turnover as a function of preshock and psychological stress treatments, by measuring contents of NA metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in discrete brain regions of male Wistar rats. Psychological stress induced by exposing to the sight, sound and odor of other rats being shocked produced higher levels of MHPG-SO4 in the hypothalamus, amygdala and locus coeruleus (LC) region, as well as higher levels of plasma corticosterone. Preshock experienced rats also showed marked increases of MHPG-SO4 levels in the same regions described above and elevated plasma corticosterone levels when placed but not shocked in the same environment in which the rats had previously received shocks. The effects of psychological stress on brain NA turnover were affected by the animal's shock history preferentially in the hypothalamus and amygdala. These results suggest that: a purely psychological stressor caused acutely enhanced NA turnover in specific brain regions; regional NA activity appeared to be reinstated simply by reexposure to the environment previously associated with shock; preshock experience further intensified the enhancement of amygdaloid NA turnover evoked by psychological stress. An additional experiment, studying the aftereffects of preshock experience, clearly showed that these findings result from sensitization or conditioning to the environment previously paired with shock, and not merely from the aftereffects of the shock per se.

Animals↗
PubMed1986

[Latent handedness and individual hemisphericity].

An attempt was made to see the relationship of latent handedness (Luria, 1966) with individual hemisphericity, which was evaluated by a version of Hemisphericity Test (HT) devised by Ogura & Hatta (1983) and Cognitive Mode Questionnaire (CMQ; Sakano & Ohgishi, 1983). Subjects were 125 undergraduates (69 males and 56 females). In males, one of those three criteria for latent handedness, i.e. arm-folding subtest, showed a connection with HT; right-arm-uppermost subjects (R group) preferred verbal to nonverbal stimuli more often than left-arm-uppermost subjects (L group). These results support Sakano's hypothesis that the arm-folding subtest reflects individual hemisphericity (Sakano, 1982). Also, HT scores differed significantly between those two groups classified by CMQ. This result indicates the connection between CMQ and individual hemisphericity, whereas those subtests for latent handedness did not show any relation with CMQ. In females, no significant relation could be found among those three tests. Possibly these sex differences are related with those sex differences responsible for the degree of cerebral asymmetry.

Adolescent↗
PubMed1986

Effects of shock controllability on rat brain noradrenaline turnover under FR-1 and FR-3 Sidman avoidance schedules.

We examined changes in brain noradrenaline (NA) turnover as a function of shock controllability and the task complexity (fixed ratio, FR-1 and FR-3) under a 21-hr continuous discriminated Sidman avoidance schedule with shock intensity of 0.7-1.0 mA, shock duration of 1.0 sec, shock-shock interval of 1.5 sec, response-shock interval of 100 sec and signal-shock interval of 10 sec, by measuring levels of a principal metabolite of NA, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in discrete brain regions of male Wistar rats. In an FR-1 operant schedule, experimental rats which could avoid or escape shock by pulling a disk manipulandum only once showed significantly lower levels of MHPG-SO4 in the hypothalamus, amygdala, thalamus, locus coeruleus (LC) region and cerebral cortex than did yoked rats which received the same amount of shock but could not perform any effective avoidance and/or escape responses. The MHPG-SO4 levels for the experimental rats did not differ significantly from "non-shock" control rats in most regions. In an FR-3 operant schedule, however, the experimental rats which could control shock by emitting three disk-pulling responses showed significantly higher levels of MHPG-SO4 in most brain regions, as compared to FR-1 experimental rats. The FR-3-experimental rats exhibited levels of MHPG-SO4 similar to those seen in the FR-3 yoked rats in all brain regions. These two groups of shocked rats showed significantly higher levels of MHPG-SO4 in all brain regions with the exception of the basal ganglia, as compared to the FR-3 control rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Attenuating effect of diazepam on stress-induced increases in noradrenaline turnover in specific brain regions of rats: antagonism by Ro 15-1788.

One-hour immobilization stress increased levels of the major metabolite of brain noradrenaline (NA), 3-methoxy-4-hydroxyphenyl-ethyleneglycol sulfate (MHPG-SO4), in nine brain regions of rats. Diazepam at 5 mg/kg attenuated the stress-induced increases in MHPG-SO4 levels in the hypothalamus, amygdala, hippocampus, cerebral cortex and locus coeruleus (LC) region, but not in the thalamus, pons plus medulla oblongata excluding the LC region and basal ganglia. The attenuating effects of the drug on stress-induced increases in metabolite levels in the above regions were completely antagonized by pretreatment with Ro 15-1788 at 5 or 10 mg/kg, a potent and specific benzodiazepine (BDZ) receptor antagonist. When given alone, Ro 15-1788 did not affect the increases in MHPG-SO4 levels. Behavioral changes observed during immobilization stress such as vocalization and defecation, were also attenuated by diazepam at 5 mg/kg and this action of diazepam was antagonized by Ro 15-1788 at 10 mg/kg, which by itself had no effects on these behavioral measurements. These findings suggest: (1) that diazepam acts via BDZ receptors to attenuate stress-induced increases in NA turnover selectively in the hypothalamus, amygdala, hippocampus, cerebral cortex and LC region and (2) that this decreased noradrenergic activity might be closely related to relief of distress-evoked hyperemotionality, i.e., fear and/or anxiety in animals.

Animals↗
PubMed1985

Methionine-enkephalin inhibits stress-induced increases in noradrenaline turnover in brain regions of rats.

Met-Enkephalin injected i.c.v. attenuated stress-induced increases in levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate, the major metabolite of brain noradrenaline, in the hypothalamus, amygdala, hippocampus, thalamus, midbrain and LC region in rats. The data suggest that Met-enkephalin acts to attenuate stress-induced increases in noradrenaline turnover in these brain regions in rats.

Animals↗
PubMed1985

State-dependent effects of beta-endorphin on core temperature in stressed and non-stressed rats.

beta-Endorphin, gamma-endorphin, delta-endorphin and morphine injected i.c.v. caused hyperthermia in non-stressed rats; however, the same dose of beta-endorphin and morphine caused hypothermia in stressed animals. These effects of beta-endorphin were antagonized by naloxone. The results suggest that effects of beta-endorphin are different depending on the animal's state and that these effects are mediated via opioid receptors.

Animals↗
PubMed1984

Recovery of stress-induced increases in noradrenaline turnover is delayed in specific brain regions of old rats.

Male Wistar rats at 2 and 12 months of age were sacrificed before, immediately following, and at 6 and 24 hours after a 3-hour immobilization stress period. Levels of noradrenaline (NA) and its major metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), in eight brain regions and plasma corticosterone levels were fluorometrically determined. Immobilization stress caused significant increases of MHPG-SO4 levels in all brain regions examined and significant elevations in plasma corticosterone levels in both 2 and 12 month old rats. In 2 month old rats, the MHPG-SO4 levels in all brain regions returned to control levels within 6 hours after release from the stress. However, in 12 month old rats, the metabolite levels in the hypothalamus, amygdala, pons plus medulla oblongata (pons+med. obl .) and midbrain still remained at significantly increased levels at 6 and 24 hours after the stress. Moreover, in the amygdala of older rats, stress-induced decreases in NA levels persisted even 6 hours after stress. Plasma corticosterone levels also showed significant elevations at 6 and 24 hours after the stress only in 12 month old rats. These results suggest that brain NA metabolism during recovery periods from an acute exposure to a stressful situation is altered by the aging process in such a manner that NA neurons in the hypothalamus, amygdala, pons+med. obl . and midbrain in older rats remain activated by stressful stimuli for prolonged periods of time following release from stress.

Aging↗
PubMed1983

Differential effects of morphine on noradrenaline release in brain regions of stressed and non-stressed rats.

Effects of morphine on noradrenaline (NA) turnover in the 8 brain regions were investigated in non-stressed and stressed rats. Morphine at 3 mg/kg and 6 mg/kg caused dose-dependent increases in levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-SO4), the major metabolite of brain NA, in the hypothalamus, amygdala, thalamus, hippocampus and midbrain and decreases in NA levels in the first 4 of these regions. In contrast to these enhancing effects of morphine on NA release in non-stressed rats, pretreatment with morphine at 6 mg/kg significantly attenuated immobilization-stress-induced increases in MHPG-SO4 levels in the above regions. The morphine effects in both states, non-stressed and stressed, were reversed by naloxone at 0.5 mg/kg and 5 mg/kg in the hypothalamus, amygdala and thalamus. These neurochemical changes are apparently related to the distress-evoked hyperemotionality. Behavioral changes observed during the restraint stress such as struggling, vocalization and defecation were attenuated by morphine at 6 mg/kg and enhanced by naloxone at 5 mg/kg, and this action of morphine was also reversed by naloxone at 5 mg/kg. These results suggest that morphine acts to attenuate stress-induced increases in NA release in the hypothalamus, amygdala and thalamus via opiate receptors, although the drug facilitates NA release in these regions in non-stressed rats. Together with previous findings that naloxone enhances stress-induced increases in NA release selectively in these regions, it is further suggested that endogenous opioids released during stress might act to inhibit NA release in these specific brain areas and that these decreased noradrenergic activities might be closely related to the relief of the distress-evoked hyperemotionality in animals.

Animals↗
PubMed1983

Differential modification by opioid agents of acutely enhanced noradrenaline release in discrete brain regions.

Although immobilization stress-induced increases in MHPG-SO4 level in the hypothalamus, amygdala and thalamus were enhanced by naloxone and attenuated by morphine, both agents failed to exert significant effects upon regional MHPG-SO4 levels in methamphetamine-treated rats. The results indicate that there is a differential modification by opioid agents of acutely enhanced noradrenaline release induced by physiological and by pharmacological manipulations.

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↗