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PubMed1990

A possible alarm substance in the forced swimming test.

Rats were tested in a forced swimming paradigm under a number of conditions which showed that time of day of testing did not significantly affect duration of immobility and a shorter ten-minute test period was as effective as the traditional longer protocol which tests animals 24 hours after initial immersion. Prior foot shock and noise decreased the immobility response. In addition, swimming in a cylinder in which another rat had been swimming also decreased the immobility response. The latter was not due to fecal or urinary contamination but appeared to be due to an alarm substance released during immersion in the water. Animals were affected by this proposed substance whether they released it themselves or it was released by a stranger. The proposed substance was released after a 3.5-minute or longer swimming period.

Animal Communication↗
PubMed1992

Effects of acute swim stress on LiCl-induced conditioned taste aversions.

The present study examined the effects of a 5-min period of swim stress experienced between a flavor (saccharin) and illness (LiCl) on conditioned taste aversion learning. Experiment 1 obtained a stress-induced attenuation of learning. Experiment 2 replicated the findings of Experiment 1, and also obtained a similar attenuation when stress was administered 30 min prior to the saccharin presentation. Experiment 3 examined the effects of swim stress either 15 min or 90 min after the LiCl had been administered. It was found that swim stress 15 min after LiCl significantly attenuated CTA, but swim stress 90 min after LiCl did not. These results are discussed with regard to current views of the relationship between external events and conditioned taste aversions.

Animals↗
PubMed1994

A further analysis of physiological changes in rats in the forced swim test.

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.

Acid-Base Equilibrium↗
PubMed1988

Gender determinants of opioid mediation of swim analgesia in rats.

Continuous cold-water swims (CCWS) and intermittent cold-water swims (ICWS) elicit respective nonopioid and opioid analgesic responses in adult male rats. The present experiment evaluated whether gender differences were observed in naloxone's (14 mg/kg, SC) ability to alter differentially CCWS and ICWS analgesia on the tail-flick and jump tests in age-matched and weight-matched intact rats and in gonadectomized rats. CCWS analgesia was unaffected by naloxone on either test in age-matched males and females. Naloxone significantly reduced ICWS analgesia on the tail-flick (45%) and jump (37%) tests in intact males, but not age-matched females. Naloxone significantly reversed ICWS analgesia in weight-matched males on the tail-flick (1-14 mg/kg, 30-32%) and jump (14 mg/kg, 31%) tests. Naloxone also significantly reduced ICWS analgesia on the tail-flick (32%) and jump (41%) tests in castrated males, but not ovariectomized females. Changes in swim hypothermia could not account for the above effects. These data indicate gender differences in naloxone's differential modulation of swim analgesia, and reflect further differences in pain-inhibitory responses as a function of gender.

Analgesia↗
PubMed1991

Chronic forced swim stress produces subsensitivity to nicotine.

Twice daily injections of saline reduce the thermic response to nicotine in the rat. The authors hypothesized that this was due to the stress of twice-daily handling and injection. However, the injection of saline is not a classic stressor. The hypothesis that stress blunts thermic responsiveness to nicotine was, therefore, tested using a classic form of chronic inescapable stress. Rats (n = 12) were subjected to a 14-day, twice daily course of inescapable cold water swim stress using a repeated measures design. Thermic responsiveness of nicotine was measured at baseline and every 7 days thereafter for 49 days. The mean response to nicotine (1.0 mg/kg IP) differed significantly across time, F(7,88) = 10.6, p less than 0.0001. Mean thermic responsiveness (+/- SEM) decreased from -0.75 +/- 0.09 at baseline to -0.41 +/- 0.18 degrees C (54.7% of baseline) following 14 days of forced swim stress. This change was not significant. However, the thermic response to nicotine was -0.14 +/- 0.13 degrees C (p less than 0.05), +0.55 +/- 0.12 degrees C (p less than 0.05), and +0.04 +/- 0.11 degrees C (p less than 0.05) 7, 14, and 21 days following the discontinuation of forced swim stress. The mean response did not differ from baseline 28 days following the last session of forced swim stress. The data suggest that in the recovery phase the animals ceased to be sensitive to nicotine. These findings support the hypothesis that a chronic stressor can produce subsensitivity to nicotine.

Animals↗
PubMed1993

Swim stress selectively alters the specific binding of a benzodiazepine antagonist in mice.

The ability of flurazepam to antagonize the electrical precipitation of tonic hindlimb extension is reduced 24 h after mice are forced to swim for 10 min in cold water (6 degrees C). Presumably, this reduction in flurazepam's antiseizure efficacy reflects an environmental stress-induced modification of the GABAA receptor complex. The current study employed a variety of complementary in vitro approaches to characterize the delayed effects of cold-water swim stress on binding parameters of the GABAA receptor complex that may be associated with flurazepam's reduced antiseizure efficacy. The specific binding of [3H]flunitrazepam and the potentiation of this binding by chloride ions did not change after stress in the cerebral cortex, hippocampus, and cerebellum. Moreover, swim stress did not alter the ability of GABA to inhibit the binding of [35S]t-butylbicyclophosphorothionate (TBPS), a ligand that is a specific biochemical marker of the GABA-associated chloride ionophore, to crude membranes prepared from the cerebral cortex and cerebellum. Swim stress was associated with alterations of the specific binding of [3H]Ro 15-1788, a benzodiazepine receptor antagonist, to crude hippocampal and cerebellar membranes. The results are considered in the context of new insights derived from molecular cloning studies of the GABAA receptor complex.

Animals↗
PubMed1993

Cross-tolerance between morphine and swim analgesia in mice selectively bred for high and low stress-induced analgesia.

Mice selectively bred for high (HA) and for low analgesia (LA) induced by 3-min swimming at 20 degrees C and unselected controls (C) were injected three times daily for 3 days with 20 mg/kg morphine HCl. The analgesic effect of 10 mg/kg morphine in nontolerant mice differed between the lines in the rank order of HA > C > LA and significantly decreased after repeated treatment with morphine, as revealed by the hotplate test (56 degrees C). The tolerance to morphine analgesia was more pronounced in HA than in C mice but did not develop at all in LA mice. Similarly, the magnitude of swim-induced analgesia in morphine tolerant mice decreased to a greater degree in the HA than the C line but did not change in LA mice. Naloxone HCl (1 and 10 mg/kg) attenuated swim analgesia more in nontolerant HA than C mice but had no effect in morphine-tolerant HA and C and in all LA mice. The differential degree of morphine tolerance and cross-tolerance with swim analgesia suggests that the strategy of selective breeding toward divergent magnitudes of stress-induced analgesia has differentiated opioid involvement in endogenous pain inhibition in the selected lines.

Analgesia↗
PubMed1996

Detection of serotonergic and noradrenergic antidepressants in the rat forced swimming test: the effects of water depth.

A new scoring technique is described that measures active behaviors of rats in the forced swimming test, a test that predicts antidepressant drug effects. The technique distinguishes the effects of selective serotonin reuptake inhibitors, which reduce immobility and increase swimming behavior, from selective norepinephrine reuptake inhibitors, which reduce immobility and increase climbing behavior. The magnitude of behavioral effects described for each drug (i.e., reduced immobility for both drugs, increased swimming for fluoxetine, increased climbing for desipramine) was greater when testing was conducted at the deeper 30-cm rather than the shallow 15-cm water depth. Results obtained with the technique demonstrate that selective serotonin reuptake inhibitors are not false negatives in the rat forced swimming test, as previously thought.

Animals↗
PubMed1996

The effects of different types of pre-training on the rat's retention performance in a swim-to-platform task following administration of scopolamine.

Previous research has found that centrally acting antimuscarinic drugs strongly impair the acquisition of a variety of learned behaviors in rats but have little effect on these same behaviors if training is given prior to drug treatment. We gave groups of rats different types of pre-training followed by treatment with scopolamine hydrobromide and subsequent testing on a simple swim-to-platform test. Factors such as practice in swimming without a platform to escape to, or learning to swim to a platform in a different apparatus or even to the test platform located in a different place did not protect the rats from the behavioral disruption produced by scopolamine. However, five training trials on the specific swim-to-platform task used in the retention test afforded almost complete protection against the effect of scopolamine. It appears that the protective effect of pre-training is highly specific and does not involve acquisition of some type of general rule which might survive antimuscarinic blockade.

Animals↗
PubMed1994

Sex differences in acute swim stress induced changes in the binding of AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid) and kainate to glutamate receptors in mouse forebrain.

Sex differences were found in the binding of [3H]AMPA and [3H]kainate to glutamate receptors in synaptosomal membranes prepared from mouse forebrain. The number of low affinity [3H]AMPA binding and the affinity of [3H]kainate binding was higher in membranes prepared from male mice than from females. Acute swim stress (3 min at 32 degrees C) decreased the number of low affinity [3H]AMPA binding sites and the affinity of [3H]kainate binding in membranes prepared from male mouse forebrain, but not in those prepared from female mice forebrain. As kainate is known to interact with low affinity AMPA binding sites, these observed changes may be associated with binding sites common to AMPA and kainate. They may represent a functional down-regulation of AMPA/kainate binding sites. These sex differences in binding to non-NMDA subclasses of glutamate receptors are similar to than those found in the binding of MK-801 to the NMDA subclass of glutamate receptors, in that the effects of acute swim stress were more pronounced in membranes prepared from male than from female mice. The number of low affinity [3H]AMPA binding sites were decreased by acute swim stress in membranes from male mice, whereas the number of low affinity [3H]MK-801 binding sites increased following acute swim stress.

Animals↗
PubMed1985

Determination of the energetic cost of swimming from the analysis of growth rate and body composition in juvenile chinook salmon, Oncorhynchus tshawytscha.

The standard metabolic rate was estimated to be 19.5 cal X kcal-1 X day-1. The multiple regression of growth on swimming speed and ration size was significant (P less than 0.001). The relationship was as follows: G = 22.22-2.85BL + 6.58 R where G is growth in cal X kcal X day-1, BL represents swimming speed in body lengths X sec-1 and R denotes ration in % body wt X day-1, dry weight. The multiple correlation coefficient, R2, was 0.80. Unlike coho salmon, the net cost of swimming was independent of swimming speed. Fish in all groups experienced reduction of fat with exercise with the exception of the slowest speed-highest ration (1.0-1.9 BL X sec-1, 6% X day-1) group. Nearly all of the explained variation was accounted for by food consumption rate.

Aging↗
PubMed1987

Coronary ligation reduces maximum sustained swimming speed in Chinook salmon, Oncorhynchus tshawytscha.

The maximum aerobic swimming speed of Chinook salmon (Oncorhynchus tshawytscha) was measured before and after ligation of the coronary artery. Coronary artery ligation prevented blood flow to the compact layer of the ventricular myocardium, which represents 30% of the ventricular mass, and produced a statistically significant 35.5% reduction in maximum swimming speed. We conclude that the coronary circulation is important for maximum aerobic swimming and implicit in this conclusion is that maximum cardiac performance is probably necessary for maximum aerobic swimming performance.

Animals↗
PubMed1995

Modulation of swimming in the lamprey, Petromyzon marinus, by serotonergic and dopaminergic drugs.

The effects of serotonergic and dopaminergic drugs on free swimming behavior in adult sea lampreys (Petromyzon marinus) were investigated using video image analysis. Injections of the serotonin precursor 5-hydroxy-L-tryptophan along with the serotonin reuptake blocker clomipramine into the visceral cavity of lampreys resulted in significant increases in the cycle period of swimming, but had no significant effects on the propagation time of the swim waves down the body (normalized to cycle period), or on the degree of body curvature. Injections of the dopamine agonist apomorphine resulted in significant decreases of cycle period and body curvature with no significant effects on the normalized wave propagation time. The effects on cycle period are consistent with previous findings using serotonin and apomorphine on swimming activity in the isolated spinal cord.

5-Hydroxytryptophan↗
PubMed1993

Sex differences in the antagonism of swim stress-induced analgesia: effects of gonadectomy and estrogen replacement.

Sex differences in the neurochemical mediation of swim stress-induced analgesia (SSIA) were examined in Swiss-Webster mice. Intact and gonadectomized adult mice of both sexes were tested for their analgesic response (hot-plate test) to 3 min of forced swimming in 15 degrees C and 20 degrees C water. SSIA resulting from 15 degrees C swim was previously shown to be naloxone-insensitive (i.e., non-opioid) whereas SSIA resulting from 20 degrees C swim produced an analgesia that was partially reversible by naloxone (i.e., mixed opioid/non-opioid). The non-opioid components of these SSIA paradigms were attenuated by the N-methyl-D-aspartate (NMDA) receptor antagonist, dizocilpine (MK-801). We now report that in males, but not females, dizocilpine (0.075 mg/kg, i.p.) and naloxone (10 mg/kg, i.p.) antagonized the non-opioid and opioid components of SSIA, respectively. After ovariectomy, females displayed a pattern of antagonism similar to males such that dizocilpine attenuated non-opioid SSIA, although naloxone remained ineffective in antagonizing 20 degrees C SSIA. Thus, SSIA in intact females was neither opioid- nor NMDA-mediated, yet it was of similar magnitude to the SSIA displayed by intact males. In separate experiments, estrogen replacement (estrogen benzoate; 5.0 micrograms/day, i.p.) administered to ovariectomized mice over a 6-8 day period reinstated the dizocilpine-insensitivity of 15 degrees C SSIA characteristic of intact females. However, a similar estrogen regimen administered to both intact and castrated males did not compromise the sensitivity to dizocilpine previously noted in male mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1988

Repeated swimming stress and responsiveness of the isolated rat pacemaker to the chronotropic effect of noradrenaline and isoprenaline: role of adrenal corticosteroids.

1. Repeated swimming stress (three daily sessions) resulted in an increased plasma corticosterone level and subsensitivity of the isolated rat pacemaker to noradrenaline and isoprenaline. 2. Repeated swimming stress was found to decrease the affinity of beta 1-adrenoreceptors for metoprolol. 3. Bilateral adrenalectomy performed 2 days before repeated swimming stress abolished the development of pacemaker subsensitivity to noradrenaline and isoprenaline and the decrease in beta 1-adrenoreceptors affinity for metoprolol. 4. It is concluded that adrenal corticosteroids, at least partially, mediate the swimming stress-induced subsensitivity of the isolated rat pacemaker to noradrenaline and isoprenaline.

Adrenalectomy↗
PubMed1992

Involvement of swimming-induced acute stress in the sensitivity of rat vs deferens to norepinephrine.

1. The effects of swimming-induced stress on rat sensitivity to norepinephrine were studied. 2. Through microscopic analysis of the stomach from swimming stressed rats significant ulceration was observed, confirming that the stress situation was really present. 3. Sensitivity to norepinephrine either in the presence or in the absence of cocaine and propranolol in acutely swimming stressed rats was not altered significantly. 4. Bilateral adrenalectomy was performed in rats 2 days before swimming and acute stress resulted in a supersensitivity to norepinephrine, indicating that adrenal glands may, at least, partially mediate the sensitivity to this drug in vasa deferentia isolated from these animals.

Adrenal Glands↗
PubMed1994

Forced swim stress: supersensitivity of the isolated rat pacemaker to the chronotropic effect of isoprenaline and the role of corticosterone.

1. Forced swim (three daily sessions) resulted in an increased plasma corticosterone level and supersensitivity of the isolated rat pacemaker to the chronotropic effect of isoprenaline. 2. Bilateral adrenalectomy, performed 2 days before forced swim, abolished the development of pacemaker supersensitivity to isoprenaline. 3. Administration to rats of the antiglucorticoid compound RU-38486 prevented the development of pacemaker supersensitivity to isoprenaline. Pretreatment of rats not submitted to forced swim with the synthetic glucocorticoid RU-28362 causes pacemaker supersensitivity to isoprenaline. 4. Pretreatment of rats with diazepam or imipramine which block the forced swim-induced increase in the plasma level of corticosterone prevented the development of pacemaker supersensitivity to isoprenaline. 5. It is concluded that corticosterone plays a critical role in the modulation of the sensitivity to catecholamines of the pacemaker beta-adrenoceptors during adaptation to repeated stress.

Adrenal Glands↗
PubMed1995

REM sleep deprivation treatment enhances the effect of clozapine in the forced swimming test.

1. Effect of REM sleep (REMs) deprivation treatment on clozapine response in the forced swimming test was investigated. 2. Clozapine significantly increased the swimming activity in REMs-deprived mice at a dose of 5 mg/kg (i.p.) which did not affect the activities in the control groups. 3. Physostigmine (0.3 mg/kg, i.p.), an acetylcholinesterase inhibitor, blocked the increasing effect of 5 mg/kg clozapine on swimming activity in REMs-deprived animals. 4. These results suggest that the REMs deprivation treatment-induced enhancement of effect of clozapine on swimming activity is mediated by the functional change of central cholinergic system following the treatment.

Animals↗