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PubMed1989

Positive effects of captopril in the behavioral despair swim test.

Captopril, an angiotensin II converting enzyme (ACE) inhibitor, was evaluated for potential antidepressive activity on the forced swim-induced behavioral despair (immobility) test in mice. Captopril (10.0 and 30.0, mg/kg ip) significantly reduced immobility and mimicked the effects of the antidepressants imipramine (30.0 mg/kg, ip) and mianserin (3.0, 10.0, and 30.0 mg/kg, ip). Captopril increased the motor activity of mice at these same dosages. Naloxone (2.0 mg/kg, ip) blocked the effects of captopril (30.0 mg/kg, ip) in the swim test. These data suggest that captopril has potential antidepressive activity. However, the conclusion is guarded, as the positive effects may be related to motor stimulation. The blockade of the captopril effects by naloxone suggests that brain opioid peptides play a role in this behavioral effect of captopril.

Animals↗
PubMed1982

Swimming as a method for assessing motor cortex integrity in the rat.

Rats were tested on 6 measures of swimming behavior 1, 2 and 4 weeks after sham operations or bilateral motor cortex lesions that damaged the forelimb areas and axons controlling the axial musculature. Rats with lesions performed more forelimb kicks and showed larger body angles than control animals. Number of hindlimb kicks and speed were within normal limits. Thus, some measures of swimming can be affected by small motor cortex lesions that spare the hindlimb projections.

Animals↗
PubMed1983

Time course of the changes of catecholamine levels in rat brain during swimming stress.

The time course of the changes in the levels of adrenaline, noradrenaline and dopamine was investigated in rat hypothalamus, ponsmedulla and midbrain during 4-h swimming at 35 degrees C. The adrenaline levels showed gradual decrease whereas the noradrenaline and dopamine levels were kept in almost steady-state during the swimming. These findings suggest that brainstem adrenaline levels are not so fast adaptive as the noradrenaline and dopamine levels under the stress.

Animals↗
PubMed1984

Activation of 'fictive swimming' by electrical microstimulation of brainstem locomotor regions in an in vitro preparation of the lamprey central nervous system.

Electrical microstimulation of specific areas of the brainstem in an in vitro preparation of the lamprey CNS elicits coordinated swimming motor activity recorded in spinal ventral roots. Swimming motor activity could be graded in intensity by variations in stimulus current. This 'brainstem locomotor region' extends from the mesencephalon, near the torus semicircularis, caudally through the rhombencephalon in parallel strips about 200-300 micron lateral to the midline.

Adaptation, Physiological↗
PubMed1984

Descending control and sensory gating of 'fictive' swimming and turning responses elicited in an in vitro preparation of the lamprey brainstem/spinal cord.

An in vitro lamprey nervous system preparation has been developed which consists of the head and exposed brainstem attached to the isolated spinal cord (resting on the notochord). Mechanical or electrical stimulation of the snout elicits motor activity in ventral roots which underlies a turning response (head withdrawal) away from the stimulus followed by escape swimming. Direct stimulation of the sensory division of the trigeminal nerve activates these patterns, and cutting this nerve abolishes ventral root activity elicited by stimulation of the snout. These patterns of ventral root activity are correlated with muscle activity and escape movements in intact animals. Sensory input activated by passive bending of the notochord/spinal cord gates the first burst in ipsilateral ventral roots during turning motor activity, and this response can thus be considered as a position dependent 'enhancement' reflex. Descending pathways activated by stimulation of the snout consist of axons which project for at least 20 segments, and are not significantly dependent on propagation through local circuits in the gray matter. The in vitro brainstem/spinal cord preparation survives for several days and will permit studies of the descending systems which normally initiate two types of motor acts, swimming and turning responses.

Animals↗
PubMed1992

N-methyl-D-aspartic acid (NMDA) receptor antagonist MK-801 blocks non-opioid stress-induced analgesia. II. Comparison across three swim-stress paradigms in selectively bred mice.

The effects of the specific N-methyl-D-aspartic acid (NMDA) receptor antagonist MK-801 (dizocilpine, 0.075 mg/kg, i.p.) on swim-stress-induced analgesia (SSIA) were studied in control (C) mice and in mice selectively bred for high (HA) or low (LA) SSIA. In three consecutive experiments, animals were subjected to forced swimming at water temperature of 20 degrees C, 32 degrees C and 15 degrees C and the resulting analgesia (hot-plate test) was found to be mixed opioid/non-opioid, opioid and non-opioid, respectively, as a function of the degree of antagonism by naloxone (10 mg/kg, i.p.). The major finding of this study is that MK-801 attenuated 15 degrees C SSIA, against which naloxone was ineffective, but had no effect on 32 degrees C SSIA, which naloxone blocked completely. A combination of naloxone and MK-801 significantly attenuated 20 degrees C SSIA in C and HA mice and in HA mice this attenuation was significantly larger than that produced by either drug alone. Morphine analgesia (10 mg/kg, i.p.) was unaffected by MK-801. It is concluded that low doses of MK-801 selectively block non-opioid mechanisms of SSIA.

Analgesia↗
PubMed1994

Extensor- and flexor-like modulation within motor pools of the rat hindlimb during treadmill locomotion and swimming.

EMG activity was recorded from the vastus lateralis (VL, knee extensor), rectus femoris (RF, hip flexor and knee extensor), tibialis anterior (TA, ankle flexor and digit extensor) and either the lateral or medial gastrocnemius (LG, MG, knee flexors and ankle extensors) muscles of 7 adult rats during treadmill locomotion and swimming. Most flexors and extensors are activated as a single burst but each is known to be modulated differently during locomotion. For example, the extensor EMG bursts are shortened and amplitude elevated as speed increases, whereas little change occurs in the EMG duration and amplitude in flexors. The RF and VL displayed a double burst of EMG activity per cycle during treadmill locomotion and a single burst during swimming. Kinematic and EMG analyses showed that during running, one of these EMG bursts occurred primarily during swing while the other burst occurred primarily during stance. Modulation of the burst occurring during swing approximated a flexor pattern, while the second burst was modulated like a typical extensor when running over a range of speeds and grades on a treadmill. These data suggest that motoneurons within a motor pool of a uniarticular (VL) as well as a biarticular (RF) muscle can be modulated by more than one cyclical input, probably of central origin, and that under some conditions several motor pools may share the same central commands.

Activity Cycles↗
PubMed1983

A survey of pathogenic and free-living amoebae inhabiting swimming pool water in Mexico City.

A survey of pathogenic and free-living amoebae in swimming pool waters of Mexico City was performed. Among the organisms isolated those which have public health importance were Naegleria fowleri Carter and Acanthamoeba castellanii Douglas. Amoebae of the genera Acanthamoeba, Naegleria, and Vahlkampfia were recovered in their cystic stage while those specimens of the genera Amoeba, Entamoeba, Thecamoeba, and Vanella were recovered only in their trophic stage during this study. Amoebae were concentrated through filtration procedures and subsequently cultured in different culture media. Nonpathogenic amoebae also isolated by culture included: Amoeba proteus (Pallas) Leidy, Amoeba striata Penard, Paratetramitus jugosus Page, Acanthamoeba astronyxis Ray and Hayes, Vahlkampfia avara Page, Vahlkampfia inornata Page, Thecamoeba verrucosa Ehrenberg, and Vanella mira Schaeffer. Trophozoites of Entamoeba gingivalis Gros, were also recovered, both directly and by culture. Most commonly found were amoebae of the species Naegleria gruberi Schardinger (59.02%), N. fowleri (16.77%), and A. castellanii (7.64%). Least-frequently found amoebae belonged to the species Thecamoeba verrucosa (0.12%). All isolated strains of N. fowleri and A. castellanii were thermophilic at 45 and 40 degrees C, respectively, and also pathogenic when inoculated into white mice. More populated by amoebae were those swimming pools of the indoor type with an inner side garden. It was also shown that the free residual chloride values of 0.50 to 1.5 mg/liter, ordinarily used in pool waters, are not adequate for elimination of amoebae.

Amoeba↗
PubMed1979

Forced swimming in rats: hypothermia, immobility and the effects of imipramine.

Rats when forced to swim in a restricted space not only became immobile but showed marked hypothermia. The hypothermia was greater than that observed after reserpine or Ro 4-1284 and was not antagonized by imipramine at doses which significantly reduced immobility. Hypothermia induced by forced swimming can therefore be dissociated from the immobility occurring in these conditions and also from drug-induced hypothermia.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1983

Morphine pretreatment reduces clomipramine effect in mouse forced-swimming test.

It had previously been shown that naloxone inhibits the effect of clomipramine both in a pain test in the forced-swimming test in mice which is proposed as an antidepressant study model. Evidence is reported of a decrease in activity of clomipramine in the forced-swimming test in mice after morphine pretreatment. The hypothesis of an interaction with mu-opiate receptors is considered.

Animals↗
PubMed1985

Involvement of amygdaloid catecholaminergic mechanism in suppressive effects of desipramine and imipramine on duration of immobility in rats forced to swim.

The suppressive effect of systemic injection of desipramine and imipramine on the duration of immobility in rats forced to swim was inhibited by 6-hydroxydopamine given into the medial amygdaloid nucleus as a pretreatment. Pretreatment with 5,7-dihydroxytryptamine given into the medial amygdaloid nucleus had no effect on the immobility-reducing effect of tricyclic antidepressants. The concentrations of catecholamines and serotonin in 6-hydroxydopamine- and 5,7-dihydroxytryptamine-pretreated rats, respectively, were significantly lower than those in the saline-injected rats. These results suggest that the suppressive effect of systemic injection of desipramine and imipramine on the duration of the immobility of rats forced to swim was mediated by the catecholaminergic but not the serotonergic mechanisms in the medial amygdaloid nucleus.

5,7-Dihydroxytryptamine↗
PubMed1987

Amygdaloid catecholaminergic mechanisms involved in suppressive effects of electroconvulsive shock on duration of immobility in rats forced to swim.

Chronic but not acute treatment with electroconvulsive shock (ECS) significantly reduced the duration of immobility in rats forced to swim. The immobility-reducing effect of chronic treatment with ECS was strongly antagonized by 6-hydroxydopamine but not by 5,7-dihydroxytryptamine given into the medial amygdaloid nucleus. These results indicate that ECS, like the tricyclic antidepressants, reduces the duration of immobility in rats forced to swim and that catecholaminergic mechanisms in the medial amygdaloid nucleus are involved in the suppressive effect of ECS on the duration of immobility, as are the tricyclic antidepressants.

5,7-Dihydroxytryptamine↗
PubMed1988

Stimulation of dopamine D-2 but not D-1 receptors reduces immobility time of rats in the forced swimming test: implication for antidepressant activity.

The involvement of dopamine D-1 and D-2 receptor mechanisms was investigated in the forced swimming test with rats. d,1-Sulpiride, a D-2 receptor antagonist, reported to reduce desipramine-induced anti-immobility, did not alter the brain levels of desipramine. In addition, the anti-immobility effect of desipramine was not antagonized by SCH 23390, a D-1 receptor antagonist. Amineptine (20 mg/kg i.p., 60 min before testing), a dopamine uptake blocker, and LY171555 (0.2 mg/kg i.p., 60 min before testing), a dopaminergic D-2 stimulant reduced immobility time in the forced swimming test, but benserazide + 1-DOPA (200 mg/kg p.o., 45 min before testing), which increases dopamine release, or SKF 38393A (20 mg/kg s.c., 60 min before testing), a D-1 agent, did not. The anti-immobility effect but not the stereotypy was increased following chronic (21 days) LY171555 (0.1 and 0.2 mg/kg i.p.) treatment. The effect of acute or repeated (7 days) LY171555 (0.2 mg/kg i.p.) treatment was antagonized by 1-sulpiride (50 mg/kg i.p., 90 min before testing), a D-2 receptor antagonist. Neither SKF 38393A (20 mg/kg s.c., 60 min before testing) nor SCH 23390 (0.05 mg/kg s.c., 30 min before testing) modified the acute anti-immobility effect of LY171555 (0.2 mg/kg i.p.) SCH 23390 (0.025 and 0.05 mg/kg) increased the immobility time at doses which decreased motor activity. The increase in immobility time brought about by SCH 23390 was not antagonized by SKF 38393A (20 mg/kg). The findings indicate that activation of dopamine D-2 receptors could reduce immobility time.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1990

Alpha 2-adrenoceptor blockade prevents the effect of desipramine in the forced swimming test.

The influence of alpha 2-adrenoceptor blockade on the activity of desipramine in an experimental model of depression was studied by using idazoxan and 1-(pyrimidinyl)piperazine (1-PP). The two drugs antagonists at these receptors, were studied for their ability to modify the effect of repeated treatment with the antidepressant, desipramine in the forced swimming test. Idazoxan (0.03, 0.3 and 3 mg/kg s.c.) and 1-PP (0.3 and 3 mg/kg p.o.) given with the last dose of a 7-day schedule of 10 mg/kg i.p. desipramine significantly reduced the effect of the latter on immobility. On its own neither drug modified the immobility time of rats at any dose. Infusion of various concentrations of idazoxan (1.6, 8 and 40 ng/microliters) in the rat locus coeruleus (LC), dose dependently antagonized the effect of desipramine without causing any appreciable change in motor behavior or immobility. The effect of idazoxan (8 ng/microliters) infusion in the LC was completely prevented by administering 6 micrograms 6-hydroxydopamine in the same region 12 days earlier. It thus appears that alpha 2-adrenoceptor blockade prevents the effect of desipramine in the forced swimming test, presumably by an effect on noradrenaline-containing cells in the LC. The question of how blockade or activation of alpha 2-adrenoceptors, both in the LC and in other sites, could influence antidepressant activity is discussed.

Adrenergic alpha-Antagonists↗
PubMed1990

The role of the mesolimbic dopaminergic system in the desipramine effect in the forced swimming test.

The effects of sulpiride isomers injected into the nucleus accumbens on the anti-immobility activity of desipramine in rats were studied to clarify the role of dopamine receptors. (-)-Sulpiride 100 ng/0.5 microliters injected bilaterally into the nucleus accumbens 5 min before testing reduced the effect of a 7-day treatment with 10 mg/kg per day desipramine in the swimming test but 5 micrograms/0.5 microliter (+)-sulpiride injected in the same area had no effect. Fluphenazine, 5 micrograms/0.5 microliter, or 6-hydroxydopamine-induced depletion of dopamine in the nucleus accumbens also reduced the anti-immobility effect of desipramine. The data further support the hypothesis that dopamine transmission in the nucleus accumbens has a permissive role in the effect of desipramine in the forced swimming test.

Animals↗
PubMed1991

The forced swimming test: effects of glucose administration on the response to food deprivation and adrenalectomy.

Rats food deprived for 24 h prior to a 15 min swimming test have no difficulty in acquiring the immobile response but showed significantly reduced levels of immobility (40%) on retest compared with controls (70%). This effect of food deprivation was reversed, by glucose (100 mg/kg), dexamethasone (6 micrograms/rat) and ketocyclazocine (25 micrograms/rat). Adrenalectomised animals also acquire but cannot retain the immobile response, however, adrenalectomised rats given 1000 mg/kg glucose within 2 h of the initial swimming test are immobile for 75-85% of the retest period. We interpret these findings as suggesting a complex interplay of endocrine and metabolic factors are necessary for retention of the behavioural response.

Adrenal Glands↗
PubMed1995

Effects of desipramine and alprazolam on forced swimming behaviour of adult rats exposed to prenatal diazepam.

Pregnant rats were treated with a single daily s.c. injection of diazepam (2 mg/kg) over gestation days 14-20. This treatment led to a reduction in GABA receptor complex function since adult male offspring showed a strong decrease in electrographic hippocampal responses to alprazolam and a strongly increased response to picrotoxin after intra-locus coeruleus injection of the two compounds. No difference in immobility time in the forced swimming test and in spontaneous motor activity was observed between prenatally vehicle- and diazepam-exposed offspring. Conversely, prenatal exposure to diazepam potentiated the anti-immobility effect of subchronic desipramine (10 mg/kg i.p.) and made active a dose of desipramine (5 mg/kg i.p.) that was ineffective in prenatally vehicle-exposed rats. This effect was observed only in pretested rats. Prenatal exposure to diazepam blocked the anti-immobility effect of subchronic alprazolam (15 mg/kg i.p.) in both non-pretested and pretested rats. Spontaneous motor activity was strongly reduced in all groups. These findings suggest that a persistent reduction in GABA receptor complex function, induced by prenatal exposure to diazepam, does not alter the mobility of adult progeny in the forced swimming test, but it may have consequences when drugs acting on the GABA receptor complex are used.

Alprazolam↗
PubMed1994

The potent activity of the 5-HT1A receptor agonists, S 14506 and S 14671, in the rat forced swim test is blocked by novel 5-HT1A receptor antagonists.

The high efficacy methoxynaphtylpiperazine 5-HT1A receptor agonists, S 14506 (1-[2-(4-fluorobenzoylamino)ethyl]-4-(7-methoxynaphtyl)piper azine) and S 14671 (1-[2-(2-thenoylamino)ethyl]-4[1-(7-methoxynaphtyl]piperazin e), potently reduced the duration of immobility in the forced swimming test in rats [minimal effective dose (MED): 0.01 mg/kg, s.c., in each case]; in contrast, the prototypic 5-HT1A receptor agonist, 8-OH-DPAT [8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide], was much less potent (MED: 0.63 mg/kg). The action of S 14671 (0.16 mg/kg) was completely blocked by the potent 5-HT1A receptor antagonist, SDZ 216-525 (4-(4-[4-(1,1,3-trioxo-2H-1,2-benzoisothiazol-2- yl)butyl]-1-piperazinyl)1H-indole-2-carboxylate) (0.63 mg/kg) and by the novel, selective 5-HT1A receptor antagonist, (+)-WAY 100,135 (N-tertiobutyl-3-[4-(2-methoxyphenyl)piperazinylphenyl propanamide): the effect of the latter was expressed dose dependently (Inhibitory Dose50: 35 mg/kg). Similarly, in the presence of (+)-WAY 100,135, S 14506 (0.63 mg/kg) failed to reduce immobility. Pretreatment with parachlorophenylalanine (3 x 300 mg/kg per day, i.p.), which profoundly depleted cerebral pools of 5-HT, modified neither baseline immobility nor the actions of S 14506 and S 14671. It is concluded that S 14506 and S 14671 possess exceptionally potent activity in the forced swimming test and that their actions reflect the activation of postsynaptic 5-HT1A receptors.

Animals↗