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PubMed1982

Effects of in utero or suckling exposure to cerium (citrate) on the postnatal development of the mouse.

Gravid female mice received either a single subcutaneous dose of cerium citrate (80 mg Ce/kg) or an equivalent (in citrate) dose of sodium citrate on d 7 or 12 of gestation or on d 2 postpartum. To separate effects of prenatal and postnatal exposure, a cross-fostering design was employed. The weight and gross activity of the neonates were assessed on d 8 or 13 postpartum. Open-field behavioral parameters, accelerating rotarod performance, and passive avoidance learning were assessed on d 60-65 postpartum. Maternal offspring retrieval latency was measured on d 3 postpartum. Analyses revealed that neonatal weight was reduced both in offspring exposed to Ce in utero and in the offspring of mothers receiving Ce during lactation/suckling. Ce also appeared to affect maternal/offspring interaction: pups exposed prenatally to Ce were retrieved in less time than control pups. Except for an increased frequency of rearings in the open field of adult offspring exposed to Ce in utero, Ce exposure had no apparent effect on behavioral parameters, either in neonatal or adult offspring.

Animal Population Groups↗

PubMed1986

Severe deficits of adaptive behaviour after lesions of rat's nucleus reticularis pontis oralis.

Hooded rats of the Long-Evans strain with bilateral symmetric lesions of the nucleus reticularis pontis oralis (RPO) displayed locomotor hyperactivity in the open field (OF) compared with their preoperative values. Their locomotor velocity and their climbing rate were significantly enhanced. Habituation in the OF was significantly weakened. The lesioned rats were unable to acquire any active avoidance responses in a Y-maze or a jump test. They were unable to correctly perform preoperatively learned avoidance responses and could not relearn the tasks. Reaction times to the conditioned stimulus increased and more often the rats escaped only after the onset of the punishment; even their escape responses were instable. The lesioned rats were neurologically inconspicuous. One can assume that the RPO participates in a functional system for control and recall of learned (not inborn) programs.

Animals↗

PubMed1989

Cholinomimetic activities of minaprine.

The cholinomimetic activities of the antidepressant drug minaprine have been investigated, in vitro and in vivo, in rodents. Minaprine, and its metabolite SR 95070B [3-(2-morpholinoethylamino)-4-methyl-6-(2-hydroxyphenyl) pyridazine hydrochloride] selectively displaced [3H]-pirenzepine from its cortical and hippocampal binding sites, and only weakly inhibited the binding of [3H]-N-methylscopolamine in either the rat cerebellum, heart and salivary glands, or the guinea-pig ileum. In mice, none of these drugs induced the typical cholinergic side-effects up to lethal doses. Minaprine and SR 95070B antagonized rotations induced by an intrastriatal injection of pirenzepine in mice, after intraperitoneal and/or oral administration. Minaprine also antagonized atropine-induced mydriasis in mice. Both minaprine and SR 95070B potentiated the tremorigenic effect of oxotremorine without inducing tremor when injected alone. Finally, minaprine and SR 95070B, after parenteral and/or oral injection, antagonized the scopolamine-induced deficit in passive avoidance learning, and enhanced short-term retention in the social memory test, in rats. The muscarinic agonists arecoline, oxotremorine and RS 86 [2-ethyl-8-methyl-2,8 diazaspiro-4,5 decan-1,3 dion hydrobromide], as well as the acetylcholine esterase inhibitors physostigmine and tacrine were active in most of these models. These results indicate that minaprine, and its metabolite SR 95070B, have cholinomimetic activities which could be, at least in part, mediated by their selective affinity for M1 muscarinic receptors. Thus minaprine could represent a potential useful drug for the treatment of senile dementias and cognitive impairments occurring in elderly people.

Animals↗

PubMedDate not supplied

Opposite effects of naltrexone on ETOH intake by Syracuse high and low avoidance rats.

Rats which were selectively bred for good (Syracuse High Avoidance: SHA) and poor (Syracuse Low Avoidance: SLA) shuttle-box avoidance learning were used to assess the effects of naltrexone on ethanol ingestion. Male rats from both strains were offered a free choice of water and ethanol (10%, v/v) for two 8-day periods between which was inserted a 4-day period of forced ethanol consumption. The net ethanol consumption and ethanol preference ratio were significantly greater in control SHA rats than in control SLA rats in the first choice period, but they did not differ in the forced and the second choice periods. Chronic naltrexone administration from an implanted 30-mg pellet showed bidirectional effects, i.e., suppression of ethanol consumption in SLA animals and enhancement in SHA rats.

Alcohol Drinking↗

PubMed1999

Piracetam improves cognitive performance by restoring neurochemical deficits of the aged rat brain.

In order to test the hypothesis that piracetam improves cognitive functions by restoring biochemical deficits of the aging brain, we investigated the effects of piracetam treatment (300 mg/kg daily for 6 weeks) on the active avoidance performance of young and aged rats. After testing, the rats were killed and membrane fluidity and NMDA as well muscarinic cholinergic receptor densities were determined in the frontal cortex, the hippocampus, the striatum, as well as the cerebellum. Piracetam treatment improved active avoidance learning in the aged rats only and elevated membrane fluidity in all brain regions except the cerebellum in the aged animals. Moreover, we observed a positive effect of piracetam treatment on NMDA receptor density in the hippocampus and on muscarinic cholinergic receptor densities in the frontal cortex and the striatum and to a lesser extent in the hippocampus. Again, these effects were only observed in aged animals. Discrimination analysis indicated that piracetam effects on membrane fluidity in the frontal cortex, the hippocampus, and the striatum and its effects on NMDA densities in the hippocampus might be involved in its positive effects on cognitive performance.

Age Factors↗

PubMed1991

Different responsiveness of spleen lymphocytes from two lines of psychogenetically selected rats (Roman high and low avoidance).

Roman high- (RHA) and low-avoidance (RLA) rats have been genetically selected on the basis of their active avoidance behavior, and have been shown to differ on numerous behavioral, neurochemical and neuroendocrine parameters, especially in response to stress. We investigated the activity of splenic lymphocytes in vitro. Natural killer cell activity against YAC-1 tumoral cells and the mitotic response to plant lectins concanavalin A and phytohemagglutinin were much lower for lymphocytes isolated from RHA rats, in males as well as in females. The difference between the two strains was even larger when measured in a stressed state, immediately after active avoidance learning. On the other hand, the mitotic response to bacterial lipopolysaccharide, a B-cell-specific mitogen, was not different between the two lines, indicating that the difference in lymphocyte reactivity is limited to the T-lineage. The lower activity of T-cells in the RHA line had no consequence upon the ability of these animals to build up an antibody response against sheep red blood cells. These results indicate that Roman lines are an interesting animal model for the study of the relationships between the brain and the immune system, as well as for the analysis of the genes involved in the control of behavior.

Animals↗

PubMed1984

Hormonal influence on the duration of short-term and intermediate stages of memory.

In day-old chicks trained on a single trial passive avoidance learning task, ACTH1-24 and corticosterone delayed the formation of long-term memory and the decay of the immediately preceding intermediate memory. This action of ACTH1-24 was attributed to its glucocorticoid activity since ACTH4-10 did not yield the same effect. ACTH1-24 and ACTH4-10, but not corticosterone, enhanced short-term memory retention levels. The effects of arginine vasopressin and arginine vasotocin were similar to those observed with ACTH1-24, but they also delayed the decay of short term memory and hence the formation of intermediate memory. These findings were discussed in the context of hormonal modulation of memory formation and counteraction of antibiotic-induced amnesia.

Adrenocorticotropic Hormone↗

PubMed1998

Pharmacological characterization of 6-bromo-3'-nitroflavone, a synthetic flavonoid with high affinity for the benzodiazepine receptors.

6-Bromo-3'-nitroflavone is a synthetic flavone derivative that selectively recognizes benzodiazepine receptors and has potent anxiolytic-like effects. Here, we describe in detail its pharmacological characterization. When i.p. injected in mice, 6-bromo-3'-nitroflavone (0.01-0.3 mg/kg) had an anxiolytic-like effect in the elevated plus-maze test. This effect was blocked by the specific benzodiazepine receptor antagonist, flumazenil. In addition, it exhibited anxiolytic-like actions when given orally (1 mg/kg). 6-Bromo-3'-nitroflavone did not exhibit myorelaxant effects (up to 30 mg/kg, i.p.). Unlike diazepam, this flavonoid produced no anterograde amnesia in a one-trial inhibitory avoidance learning. On the other hand, 6-bromo-3'-nitroflavone possessed mild anticonvulsant activity (0.1 mg/kg, i.p.) and provoked sedative-depressant actions only at doses 100-1000 times higher than those producing anxiolytic-like effects. 6-Bromo-3'-nitroflavone (0.1-1 mM) produced a lower potentiation of gamma-amino-butyric acid (GABA)-stimulated 36Cl- influx (126-138%) in comparison to diazepam (0.1 mM: 166%) in cerebral cortical membrane vesicles. Taken together, these findings suggest that 6-bromo-3'-nitroflavone has anxiolytic-like action possibly behaving as a partial agonist of the benzodiazepine receptors.

Animals↗

PubMed1998

Long-term effects of repeated maternal separation on three different latent inhibition paradigms.

In the present study we investigated the effect of repeated maternal separation on postnatal days 12, 14, 16, and 18 for 6 h/day on Wistar rats on three latent inhibition (LI) paradigms: two-way active avoidance, conditioned emotional response (CER), and conditioned taste aversion (CTA). In addition, hyperactivity induced by d-amphetamine and stereotypies induced by apomorphine were evaluated. In all three LI experiments, the control animals showed only marginal LI, whereas the maternally separated animals showed enhanced LI (only males in CTA). In two-way active avoidance within the nonpreexposed condition maternally separated animals showed improved acquisition of avoidance learning compared with the control animals. Sensitivity in response to amphetamine and apomorphine was not altered by the maternal separation procedure. Thus, maternal separation in this study, contrary to previous reports, but in line with results obtained following early handling before weaning, led to enhancement of the LI phenomenon as assessed in each of the three procedures. As our maternal separation procedure (6 h on days 12, 14, 16, and 18) led to behavioral outcomes that differed from those reported by Ellenbroek and Cools (24 h on day 10), it is suggested that maternal separation regimens that are dissimilar may lead to different and sometimes opposite behavioral effects.

Amphetamine↗

PubMed1990

Facilitation of memory retrieval by pretest morphine mediated by mu but not delta and kappa opioid receptors.

Mice were trained to avoid electric shock (0.6 mA) in a step-through type passive avoidance learning task, retention being measured 24 h after the training trial. Morphine 10 mg/kg administered 30 min before the test trial (pretest) facilitated memory retrieval, and the effect was completely antagonized by 1 mg/kg naloxone, a selective mu-opioid receptor antagonist. On the other hand, pretest administration of 0.01-10 mg/kg DTLET, a selective delta-opioid receptor agonist, did not produce the same effect as morphine. Nor-binaltorphimine, a kappa-opioid receptor antagonist, did not antagonize the effect of pretest morphine, at doses of 1 and 2 mg/kg. These results suggest that the facilitation of memory retrieval by pretest morphine is mediated through mu- but not delta- or kappa-opioid receptors.

Analgesics↗

PubMed1982

Characteristics of retrograde amnesia following reactivation of memory in mice.

Amnesia for approach-avoidance learning was induced in mice by injecting the protein synthesis inhibitor anisomycin (ANI) immediately, 1, or 2 hours, but not 3 hours after training. A robust amnesia could be demonstrated if ANI was administered 3 hours after training, immediately following a 60 second exposure to the training apparatus or to a structurally similar environment. The temporal gradient of effectiveness of amnesia production by ANI was significantly steeper following reactivation treatment than it was following initial training. In addition, while amnesia produced by the conventional procedure remained stable for 6 days, the amnesia induced following reactivation treatment spontaneously recovered 4 days after training. These findings are discussed in terms of their relevance to interpretations of retrograde amnesia studies.

Animals↗

PubMed2004

Facilitation of a weak training experience in the 1-day-old chick using diphenylhydantoin: a pharmacological and biochemical study.

This series of studies used a weakly trained (20% methyl anthranilate) version of the passive avoidance learning task in the 1-day-old chick to investigate memory facilitation effects by diphenylhydantoin (DPH). The results indicated that the pairing of the weak training experience with DPH results in facilitation of memory that can be observed from 40 min following training with the weak training experience. The results from a biochemical experiment indicated that DPH facilitates the activity of Na(+)/K(+)-ATPase at the majority of times sampled in a large percentage of the sections of the chick brain. The most marked level of elevation in the activity of the enzyme was observed at the 20-min time point following weak training in the section of the chick brain, which contained several memory relevant neuroanatomical loci. This represents a 68% increase in the activity of the enzyme in those areas considered to be crucial to the processing of memory in the paradigm at a time predicted by previous investigation to be crucial in the development of the intermediate-term memory stage of memory. The results of this series of studies support the notion that Na(+)/K(+)-ATPase plays an important role in memory processing following passive avoidance training in the 1-day-old chick.

Animals↗

PubMed2001

Regular exercise improves cognitive function and decreases oxidative damage in rat brain.

The biochemical mechanisms by which regular exercise significantly benefits health and well being, including improved cognitive function, are not well understood. Four-week-old (young) and 14-month-old (middle aged) Wistar rats were randomly assigned to young control and young exercised, middle-aged control and middle-aged exercised groups. Exercise groups were exposed to a swimming regime of 1 h a day, 5 days a week for 9 weeks. The passive avoidance test showed that middle-aged exercised rats had significantly (P<0.05) better short- (24 h) and long-term (72 h) memory than aged-matched control rats. Conditioned pole-jumping avoidance learning was improved markedly in both age groups by exercise. Brain thiobarbituric acid-reactive substances and 8-hydroxy-2'deoxyguanosine content in the DNA did not change significantly, while the protein carbonyl levels decreased significantly (P<0.05) in both exercised groups. This decrease was accompanied by an increase in the chymotrypsin-like activity of proteasome complex in the exercised groups, whereas trypsin-like activity did not differ significantly between all groups. The DT-diaphorase activity increased significantly (P<0.05) in the brain of young exercised animals. These data show that swimming training improves some cognitive functions in rats, with parallel attenuation of the accumulation of oxidatively damaged proteins.

Age Factors↗

PubMed1996

Impairment of schedule-controlled behavior by pre- and postnatal exposure to hexachlorobenzene in rats.

Hexachlorobenzene (HCB) is still frequently found at elevated levels in human adipose tissue and breast milk. As intoxication with HCB causes neurological disturbance in human beings, the purpose of the present study was to examine neurobehavioral functions in rats after pre- and postnatal exposure. Female rats were fed diets with 0, 4, 8, or 16 mg HCB/kg diet. Exposure started 90 days prior to mating and was continued throughout mating, gestation, and lactation. Thereafter, the offspring were given the same diets as their respective mothers. HCB levels were determined in the brain, the liver, and in the adipose tissue from virgin rats, dams, and the offspring. Concentrations on a lipid basis were found to decline in the order adipose > liver > brain. The exposure levels chosen did not cause gross toxic effects in dams or offspring. There were dose-related increases in liver-to-body-weight ratios in exposed dams, but not in unmated females treated alike. Behavioral testing was conducted in the offspring. Examination of open-field activity on PND 21, and of active avoidance learning on PND 90 failed to reveal significant differences between groups. Training of operant behavior started at the age of 150 days in the offspring from the control, the 8-mg group, and the 16-mg group. Animals were trained on a fixed interval schedule of 1 min (FI-1). On this schedule, responses were reinforced by a food pellet every time 1 min had elapsed after the preceding reinforcement. There were dose-dependent reductions in the post-reinforcement pause, e.g. the time between each reinforcement and the first reaction emitted after it. In addition, the index of curvature, which describes the efficiency of performance on the FI-1 schedule, was decreased in a dose-dependent fashion.

Adipose Tissue↗

PubMed1997

Effects of the dopamine D3 receptor agonist, R(+)-7-hydroxy-N,N-di-n-propyl-2-aminotetralin, on memory processes in mice.

The putative dopamine D3 receptor agonist, R(+)-7-hydroxy-N,N-di-n-propyl-2-aminotetralin (R(+)-7-OH-DPAT) (0.1-100 microg/kg, s.c.), administered before training, immediately after training, and before retention significantly shortened step-down latency of passive avoidance learning, indicating the amnesic effects of R(+)-7-OH-DPAT. Neither the dopamine D1 receptor antagonist, R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzaz epine maleate R(+)-SCH23390) (2.5 and 5 microg/kg, i.p.), nor the dopamine D2 receptor antagonist, S(-)-sulpiride (10 and 30 mg/kg, i.p.), markedly influenced the R(+)-7-OH-DPAT (10 and 100 microg/kg, s.c.)-induced amnesia. In addition, only a 1000 microg/kg dose of R(+)-7-OH-DPAT decreased locomotor activity; 1 and 100 microg/kg doses of the drug were ineffective. These results suggest that the amnesic effects of the dopamine D3 receptor agonist, R(+)-7-OH-DPAT, are not mediated via dopamine D1 or D2 receptors in the brain.

Animals↗

PubMedDate not supplied

Behavioral toxicity of chloral in mice: an approach to evaluation.

The potential for behavioral toxicity of the water contaminant chloral (CHL) was ascertained from acute, 14 day and 90 days of exposure in adult mice and perinatal exposure. Acute motor incoordination produced by CHL occurred 5 min after gavage and persisted for about 2 hr. The ED50 for acute CHL effects was 84.2 mg/kg, a value less than 1/10th of the acute LD50. Exposure for 14 days to either 14.4 or 144.0 mg/kg/day of CHL by gavage did not produce any deleterious effects on body weight, behavioral observations, locomotor activity, motor coordination or swimming endurance which were measured 24-48 hr after exposure was terminated. Subchronic, 90 day exposure to 0.70 or 0.07 mg/ml CHL in drinking water (15.7 and 159.8 mg/kg/day) did not affect the palatibility of drinking water since total fluid intakes were not reduced. Mice exposed to these doses of CHL did not gain weight as rapidly as control mice. Exposure to 159.8 mg/kg/day produced a decrease in body temperature after 45 days of exposure and a second temperature measurement indicated that mice exposed to both 15.7 and 159.8 mg/kg/day were hypothermic on day 91. Mice were also evaluated on various behavioral tests and none of these measures were altered by 90 days of CHL exposure. Mice perinatally exposed to 21.3 and 204.8 mg/kg/day CHL in drinking water had normal body weights, normal development of neurobehavioral reflexes and normal motor coordination. The retention of passive avoidance learning was reduced on both the 1 hr and 24 hr retention tests for mice exposed to the higher CHL concentration. CHL did not produce motor incoordination at relatively low doses following a single acute exposure. Repetitive exposure to CHL at levels of about 1/10th and 1/100th the acute LD50 for 14 or 90 days did not produce delayed or persistent behavioral changes. Non-specific effects on body temperature and body weight gains were observed for mice exposed for 90 days. There is little evidence that exposure to CHL is likely to result in delayed or persistent behavioral toxicity to adults exposed to contaminated drinking water supplies while CHL during the prenatal and early postnatal period at levels as high as 204.8 mg/kg/day can result in detrimental behavioral effects.

Animals↗

PubMed1987

Behavioral and neurochemical changes produced by postnatal pretreatments with methamphetamine in rats.

Male neonates of Wistar strain rats were given s.c. 1-4 mg/kg/day of methamphetamine (MAP) for 7 successive days from days 6 to 12 after birth. The acquisition processes of the discriminative lever-press avoidance response were investigated from day 60 after birth. Effects of the postnatal pretreatments with MAP on saturation constants for specific bindings of 3H-spiperone (SPP) and 3H-WB4101, respectively, in 8 brain regions were also investigated at 100-120 days after birth. In addition, dopamine, noradrenaline and the levels of their metabolites were measured in the brain. No significant difference was detected in body weight, gross behaviors and avoidance learning between saline- and MAP-pretreated groups. However, effects of MAP and apomorphine on the locomotor activity significantly increased in the MAP-pretreated group. Significant decreases in Bmax and Kd values of 3H-SPP binding sites in the striatum were detected in the MAP-pretreated group, while significant decreases in Bmax values of 3H-WB4101 binding sites in the cortex and hippocampus as well as those in Kd values in the hippocampus were found in the treated group. Dopamine and noradrenaline levels significantly decreased in the MAP-pretreated group, but on the contrary, their metabolites levels significantly increased. These results suggest that postnatal pretreatments with MAP produce long-lasting behavioral changes associated with an impaired development of catecholaminergic neurons in the rat brain after maturity.

Animals↗

PubMed1982

Behavioral toxicity of trihalomethane contaminants of drinking water in mice.

The behavioral toxicity of trichloromethane (TCM), dichlorobromomethane (DCBM), dibromochloromethane (DBCM) and tribromomethane (TBM) was evaluated following oral administration in mice. A variety of dosage regimens and behavioral measures were used. Studies included acute dose effect, 14-and 90-day treatments at 300 and 3000 times the estimated average human daily intake of contaminated drinking water, 30 days of 100 mg/kg/day, and 60 days of 100 and 400 mg/kg/day. In addition, TCM was tested for the production of taste aversions with 10-day administration and for behavioral teratology in offspring following extensive perinatal exposure. The ED50 for acute effects on a screen test of motor performance was about 500 mg/kg for all four trihalomethanes. The 14-day treatments had no effect on swimming behavior and the 90-day treatments had no effect on bar clinging, a test of motor coordination, and a measure of exploratory behavior. None of the compounds produced effects on passive-avoidance learning following 100 mg/kg/day for 30 days. TCM, DBCM and TBM elicited clear effects at both 100 and 400 mg/kg/day on operant behavior when administered for 60 days. DBCM elicited clear effects at 400 mg/kg/day. These effects on operant behavior were seen following the first dose and tolerance tended to develop. Thus, there was no evidence from these studies for a progressive neurotoxicity from trihalomethanes in adult mice. A behavioral teratology study was also conducted with TCM. Both parents were treated with 31.1 mg/kg/day TCM, and treatment of the dam continued throughout gestation and lactation. No clear evidence for behavioral effects in the offspring were observed. The most sensitive measure for the effects of TCM was the taste aversion paradigm in which saccharin aversions were produced after a single treatment of 30 mg/kg.

Administration, Oral↗