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PubMed2002

Individual response profiles of male Wistar rats in animal models for anxiety and depression.

Previous work has shown that systematic individual differences between male Wistar rats can be detected in tasks like the elevated plus-maze, or the open field. Here, we investigated whether individual profiles of anxiety, as measured with the plus-maze, may predict behavioral response profiles in other tasks where anxiety, aversion, or depressive behaviors are important. Male Wistar rats were initially screened: (A) in an open field; and (B) in an elevated plus-maze. Based on their plus-maze behavior, that is, the time spent in the open arms, the animals were divided into two subgroups with either 'low' or 'high' anxiety (LA or HA) levels. These subgroups were exposed to other experimental anxiety paradigms, namely object burying and two-way active avoidance, and an animal model of depression, the forced swim test. In the plus-maze, the percentage of time spent on, and the number of entries into the open arms were lower in HA than in LA rats. In the object burying task, HA rats showed more burying behavior of Tabasco-coated marbles, and in the active avoidance task, they showed slower acquisition of avoidance learning and higher escape latency as compared to LA rats. Finally, LA and HA rats behaved similarly in the forced swim test; however, the percentage changes of immobility time between test days 1 and 2 were negatively correlated to open field behavior, namely locomotor activity and center entries. On the other hand, the frequencies of rearing in the open field, which can also gauge functional differences between rats (for example responsiveness to novelty, psychomotor activation), were not substantially related to the behavioral profiles in the tests of anxiety and depression. These results show that individual differences of anxiety in the plus-maze can be predictive of behavior in other anxiety models, but not in forced swim test, indicating that they may be determined partly by similar functional and physiological mechanisms.

Adaptation, Psychological↗

PubMed2004

Endocrine-disrupting activity of chemicals in diesel exhaust and diesel exhaust particles.

Diesel exhaust (DE) is known as the main cause of air pollution. DE is a complex mixture of particulate and vapor-phase compounds. The soluble organic fraction of the particulate materials in DE contains thousands of compounds including a variety of polycyclic aromatic hydrocarbons and heavy metals. To clarify the endocrine-disrupting activities of DE, we have reviewed the reports about the effects of DE on the reproductive and brain-nervous systems, and the endocrine-disrupting action of diesel exhaust particles (DEP). In utero exposure to low levels (0.1 mg DEP/m3) of DE from day 2 postcoitum (p.c.) until day 13 p.c. reduced the expression level of Ad4BP/SF-1 mRNA and thereby might affect the development of gonads. Low levels of DE also reduced the expression of several genes known to play key roles in gonadal development, including an enzyme necessary for testosterone synthesis. Mature male rats exposed to DE during the fetal period showed an irreversible decrease in daily sperm production due to an insufficient number of Sertoli cells. DE exposure during the fetal period influenced the brain tissue in newborn mice. In the 3 mg DEP/m3 exposure group at 10 weeks of age, a significant reduction in performance was observed in the passive avoidance learning test in both male and female mice. In addition, the fetal exposure of mice to DE affected the emotional behaviors associated with the serotonergic and dopaminergic systems in the mouse brain. In toluidine blue-stained specimens from the DE-exposed group, edema around the vessels where fluorescent granular perithelial (FGP) cells exist and degenerated granules within the FGP cytoplasm were observed; similar findings were obtained by electron microscopic examination. DEP contain many substances that stimulate Ah receptors, such as the polycyclic aromatic hydrocarbon containing benzo[a]pyrene. DEP also contain substances with estrogenic, antiestrogenic and antiandrogenic activities. The neutral substance fraction of DEP has the causal substance that reduces estrogen receptor mRNA expression. Evaluating the influence of these chemicals present in the environment on human health is an important task.

Animals↗

PubMed2001

Differences in the behaviour of Sprague--Dawley and Lewis rats during repeated passive avoidance procedure: effect of amphetamine.

The present paper investigated the differences in passive avoidance learning between Sprague--Dawley and Lewis rats. After initial habituation (experimental Part 1), measured as latencies to enter the dark, preferable compartment, the effect of treatment with amphetamine (8 mg kg(-1)b.w.), the retention performance compared with controls (saline) was tested in both rat strains in Parts 2--4. The intervals between Parts 2--4 were 24 or 49 days. Each experimental part consisted of testing lasting 6 days. On the 7th day the rats received drug treatment 1 h before the application of foot shock. The differences between rat strains were already detectable at the beginning of the study. During the repeated exposures of rats in Part 1, only Lewis rats, in contrast to Sprague--Dawley rats, exhibited the habituation. The repeated testing of rats in Parts 2--4, due to previous experience with an aversive stimulus, was considered as the retention test. In Parts 2--3 we observed only minor differences in the responses of both rat strains tested. Also no significant differences were observed between rat strains after amphetamine treatment that induced an amnesia-like effect in all retention trials. However, data shown in Part 4 revealed the largest differences between both strains. Control Lewis rats exhibited significantly higher retention responses than Sprague--Dawley rats. In the latter strain we observed no differences in avoidance latencies between controls and amphetamine treated rats. In Lewis rats the difference in avoidance performance between controls and amphetamine treated animals was highly significant due to their enhanced retention performance. In conclusion, the results presented in this study extend the known behavioural differences in tested rat strains to the passive avoidance procedure that, in addition, was performed for a total period of 4 months. Due to a known deficiency of hypothalamo-pituitary-adrenal axis activity in Lewis rats it can be hypothesized that the behavioural dissociation of this strain from Sprague--Dawley rats could be related to the different activity of this regulatory axis in the rat strains tested.

Amphetamine↗

PubMed1999

N-acetylserotonin, melatonin and their derivatives improve cognition and protect against beta-amyloid-induced neurotoxicity.

After a single injection of cholinergic neurotoxin ethylcholine aziridinium (AF64A, 3 nmol intracerebroventricularly (i.c.v.)), rats failed to perform the tasks in the active avoidance (learning and retention paradigms) and water maze tests. N-Acetylserotonin (NAS), melatonin and their newly synthesized derivatives, CA-15 and CA-18, (0.3-3.0 mg/kg daily for 12-14 days) reversed the effect of AF64A in a dose-dependent manner with CA-18 being the most active. Melatonin and NAS caused sedation absent in CA-18-treated rats. The studied compounds (25-500 microM for 72 hr) protected against beta-amyloid peptide (beta AP) fragment 25-35-induced neurotoxicity in cerebellar granule cell culture. Our results suggest that neuroprotecting properties of these compounds might mediate their cognition-enhancing effects. The results obtained warrant the further search for the novel types of safe neuroprotectors among the synthetic NAS/melatonin derivatives.

Alzheimer Disease↗

PubMed1984

The neuroteratogenicity of procarbazine in the rat: behavioral, morphological, and neurochemical aspects.

Pregnant female Sprague-Dawley rats were treated from day 12 through day 15 of gestation with procarbazine, an antineoplastic drug, and their offspring were subjected to tests of locomotor development and behavior. Treatment levels ranged from 0.5 mg/kg/day, a dose that produced no abnormalities, to 10 mg/kg/day, a dose that caused a marked micrencephaly in the absence of other teratological changes. Despite marked morphological brain changes, preweaning locomotor development, as assessed by open-field swimming activity and vertical grid climbing, was normal in all offspring. Post-weaning passive avoidance learning and retention were also normal. Groups that had been treated prenatally with teratogenic doses (5.0 and 10.0 mg/kg/day) displayed less rearing behavior in the open field, while ambulation in the periphery of the open field arena was unaffected. Groups treated with subteratogenic doses (0.5 and 1.0 mg/kg/day) did not differ from control. In addition to the behavioral studies, sodium-dependent high-affinity choline uptake and choline acetyltransferase activity (CAT) were measured (per mg protein) in the cortex and hippocampus of animals that had been exposed prenatally to either teratogenic or subteratogenic doses of procarbazine. In spite of a substantial reduction in size of both brain structures in the group receiving a teratogenic dose, choline uptake and CAT did not differ from control.

Abnormalities, Drug-Induced↗

PubMed1983

Effects of experimental suppression of active (REM) sleep during early development upon adult brain and behavior in the rat.

In order to test the hypothesis that active sleep (AS) is important for the normal development of the central nervous system, 3 different deprivation methods were applied to male Wistar rat pups during the first month of life. Daily injection of clomipramine from 8 to 21 days of age reduced the high level of AS to less than the adult value throughout most of the experimental period. Administration of clonidine from 8 to 21 days of life induced an almost total suppression of AS. Instrumental deprivation, using the 'pendulum' method, led to a significant (but less severe) AS reduction during 2-4 weeks of postnatal age. Open-field behavior testing in adulthood revealed a higher than normal level of ambulation in all 3 experimental groups. Masculine sexual responses were deficient, due to a low level of both mounts and ejaculations, in both clomipramine- and clonidine-treated animals. Neither passive avoidance learning nor dark preference tests revealed any differences between the experimental and control rats. Sleep observations showed that there was an abnormally high incidence of large myoclonic jerks during AS in both clomipramine- and clonidine-treated rats. Subsequent measurement of regional brain weights showed a significant reduction in the cerebral cortex and medulla oblongata, as compared with the respective control groups, in both the clomipramine- and the clonidine-treated rats. In addition, DNA and protein determination in the affected brain areas showed a proportional reduction in the cortex and in the medulla. These results demonstrate that interference with normal functioning either of AS per se or of specific monoaminergic transmitter systems during early development can produce long-lasting behavioral as well as brain morphological and biochemical abnormalities in later life.

Animals↗

PubMed2005

Do unprofitable prey evolve traits that profitable prey find difficult to exploit?

Prey that are unprofitable to attack (for example, those containing noxious chemicals) are often conspicuously patterned and move in a slower and more predictable manner than species lacking these defences. Contemporary theories suggest these traits have evolved as warning signals because they can facilitate both associative and discriminative avoidance learning in predators. However, it is unclear why these particular traits and not others have tended to evolve in unprofitable prey. Here we show using a signal detection model that unprofitable prey will evolve conspicuous colours and patterns partly because these characteristics cannot readily evolve in profitable prey without close mimicry. The stability of this signal is maintained through the costs of dishonesty in profitable prey. Indeed, unprofitable prey will sometimes evolve a conspicuous form to reduce mimetic parasitism, even in the unlikely event that this form can be more closely mimicked. This is one of the first mathematical models of the evolution of warning signals to allow for the possibility of mimicry, yet our analyses suggest it may offer a general explanation as to why warning signals take the form that they do. Warning signals and mimicry may therefore be more closely related than is currently supposed.

Animals↗

PubMed2006

Effects of Salvia officinalis L. (sage) leaves on memory retention and its interaction with the cholinergic system in rats.

OBJECTIVE: The leaves of sage (Salvia officinalis L., Lamiaceae) are reported to have a wide range of biological activities, such as anti-bacterial, fungistatic, virustatic, astringent, eupeptic and anti-hydrotic effects. To determine the mnemogenic effect of sage leaves, we investigated the effects of ethanolic extract of sage leaves and its interaction with cholinergic system on memory retention of passive avoidance learning in rats. METHODS: Post-training intracerebroventricular (i.c.v.) injections were carried out in all the experiments except ethanolic extract (i.p. intraperitoneally). RESULTS: Administration of ethanolic extract (50 mg/kg), pilocarpine (0.5 and 1 mg/rat), the muscarinic cholinoceptor agonist, and nicotine (0.1 and 1 microg/rat) increased, while mecamylamine (1, 5 microg/rat), the muscarinic cholinoceptor antagonist, and mecamylamine (0.01 and 0.1 microg/rat), the nicotine cholinoceptor antagonist decreased memory retention in rats. Activation of muscarinic cholinoceptors by pilocarpine potentiated the response of ethanolic extract. Also, pharmacological blockade of scopolamine attenuated potentiating effect of ethanolic extract. Activation of nicotinic cholinoceptor by nicotine potentiated the response of ethanolic extract. Blockade of nicotinic cholinoceptor by mecamylamine attenuated the response of ethanolic extract. CONCLUSION: It is concluded that the ethanolic extract of salvia officinalis potentiated memory retention and also it has an interaction with muscarinic and nicotinic cholinergic systems that is involved in the memory retention process.

Andorra↗

PubMed1979

Piracetam impairs the overshadowing of background stimuli by an informative CS.

The effects of Piracetam (100 mg/kg) on passive avoidance learning was investigated in a situation in which rats received multiple conditioning trials. The test was based on the untrained preference of rats for a dark, rather than a brightly lit compartment. After the initial black-white preference was tested, rats were restricted to the black compartment for conditioning. Different groups received different percentages of tone-shock pairings. After the conditioning trials the black-white preference was again tested. The saline-injected rats showed overshadowing of the background stimulus by the tone, in the group that had received 100% tone-shock pairings; and an acquired aversion to the background stimuli in the group that had received 0% tone-shock pairings. In the rats injected with 100 mg/kg Piracetam associative strength was partitioned indiscriminately between the tone and the background stimuli, regardless of the tone-shock pairings that had been received during conditioning.

Animals↗

PubMed1997

Learning/memory processes under stress conditions.

Using mice, changes in the learning/memory processes under various stress conditions were investigated in one-trial step-through type passive avoidance learning task. Pre-, post-training and pre-test foot shock (FS)-stress induced long-lasting, at least 96 h, facilitation of test trial latencies. Pre-training psychological (PSY)-stress induces facilitation and pre-test swimming (SW)-stress provokes impairment of test trial latencies. These effects of FS-, PSY- and SW-stress are all dependent on the timing of their exposure and due to their acute effect. Intraperitoneal administration of 1 mg/kg scopolamine 30 min pre-training caused impairment of test latencies in naive and pre-test FS-stressed animals but failed to affect both pre- and post-training FS-induced enhancement. Taken all these data together, it seems that cholinergic mechanism is partly involved in the FS-stress induced facilitation of test latencies, though the research on the changes in ACh levels at the action site in brain after FS-stress exposure is necessary for a definite conclusion.

Animals↗

PubMed1996

The involvement of Ca2+/calmodulin-dependent protein kinase in memory formation in day-old chicks.

Day-old chicks trained on a single trial passive avoidance learning task showed a significant increase, relative to untrained controls, in activity of the Ca2+/calmodulin-dependent protein kinase (CaMK) in the particulate fraction from tissues from the intermediate medial hyperstriatum ventrale region of the forebrain. The increased kinase activity was observed within 10 min following training and persisted for at least 70 min posttraining. Amnesia for the task was induced by micromolar concentrations of the specific CAMK II antagonist, KN-62, administered into the neostriatal/hyperstriatal region of the forebrain. The effect of KN-62 was lateralized. In the right hemisphere, KN-62 induced amnesia only when injected within 2. 5 min following training, with memory loss evident by 5 min posttraining. In contrast, in the left hemisphere amnesia was induced by KN-62 administered as late as 5 min posttraining, with onset of amnesia occurring after 10 min posttraining. The findings were interpreted within the context of a three-stage model of memory formation.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1993

Behavior, cortical ectopias, and autoimmunity in BXSB-Yaa and BXSB-Yaa+ mice.

The BXSB-Yaa recombinant inbred strain was created by crossing a male SB/Le with a female C57BL/6J. A Y chromosome factor derived from the SB/Le male, known as the autoimmune accelerator (Yaa), leads to an earlier onset and greater severity of autoimmune disease in males. In contrast, male BXSB mice, which lack the Yaa gene (called BXSB-Yaa+) because their Y chromosome is derived from the C57BL/6J, do not develop an autoimmune condition. To examine the influence of the Y chromosome on behavior, cortical ectopia incidence, and immune functioning, males and females of these two strains were compared. Significant strain differences (for both sexes) were found for behavioral measures including discrimination, spatial and avoidance learning, and activity. For immunological parameters, a sex difference was seen in the BXSB-Yaa (males more autoimmune), but not in the BXSB-Yaa+ strain. As expected, male BXSB-Yaas were more autoimmune than male BXSB-Yaa+s. However, there was also a strain difference for IgG in the females (BXSB-Yaa+ greater). No strain difference was found for the presence of ectopias. However, there was a sex difference across both strains, with males having a higher incidence. BXSB-Yaa and BXSB-Yaa+ mice have behavioral and immunological differences greater than would be predicted by their known genetic differences. The significant differences between the two female groups suggest that the two strains differ with respect to autosomal genes, in addition to the Y chromosome. The incidence of ectopias is independent of this genetic difference and is influenced by the subject's sex.

Animals↗

PubMed1999

Memory improvement by post-trial injection of lidocaine into the tuberomammillary nucleus, the source of neuronal histamine.

Brain histamine is exclusively contained within and released from neurons whose cell bodies are clustered in the tuberomammillary nucleus (TM) of the posterior hypothalamus. This experiment examined the effects of a transient inactivation of the TM on inhibitory avoidance learning. Rats with chronically implanted cannulae were tested on a 1-trial step-through avoidance task. Immediately following training, the rats received unilateral intra-TM infusions (0.5 microl) of lidocaine (5 or 20 microg). Control groups included vehicle-injected rats and a group given an injection of 20 microg lidocaine 5 h after training. When tested 24 h later, rats treated with 20 microg lidocaine exhibited longer step-through latencies than vehicle-treated controls, indicative of superior learning of the task. The failure of the delayed post-trial injection of lidocaine to significantly influence step-through latencies indicates that the compound influenced learning by modulating memory storage processes rather than by acting on performance variables during retrieval of the task. Thus, inactivation of the TM by lidocaine can exert facilitatory effects on mnemonic processing, which might be related to a temporary reduction of histaminergic activity during the early phase of memory consolidation.

Anesthetics, Local↗

PubMed2001

Critical periods for the effects of alcohol exposure on learning in rats.

Critical periods for alcohol-induced deficits in spatial navigation and passive avoidance learning were investigated with a rat model of fetal alcohol syndrome. Rats were exposed to alcohol prenatally (Gestational Days 1-10 or 11-22) or postnatally (Postnatal Days 2-10) or throughout all 3 periods. Offspring were tested in either a spatial navigation or an avoidance task as juveniles or adults. As juveniles, the combined exposure group took longer to learn the spatial navigation task compared with all other groups. This effect was not seen in adults. Passive avoidance performance was not affected. These results suggest that long-term exposure to alcohol during development has adverse effects on spatial learning. The lack of differences in the short-term exposure groups implies that there may not be 1 critical period of alcohol exposure, but that the adverse effects of alcohol during development may be cumulative on some behaviors.

Age Factors↗

PubMed1990

Differential effects of olfactory bulbectomy on beta-adrenoceptors in rat amygdala, hippocampus and cerebral cortex.

Rats were bilaterally olfactory bulbectomized. At 15 days post-lesion, olfactory bulbectomized (OB) rats exhibited significant deficits in the acquisition of passive avoidance learning compared to sham lesioned rats. beta-Adrenoceptor binding in the amygdala, hippocampus and cerebral cortex was assayed with (-)-[125I]iodocyanopindolol (ICYP). Scatchard analyses revealed no difference between OB and sham rats in maximal binding density (Bmax) in any of the three tissues. However, in the OB rats, the affinity of the beta-adrenoceptor for the ligand was significantly increased in the amygdala and hippocampus but not in the cortex. Bulbectomy did not affect the ratio of beta 1- to beta 2-adrenoceptor subtypes in the three brain tissues. In amygdala and hippocampus but not cerebral cortex, bulbectomy resulted in an increase in the proportion and the affinity of the high-affinity beta-adrenoceptor binding sites for isoproterenol. The affinity of the low-affinity sites in the hippocampus was also increased in the OB rats. The results suggest that olfactory bulbectomy causes supersensitivity of the amygdaloid and hippocampal beta-adrenoceptor by increasing the degree of coupling of the receptor with the stimulatory guanine nucleotide binding protein (Gs protein).

Amygdala↗

PubMed1988

Selective behavioural impairment after acute intoxication with trimethyltin (TMT) in rats.

A series of experiments was conducted to characterize the long term behavioural consequences of acute intoxication with trimethyltin (TMT) (5,6,7, mg/kg p.o.). The acute toxicity syndrome, including weight loss, convulsions, irritability and hyper-reactivity was confirmed in treated rats. These symptoms subsided to reveal marked increases in locomotor activity in a novel environment but no lasting effects on consummatory behaviour or sensorimotor integration. Neither two-way active avoidance nor passive avoidance learning were impaired by doses of up to 7 mg/kg p.o. although intertrial activity was elevated in the shuttle box and extinction responding was increased. Place navigation in a water maze was impaired, particularly at the highest dose of TMT (7 mg/kg p.o.) and when a brief training phase (8 trials) was used. Finally, TMT lesioned rats were compared with controls on spatial and non-spatial discrimination tasks. Following 7 mg/kg p.o. TMT rats were highly impaired on the spatial discrimination but not the non-spatial discrimination despite the greater difficulty of the latter task. Histological studies confirmed the pathological effects of TMT in limbic structures, particularly the pyramidal cells of CA1 and CA4, and also revealed increased acetylcholinesterase activity within the molecular layer of the dentate gyrus. The selective, long term behavioural impairments caused by TMT are discussed in the light of their qualitative similarity to the effects of hippocampectomy or hippocampal denervation. TMT lesioned rats may provide a suitable functional model for the partial hippocampal and temporal lobe pathology characteristic of Alzheimer's disease.

Animals↗

PubMed2004

The effect of prenatal hypoxia and malnutrition on memory consolidation in the chick.

The contribution of hypoxia and malnutrition to cognitive impairments was investigated in chicks incubated in conditions of reduced gas exchange. Previous research has shown that reducing gas exchange during incubation by wrapping half the eggshell with an impermeable membrane results in impaired cognitive ability in young chicks. The results were interpreted within a three stage sequential model of memory using discriminated bead avoidance learning. Reducing gas exchange for 4 days from day 10 or 14, of the 21-day incubation, inhibits memory formation and consolidation into permanent storage. The nature of the cognitive deficit depended on the timing of the insult. Environmental hypoxia (14% oxygen), induced from days 10 to 14 and from days 14 to 18, replicated the memory deficits found previously when eggs were partially wrapped with a membrane. Oxygen is necessary to break down food and to provide energy to build tissue proteins, and therefore hypoxia (partial wrapping or environmental incubation) may indirectly cause malnutrition. Malnutrition, induced by removing 5%, 7.5% or 10% albumin from the egg prior to incubation, had no significant effect on memory consolidation. Raised corticosterone levels occurred in chicks malnourished by 5% and 7.5%, but brain sparing was only evident in chicks with 7.5% albumin removal. Hatch rates were very low in 10% malnourished chicks. Using the chick as a model of prenatal stress, we have been able to isolate the effects of hypoxia from contributing maternal factors.

Age Factors↗

PubMed1995

Inhibitors of cAMP-dependent protein kinase impair long-term memory formation in day-old chicks.

There is substantial evidence that protein kinases, through the phosphorylation of substrate proteins, play a significant role in information processing in the brain, including processes underlying memory formation. Inhibition of the activity of the cyclic-adenosine monophosphate-dependent protein kinase A by the highly specific inhibitor, halofantrine, resulted in impairment of memory formation in day-old chicks trained on a single-trial passive avoidance task. A dose of 9.6 ng/chick halofantrine induced amnesia at the beginning of a protein synthesis-dependent long-term memory stage, the last of three stages of memory postulated to underly memory formation in the chick following passive avoidance learning. The concentration of halofantrine required for 50% inhibition of chick brain protein kinase A was found to be similar to that observed for bovine heart and rat liver. The amnestic effect of halofantrine is tentatively attributed to interference with de novo protein synthesis necessary for long-term memory consolidation. Neither anthraquinone nor the anthraquinone derivative anthraflavic acid, which have little effect on protein kinase A activity, affected memory retention. On the other hand, two other anthraquinone derivatives, chrysophanic acid and purpurin, which inhibit PKA activity, at doses of 0.25 and 0.5 ng/chick also yielded retention deficits. In these cases, however, retention losses occurred earlier than observed with halofantrine, at about 30 min post-training. The earlier effects of these inhibitors may be due to the additional inhibitory action of these compounds on protein kinase C activity, which has been demonstrated in previous studies to be implicated, possibly through phosphorylation of the GAP43 phosphoprotein, in memory processing in the stage of memory immediately preceding the protein synthesis-dependent long-term stage.

Animals↗