Active Avoidance Performance Research Articles

Research on Active Collision Avoidance and Hysteresis Reduction of Intelligent Vehicle Based on Multi-Agent Coordinated Control System

This paper provides a multi-agent coordinated control system to improve the real-time performance of intelligent vehicle active collision avoidance. At first, the functions and characteristics of longitudinal and lateral collision avoidance agents are analyzed, which are the main components of the multi-agent. Then, a coordinated solution mechanism of an intelligent vehicle collision avoidance system is established based on hierarchical control and blackboard model methods to provide a reasonable way to avoid collision in complex situations. The multi-agent coordinated control system can handle the conflict between the decisions of different agents according to the rules. Comparing with existing control strategies, the proposed system can realize multi decisions and planning at the same time; thus, it will reduce the operation time lag during active collision avoidance. Additionally, fuzzy sliding mode control theory is introduced to guarantee accurate path tracking in lateral collision avoidance. Finally, co-simulation of Carsim and Simulink are taken, and the results show that the real-time behavior of intelligent vehicle collision avoidance can be improved by 25% through the system proposed.

Stratified Control Strategy of Vehicle Longitudinal Active Collision Avoidance

In order to improve the safety and real-time performance of vehicle longitudinal active collision avoidance, a layered collision avoidance control method based on warning value, standard collision time safety model TTC and fuzzy PID is proposed in this paper. Based on the collision time safety model, the upper controller obtains the braking deceleration of the vehicle according to the relative speed and relative displacement of the obstacle in front. The lower controller is based on fuzzy PID, according to the brake deceleration speed of the upper vehicle, by controlling the pressure of the brake master cylinder of the vehicle, the control of vehicle speed is realized. Finally, using the CarSim/Simulink co-simulation platform, and taking the straight-line working condition as an example, the collision avoidance effect of the controlled vehicle under different speeds was simulated and verified. The results show that the upper controller can afford the appropriate speed of collision avoidance and deceleration according to the reference information, and the lower controller can adjust the brake deceleration speed according to the fuzzy PID, so as to realize the vehicle braking pressure, meet the requirements of longitudinal active collision avoidance.

Ventral hippocampus inactivation enhances the extinction of active avoidance responses in the presence of safety signals but leaves discrete trial operant active avoidance performance intact.

The acquisition of active avoidance (AA) behavior is typically aided by the presence of two signals-the warning signal, which predicts the future occurrence of an aversive event (e.g., shocks), and the safety signal, which is presented upon successful avoidance of oncoming shocks. While the warning signal could be conceived to act as a Pavlovian fear cue, and is likely mediated by brain areas that underlie Pavlovian fear cue conditioning, the neural substrates underlying safety signaling are less clear, largely due to the unavailability of AA tasks that are devoid of an explicit warning signal. The present study sought to investigate the role of the ventral hippocampus (VH) in safety signaled AA performance acquired without an explicit warning signal, using a novel discrete trial paradigm. Adult male Long Evans rats were divided into two groups and trained to acquire AA responses with, or without a safety signal. Analysis of the acquisition and stable state performance data revealed that the availability of a safety signal alone did not improve the acquisition or performance of AA responses. Furthermore, post-training, reversible VH inactivation did not impact stable state avoidance behavior. However, extinction of avoidance responses was facilitated in the group trained with a safety signal, and this effect was further potentiated by VH inactivation. Additional elevated plus maze (EPM), light-dark box, and locomotor tests demonstrated that VH inactivation reduced anxiety without affecting locomotor activity. Taken together, these results demonstrate the importance of VH in the extinction of persistent pathological avoidance behavior when safety is signaled.

Social isolation impairs active avoidance performance and decreases neurogenesis in the dorsomedial telencephalon of rainbow trout

Alterations in the social environment, such as isolating an individual that would normally live in a social group, can generate physiological responses that compromise an individual's capacity to learn. To investigate this, we tested whether social isolation impairs learning skills in the rainbow trout. We show that rainbow trout can achieve an active avoidance (AA) learning program with inter-individual variability. Moreover, c-Fos expression in dorsomedial telencephalon (Dm) correlates with the AA performance, indicating that this structure is involved in this cognitive task. Given that Dm participates in AA learning and this region is under plastic remodelling by addition of new-born neurons, we tested whether social isolation impinges on adult neurogenesis and, consequently, on the Dm cognitive outcome. Trout were reared for four weeks in control or isolated conditions. We found that social isolation diminished the percentage of adult-born neurons that are being incorporated into Dm network. Interestingly, the same isolation treatment also induced a severe deficit in the AA performance. Our results demonstrate a structure-to-function relationship between the Dm and the learning ability in an AA task, indicate that social isolation reduces the incorporation of adult-born neurons into Dm, and show that social isolation impairs the Dm-related cognitive function.

Density of acetylcholine esterase (AchE) and tyrosine hydroxylase (TH) containing fibers in the amygdala of roman high- and low-avoidance rats

The cholinergic and dopaminergic innervation of the amygdala plays an important role in attention, emotional arousal, aversive forms of associative learning, conditioned responses, and stress responsivity. Roman High- (RHA) and Low-Avoidance (RLA) rats are an ideal model to study the potential impact of this innervation on behavioral responses, because they were selected bidirectionally for differences in their two-way active avoidance performance. RHA rats are known to quickly acquire two-way active avoidance and show indications of enhanced impulsive behavior, novelty seeking, and vulnerability to substance abuse, whereas RLA rats exhibit a passive coping style with high levels of immobility and enhanced stress responsivity. In the present study, the density of acetylcholine esterase (AchE)-positive cholinergic fibers and tyrosine hydroxylase immunoreactive (TH-ir) fibers were analyzed in various amygdala nuclei. In comparison to RLA rats, RHA rats displayed a significantly higher density of AchE-positive fibers in the lateral nucleus (La), the major sensory input area of the amygdala. In contrast, RLA rats showed a higher density of TH-ir fibers in the lateral division of the central nucleus (CeL), which modulates amygdala output and is known to contain more corticotropin-releasing hormone (CRH) positive neurons in RLA than in RHA rats. The findings suggest that a higher density of AchE-positive fibers in the La of RHA rats may facilitate attentional mechanisms and aversive forms of associative learning in RHA rats, whereas the increased density of TH-ir fibers in the CeL of RLA rats may be involved in the regulation of enhanced CRH expression and stress responsivity.

P.1.h.031 Dopamine is involved in the different copulatory patterns of Roman high and low avoidance rats: studies with apomorphine and haloperidol

The cholinergic and dopaminergic innervation of the amygdala plays an important role in attention, emotional arousal, aversive forms of associative learning, conditioned responses, and stress responsivity. Roman High- (RHA) and Low-Avoidance (RLA) rats are an ideal model to study the potential impact of this innervation on behavioral responses, because they were selected bidirectionally for differences in their two-way active avoidance performance. RHA rats are known to quickly acquire two-way active avoidance and show indications of enhanced impulsive behavior, novelty seeking, and vulnerability to substance abuse, whereas RLA rats exhibit a passive coping style with high levels of immobility and enhanced stress responsivity. In the present study, the density of acetylcholine esterase (AchE)-positive cholinergic fibers and tyrosine hydroxylase immunoreactive (TH-ir) fibers were analyzed in various amygdala nuclei. In comparison to RLA rats, RHA rats displayed a significantly higher density of AchE-positive fibers in the lateral nucleus (La), the major sensory input area of the amygdala. In contrast, RLA rats showed a higher density of TH-ir fibers in the lateral division of the central nucleus (CeL), which modulates amygdala output and is known to contain more corticotropin-releasing hormone (CRH) positive neurons in RLA than in RHA rats. The findings suggest that a higher density of AchE-positive fibers in the La of RHA rats may facilitate attentional mechanisms and aversive forms of associative learning in RHA rats, whereas the increased density of TH-ir fibers in the CeL of RLA rats may be involved in the regulation of enhanced CRH expression and stress responsivity.

Targeting Neural Synchrony Deficits is Sufficient to Improve Cognition in a Schizophrenia-Related Neurodevelopmental Model

Cognitive symptoms are core features of mental disorders but procognitive treatments are limited. We have proposed a “discoordination” hypothesis that cognitive impairment results from aberrant coordination of neural activity. We reported that neonatal ventral hippocampus lesion (NVHL) rats, an established neurodevelopmental model of schizophrenia, have abnormal neural synchrony and cognitive deficits in the active place avoidance task. During stillness, we observed that cortical local field potentials sometimes resembled epileptiform spike-wave discharges with higher prevalence in NVHL rats, indicating abnormal neural synchrony due perhaps to imbalanced excitation–inhibition coupling. Here, within the context of the hypothesis, we investigated whether attenuating abnormal neural synchrony will improve cognition in NVHL rats. We report that: (1) inter-hippocampal synchrony in the theta and beta bands is correlated with active place avoidance performance; (2) the anticonvulsant ethosuximide attenuated the abnormal spike-wave activity, improved cognitive control, and reduced hyperlocomotion; (3) ethosuximide not only normalized the task-associated theta and beta synchrony between the two hippocampi but also increased synchrony between the medial prefrontal cortex and hippocampus above control levels; (4) the antipsychotic olanzapine was less effective at improving cognitive control and normalizing place avoidance-related inter-hippocampal neural synchrony, although it reduced hyperactivity; and (5) olanzapine caused an abnormal pattern of frequency-independent increases in neural synchrony, in both NVHL and control rats. These data suggest that normalizing aberrant neural synchrony can be beneficial and that drugs targeting the pathophysiology of abnormally coordinated neural activities may be a promising theoretical framework and strategy for developing treatments that improve cognition in neurodevelopmental disorders such as schizophrenia.

Influence of the Green Tea Leaf Extract on Neurotoxicity of Aluminium Chloride in Rats

Aluminium may have an important role in the aetiology/pathogenesis/precipitation of Alzheimer's disease. Because green tea (Camellia sinensis L.) reportedly has health-promoting effects in the central nervous system, we evaluated the effects of green tea leaf extract (GTLE) on aluminium chloride (AlCl3 ) neurotoxicity in rats. All solutions were injected into the cornu ammonis region 1 hippocampal region. We measured the performance of active avoidance (AA) tasks, various enzyme activities and total glutathione content (TGC) in the forebrain cortex (FbC), striatum, basal forebrain (BFb), hippocampus, brain stem and cerebellum. AlCl3 markedly reduced AA performance and activities of cytochrome c oxidase (COX) and acetylcholinesterase (AChE) in all regions. It decreased TGC in the FbC, striatum, BFb, hippocampus, brain stem and cerebellum, and increased superoxide dismutase activity in the FbC, cerebellum and BFb. GTLE pretreatment completely reversed the damaging effects of AlCl3 on AA and superoxide dismutase activity, markedly corrected COX and AChE activities, and moderately improved TGC. GTLE alone increased COX and AChE activities in almost all regions. GTLE reduces AlCl3 neurotoxicity probably via antioxidative effects and improves mitochondrial and cholinergic synaptic functions through the actions of (-)-epigallocatechin gallate and (-)-epicatechin, compounds most abundantly found in GTLE. Our results suggest that green tea might be beneficial in Alzheimer's disease.

P.5.005 Effects of a novel neuroprotective calcium salt of N-(5-hydroxy-nicotinoyl)-L-glutamate in a model of Alzheimer's disease and in aging rodents

The nootropic drug oxiracetam (50 and 100 mg/kg) had no effect on one-trial passive avoidance acquisition in CD-1 mice, while the acetylcholinesterase inhibitor physostigmine improved passive avoidance performance at doses of 0.025 and 0.05 mg/kg given either pre- or posttraining. In a multitrial avoidance task (shuttle-box), a consistent tendency to better performance was displayed by mice receiving oxiracetam (50 and 100 mg/kg) or physostigmine (0.01 and 0.025 mg/kg, but not 0.05 mg/kg). Combinations of the two drugs never improved active or passive avoidance performance more than drugs given separately. This indicates no advantage in combining nootropics and anticholinesterase inhibitors to improve learning and memory.

Diet composition exacerbates or attenuates soman toxicity in rats: Implied metabolic control of nerve agent toxicity

To evaluate the role of diet composition on nerve agent toxicity, rats were fed four distinct diets ad libitum for 28 d prior to challenge with 110μg/kg (1.0 LD50, sc) soman. The four diets used were a standard rodent diet, a choline-enriched diet, a glucose-enriched diet, and a ketogenic diet. Body weight was recorded throughout the study. Toxic signs and survival were evaluated at key times for up to 72h following soman exposure. Additionally, acquisition of discriminated shuttlebox avoidance performance was characterized beginning 24h after soman challenge and across the next 8 d (six behavioral sessions). Prior to exposure, body weight was highest in the standard diet group and lowest in the ketogenic diet group. Upon exposure, differences in soman toxicity as a function of diet became apparent within the first hour, with mortality in the glucose-enriched diet group reaching 80% and exceeding all other groups (in which mortality ranged from 0 to 6%). At 72h after exposure, mortality was 100% in the glucose-enriched diet group, and survival approximated 50% in the standard and choline-enriched diet groups, but equaled 87% in the ketogenic diet group. Body weight loss was significantly reduced in the ketogenic and choline-enriched diet groups, relative to the standard diet group. At 1 and 4h after exposure, rats in the ketogenic diet group had significantly lower toxic sign scores than all other groups. The ketogenic diet group performed significantly better than the standard diet group on two measures of active avoidance performance. The exacerbated soman toxicity observed in the glucose-enriched diet group coupled with the attenuated soman toxicity observed in the ketogenic diet group implicates glucose availability in the toxic effects of soman. This increased glucose availability may enhance acetylcholine synthesis and/or utilization, thereby exacerbating peripheral and central soman toxicity.

The effect of sodium metabisulphite on active avoidance performance in hypercholesterolemic rats

The purpose of this study was to investigate the effects of hypercholesterolemia and sulphite on active avoidance learning. Male Wistar rats were divided into eight groups as follows: Control (C), Sulphite (S), Vitamin E (E), Sulphite + Vitamin E (SE), Hypercholesterolemia (H), Hypercholesterolemia + Sulphite (HS), Hypercholesterolemia + Vitamin E (HE), and Hypercholesterolemia + Sulphite + Vitamin E (HSE). At the end of the experimental period, the serum cholesterol level (mean ± SD) was significantly higher in H group (111.5 ± 11.11 mg dL(-1) ) as compared to C group (63.5 ± 4.9 mg dL(-1) ). Levels of thiobarbituric acid reactive substances (TBARS) were increased in HS group as compared to C, H, and S groups. Vitamin E reduced TBARS levels in HSE group compared with HS group. Active avoidance results indicated that hypercholesterolemia was associated with learning impairment. Our data clearly revealed that the combination of hypercholesterolemia and sulphite results in exaggerated impairment of active avoidance. Vitamin E improved active avoidance in HSE group compared with HS group. Therefore, the synergistic effect of hypercholesterolemia and sulphite may be associated with a considerable health risk.

Amygdala Activity, Fear, and Anxiety: Modulation by Stress

Amygdala Activity, Fear, and Anxiety: Modulation by Stress

Reelin haploinsufficiency reduces the density of PV+ neurons in circumscribed regions of the striatum and selectively alters striatal-based behaviors

Reelin, a large extracellular matrix glycoprotein, is down-regulated in the brain of schizophrenic patients and of heterozygous reeler mice (rl/+). The behavioral phenotype of rl/- mice, however, matches only partially the schizophrenia hallmarks. We recently reported (Marrone et al., Eur J Neurosci 24:20062-22070, 2006) that homozygous reeler mutants (rl/rl) exhibit reduced density of parvalbumin-positive (PV+) GABAergic interneurons in anatomically circumscribed regions of the neostriatum. Assuming that in rl/+ mice may also show regional reduction of striatal GABAergic interneurons, behavioral impairments should selectively emerge in tasks depending on specifically altered striatal circuits. We mapped the density of striatal PV+ interneurons in rl/+ and wild-type (+/+) mice and measured their performance in tasks depending on distinct striatal subregions. Our findings show that, contrary to what would be expected on the basis of gene dosage criteria, the striatal regions in which rl/rl mice exhibited decreased density of PV+ interneurons were either unaltered (rostral striatum) or equally altered (dorsomedial and ventromedial intermediate striatum, caudal striatum) in rl/+ mice. The anatomical findings were paralleled by behavioral deficits in fear extinction and latent inhibition, respectively, requiring the dorsomedial and ventromedial striatal regions. Conversely, active avoidance performance, which requires the dorsolateral region, was unaffected. Reelin haploinsufficiency alters the density of PV+ neurons in circumscribed regions of the striatum and selectively disrupts behaviors sensitive to dysfunction of these targeted regions. This aspect should be considered when designing experiments aimed at evaluating the impact of reelin haploinsufficiency in schizophrenia-associated cognitive disturbances in rl/+ mutants.

Effects of Amygdala Inactivation on the Expression of Conditioned Fear and the Performance of Active Avoidance

Effects of Amygdala Inactivation on the Expression of Conditioned Fear and the Performance of Active Avoidance

Genetic and pharmacological approaches to evaluate the interaction between the cannabinoid and cholinergic systems in cognitive processes

The objective of this study was to investigate the possible interactions between the cannabinoid and cholinergic systems in memory and learning processes by using genetic and pharmacological approaches in two different behavioural models, the active avoidance and the object recognition test. The effects induced by nicotine, physostigmine and scopolamine were studied in CB(1) receptor knockout and wild-type mice in the active avoidance paradigm. In addition, the effects of pretreatment with the CB(1) receptor antagonist rimonabant were evaluated on the responses induced by nicotine in the active avoidance and the object recognition tasks in wild-type mice. Nicotine (0.5 mg kg(-1) s.c.) did not modify the performance of CB(1) knockout and wild-type mice in this model, whereas scopolamine (0.5 mgkg(-1) i.p.) impaired the performance in both genotypes. Physostigmine (0.1 mg kg(-1) i.p.) increased the active avoidance performance in wild-type but not in CB(1) knockout mice. Rimonabant (0.3, 1, 3, and 10 mg kg(-1)) did not modify the performance in the active avoidance test, given alone or co-administered with nicotine. In contrast, nicotine enhanced the performance in the object recognition task but this response was attenuated by rimonabant co-administration. The present findings revealed that the cognitive effects of nicotine and physostigmine were attenuated in the absence of CB(1) receptor activity. Scopolamine effects were independent from CB(1) receptors.

Neurochemical and behavioral consequences of striatal injection of 5,7-dihydroxytryptamine

It is known that central serotonin (5HT) is involved in anxiety, but the behavioral results of many studies have been inconsistent. A prevalent research approach is to destroy 5HT neurotoxically. Such lesions were mostly generated by injecting 5,7-dihydroxytryptamine into ventricles or raphé nuclei, leading to rather global losses of 5HT in the brain. However, there is evidence for differential effects of 5HT in different brain structures regarding anxiety. Therefore, we decided to study the effects of injecting 5,7-dihydroxytryptamine into the forebrain. We chose the ventral striatum as the site of injection, since there is evidence that 5HT may be involved in anxiety there. We administered the neurotoxin bilaterally in adult rats, and analyzed neurochemical and behavioral consequences in three experiments. The first one showed that the toxin dose-dependently (10–50μg) depleted 5HT in the ventral striatum, neostriatum, frontal cortex, and amygdala. Besides 5HT, dopamine was also partly depleted there. This dopaminergic lesion was prevented in a second experiment, where rats were pre-treated systemically with the dopamine reuptake inhibitor nomifensine. In the final experiment, the functional consequences of such 5HT lesions were tested, which yielded moderate anxiogenic effects in the elevated plus maze and in the open field. Also, there were lesion effects on aversively motivated ultrasonic vocalization during an active avoidance test. In contrast, active avoidance performance itself and general activity in the open field were not affected. Lesion effects became discernible there when challenging rats with MDMA. The psycho-stimulatory effectiveness of this drug, which acts largely via the availability of 5HT in the brain, was reduced to degrees that depended on the size of 5HT lesion. These results are discussed with respect to factors such as severity of lesion, anatomical specificity, and the role of 5HT in anxiety.

Beneficial effects of docosahexaenoic acid on active avoidance performance in 1K-1C hypertensive rats

The present study evaluated the role of chronic docosahexaenoic acid (DHA) supplementation on active avoidance learning task performance in experimental hypertension. Male Wistar rats were randomly divided into five experimental groups as follows: control, sham, DHA treated, 1K-1C hypertensive, and 1K-1C hypertensive + DHA treated. Hypertension was induced in 1K-1C rats via placing a silver clip (0.20-mm ID) around the left renal artery following a right uninephrectomy. DHA (36 mg/kg/day) was given to the treatment groups for 60 days by gastric gavage. Arterial blood pressure was measured by using the tail-cuff method. Active avoidance responses were determined by an automated shuttle-box. In brain (cerebrum) and hippocampus tissues, thiobarbituric acid reactive substances (TBARS) and nitrite levels were measured by fluorometric methods. DHA supplementation decreased blood pressure in hypertensive rats. Data from active avoidance training indicated that performance of active avoidance learning tasks were significantly impaired in 1K-1C hypertensive rats, but was completely restored by DHA supplementation. Increased cerebrum TBARS levels in 1K-1C rats were abolished by DHA administration. Cerebrum nitrite levels were lower in the DHA, 1K-1C and 1K-1C + DHA treated groups compared to controls. Hippocampus nitrite levels were lower in DHA treated and 1K-1C hypertensive rats compared to controls and higher in 1K-1C + DHA treated rats compared to the 1K-1C group. Our data indicates that DHA supplementation improves the performance of active avoidance learning tasks which is impaired in experimental hypertension. These affirmative changes might be due to a DHA-induced decrease in lipid peroxidation which may in turn limit the consumption of nitric oxide (NO) which promotes active avoidance learning.

Central administration of a caspase inhibitor impairs shuttle-box performance in rats

Recent studies suggest that caspase-3-mediated mechanisms are essential for neuronal plasticity. N-benzyloxycarbonyl-Asp(OMe)-Glu(OMe)-Val- Asp(OMe)-fluoromethyl ketone (z-DEVD-fmk), a caspase inhibitor with predominant specificity toward caspase-3, has been shown to block long-term potentiation in hippocampal slices. Intrahippocampal infusion of a caspase-3 inhibitor to rats has been shown to significantly impair spatial memory in the water maze. The present work was designed to study whether i.c.v. administration of a caspase-3 inhibitor z-DEVD-fmk impairs learning in other tasks related to specific forms of memory in rats. The rats received bilateral injections of z-DEVD-fmk or N-benzyloxycarbonyl-Phe-Ala-fluoromethyl ketone (z-FA-fmk) (“control” peptide) at a dose of 3nmol. Administration of z-DEVD-fmk significantly decreased the number of avoidance reactions in some blocks of trials in the active avoidance (shuttle box) learning, while z-FA-fmk had no effect as compared with intact rats. However, only a slight effect of the caspase inhibitor across the session was found. z-DEVD-fmk impaired development of some essential components of the two-way active avoidance performance, such as escape reaction, conditioned fear reaction, and inter-trial crossings. Measurement of caspase-3 activity in rat brain regions involved in active avoidance learning revealed most expressed z-DEVD-fmk-related inhibition of the enzyme activity (about 30%) in the fronto-parietal cortex. A similar effect was close to significant in the hippocampus, but not in the other cerebral structures studied. In primary cultures of cerebellar neurons z-DEVD-fmk (2–50μM) inhibited caspase-3 activity by 60–87%. We suggest that moderate inhibition of caspase-3 resulting from the central administration of z-DEVD-fmk to rats may impair active avoidance learning. Taking into account previous data on the involvement of neuronal caspase-3 in neuroplasticity phenomena we assume that the enzyme may be important for selected forms of learning.

Behavioral effects of dehydroepiandrosterone in adult male rats

It is well-documented that dehydroepiandrosterone (DHEA) exhibits various behavioral effects in rodents, at least one of which is modulation of learning/memory processes in several test paradigms. However, little is known about the influence of DHEA on cognitive performance in the adult rodents. This work was designed to determine whether chronic DHEA administration during 10 days in the high (0.7 mg/kg, s.c.) or low (0.1 mg/kg, s.c.) doses has any effect on learning/memory abilities and behavior in the adult male rats (5- to 6-month old). Effect of DHEA was estimated in active and passive avoidance tasks, behavior was registered in the elevated “plus” maze and the “open field” test. DHEA in the high dose significantly ( p<0.05) increased time spent and the number of enterings in the “open” arms of the elevated “plus” maze in intact male rats as compared with the control rats. DHEA in the low dose significantly ( p<0.05) decreased horizontal and vertical locomotor activity and grooming behavior, whereas DHEA in the high dose did not significantly modify behavior in intact rats as compared with control group. Results of the ANOVA on passive avoidance performance revealed no statistically significant differences among the groups receiving DHEA in the high or low doses as compared to the control. However, DHEA in the low dose significantly ( p<0.05) reduced the number of correct avoidance responses in intact rats as compared to the control rats, while in rats treated with the high dose DHEA, the active avoidance performance did not differ significantly from the control. Thus, chronic DHEA administration has a modulatory action on the learning and behavior of the adult male rats.

The ameliorating effects of acute and chronic administration of LiuWei Dihuang Wang on learning performance in rodents.

The ameliorating effects of LiuWei Dihuang Wang (LDW) after single, one-week or two-week treatment of scopolamine (SCOP)-induced and p-chloroamphetamine (PCA)-induced amnesia by using the passive avoidance task and the facilitatory effects on two-way active avoidance performance in rats were studied. LDW (2 g/kg) after single treatment significantly prolonged the shortened step-through latency induced by SCOP and PCA. Then, SCOP- and PCA-induced amnesia was reversed by 1 and 0.1-1 g/kg LDW with one-week consecutive treatment respectively. For two-week consecutive treatment with LDW, the reversal from SCOP- and PCA-induced amnesia required only 0.01 g/kg. However, the rats treated with LDW only at 0.5, but not 0.01-0.1 g/kg, before or after each training session showed an increasing number of avoidances and a decreasing number of escapes on days 2-5 of learning. LDW at any dose alone did not influence the step-through latency in the training trial produced by non-shock rats, the motor activity and pentobarbital-induced hypnosis in rodents. These results suggest that LDW possesses the anti-amnestic and cognitive-enhancing activities related to the memory processes, and these activities were parallel to treatment duration and dependent on the learning models.