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PubMed1984

Residual effects of prolonged cannabis treatment on shuttle-box avoidance in the rat.

Chronic oral administration of cannabis extract to rats was examined for its residual effects on shuttle-box avoidance learning. In experiment 1 avoidance learning was assessed in rats that had been tested previously on other behavioral tests. Chronic treatment (3 months) facilitated the learning of shuttle-box avoidance in cannabis-treated animals relative to vehicle controls. In experiment 2 very similar results were obtained in naive rats. These and other residual effects of chronic cannabis treatment are similar to the effects of hippocampal lesions.

Animals↗
PubMed1982

[Adrenal cortical function in elaborating a passive avoidance conditioned reflex in rats adapted to experimental conditions].

Fluorometry was used to determine the content of 11-hydroxycorticosteroids (11-HCS) in the blood plasma of 2-month-old male rats in the course of passive avoidance learning by means of single electrocutaneous irritation (ECI) of the limbs. Pre-exposure of the animals for 7 days to experimental environment (over 3 min daily) led to a distinct reduction of the basal content of 11-HCS which returned to the initial level after adaptation discontinuance. One day after ECI the content of 11-HCS in rats which learned passive avoidance, was appreciably lower as compared to that in the animals which failed to learn the behavioral task. Five days after ECI the differences in the content of the corticosteroids in the animals of the two groups were little pronounced. It appears that while using passive avoidance as a long-term memory model, account should be taken of both the behavioral and emotional responses.

11-Hydroxycorticosteroids↗
PubMed1989

Behavioral characteristics of the SAM-P/8 strain in Sidman active avoidance task.

The behavior of the senescence-accelerated mouse (SAM-P/8) at the age of 1, 2, 4 and 10-11 months in Sidman active avoidance learning was analyzed, and compared to findings in the controls (SAM-R/1). At the age of 1 and 2 months, learning was comparable in these two strains. At the age of 4 and 10-11 months, SAM-P/8 but not SAM-R/1 learned active avoidance. We propose that SAM-P/8 can serve as a valid model of deficits in learning and memory.

Aging↗
PubMed1987

Active avoidance performance in genetically defined mice.

It has been concluded by several investigators that active avoidance performance in mice is primarily influenced or even determined by a single gene. The genetically defined strains C57BL/6 and BALB/c have provided evidence that an aberrant development of pyramidal cells and mossy fiber configuration in the hippocampus of BALB/c mice also is determined by a single gene. As a test of the generality of the single gene influence on avoidance learning, and to examine the relationship of the hippocampal defect to avoidance learning, adult male mice of the inbred progenitor strains C57BL/6ByJ and BALB/cByJ and their seven recombinant inbred strains were tested in a variant of the shuttle-box paradigm used in previous studies. BALB/c were found to acquire the avoidance response at a faster rate than C57BL/6, consistent with most earlier reports, but performances of the recombinant inbred strains failed to dichotomize about the progenitor strains. The rank order of performance scores for the recombinant inbred strains was different from that reported in previous studies. Thus the present data failed to support the interpretation of a single major gene influencing active avoidance learning. It is concluded that avoidance learning and performance cannot be considered as unitary variables and that the interaction of genetic with environmental factors, including the conditions of the specific testing situation, are important considerations in any interpretation of genetic effects. No relationship between the hippocampal lamination defect and avoidance performance was demonstrated.

Animals↗
PubMed1996

Limbic thalamic, cingulate cortical and hippocampal neuronal correlates of discriminative approach learning in rabbits.

Previous research employing lesions and recording of neuronal activity has implicated cingulothalamic and hippocampal circuitry in the mediation of discriminative instrumental avoidance learning in rabbits. This study was directed at the question of whether the cingulothalamic circuitry is specialized for avoidance learning, or whether it is also involved in appetitively motivated learning. Multi-unit neuronal recordings in the aforementioned areas were obtained as adult New-Zealand white rabbits learned to approach and orally contact a drinking spout for water reward after a tone conditional stimulus (CS+), and to ignore the spout after a different, non-predictive tone conditional stimulus (CS-). As during avoidance learning, excitatory and discriminative training-induced neuronal activity (TIA) developed during the course of approach learning. Discriminative TIA refers to development of greater neuronal firing response to the CS+ than to the CS-. Excitatory TIA refers to increased neuronal discharge magnitude during training compared to the activity elicited before training, when CS presentations were unpaired with foot-shock presentations. As during avoidance learning, TIA in anterior cingulate cortical and interconnected mediodorsal (MD) thalamic neuronal records preceded TIA in posterior cingulate cortical and interconnected anterior ventral thalamic records. Delayed changes also occurred in area CA1 of the hippocampus in parallel with changes in the posterior cingulate cortex and the anterior thalamic nuclei. In contrast to the avoidance-related activity, the changes in the thalamic areas preceded or occurred concurrently with changes in the related cingulate cortical areas. This difference is hypothesized to be due to a reduced or absent contribution of amygdaloid efferents to the approach learning-related TIA. The overall magnitude of the elicited training-induced neuronal responses was reduced, relative to the discharges during avoidance conditioning. The discharge magnitude differences suggested a greater recruitment of limbic circuit functions during avoidance learning, possibly due to the aversiveness and high arousal associated with the avoidance task. In general, the results indicate that the circuitry formed by interconnected cingulate cortical, limbic thalamic and hippocampal neurons has fundamentally similar functions in both approach and avoidance learning.

Animals↗
PubMed2000

Auditory noise can prevent increased extracellular acetylcholine levels in the hippocampus in response to aversive stimulation.

The intent of this study was to investigate neurochemical and behavioural effects of aversive stimulation and the impact of auditory background noise. Using in vivo microdialysis, hippocampal acetylcholine was extracted and subjected to HPLC analysis while male Wistar rats were exposed to aversive stimulation similar to that used in conventional procedures for aversive conditioning. Three groups of animals were used. Animals in the first group were exposed to a single tone/footshock pairing followed by a tone alone 2 h later. Animals in the second group served as controls and were only exposed to the tone without shock. A third group was exposed to the same tone/shock pairing and tone as the first group while being exposed to constant background noise during the whole experiment. The results showed, that the tone/shock combination led to pronounced behavioral and cholinergic activation. In contrast, exposure to background noise prevented the increase in hippocampal ACh levels to tone/shock stimulation. The unconditioned behavioural response, however, was not prevented suggesting that hippocampal ACh is not a necessary correlate of behavioural activation or arousal. A second experiment intended to investigate the effects of background noise in a shuttle box avoidance learning paradigm where rats were trained to avoid an aversive footshock, which was signalled by a tone. There, one group of rats was exposed to background noise during avoidance learning, and the other group was not exposed to noise. Whereas both groups learned to avoid the shock to some degree over training, the noise exposed animals did not show improvement in escape performance over the course of training, indicating that the noise hindered development of an adaptive response to the shock. In summary, our data indicate that background noise can prevent increased extracellular hippocampal ACh levels in response to an aversive stimulus, and can also lead to deficits in learning to escape from shock.

Acetylcholine↗
PubMed1995

Attenuation of memory with Tyr-D-Arg-Phe-beta-Ala-NH2, a novel dermorphin analog with high affinity for mu-opioid receptors.

The involvement of mu-opioid receptors in memory retrieval was examined in mice by using Tyr-D-Arg-Phe-beta-Ala-NH2 (TAPA), a novel dermorphin analog with high affinity for mu-opioid receptors, and passive avoidance learning. TAPA was intracerebroventricularly administered to mice before retention tests of passive avoidance learning. A 0.3-ng dose of TAPA markedly shortened step-down latency of passive avoidance learning, and the shortening of step-down latency was reversed by treatment with beta-funaltrexamine (5 micrograms), a mu-opioid receptor antagonist, indicating that TAPA (0.3 ng) attenuates memory retrieval. Although the attenuating dose (0.3 ng) of TAPA failed to affect horizontal or vertical locomotor activity, a 3-ng dose of TAPA showed a tendency to decrease vertical locomotor activity. A 30-ng dose of TAPA produced a significant increase in horizontal locomotor activity accompanied by a marked reduction of vertical locomotor activity. TAPA (3 ng) produced a significant increase in step-down latency of passive avoidance learning with lower intensity of electroshock or without electroshock during training. These results suggest that the activation of mu-opioid receptors impairs memory retrieval.

Amino Acid Sequence↗
PubMed1990

Retrograde amnesia in praying mantis after two successive learning processes.

Learning and memory consolidation was investigated in the mantis Stagmatoptera biocellata, by two successive trainings: a) the attack (A) avoidance training in which animals were not allowed to catch a mobile star, followed by the deimatic reaction (DR) avoidance training of not displaying this defensive response, or b) DR-avoidance training followed by A-avoidance training. The results showed that the presence and the 1 of A-avoidance learning and DR-avoidance learning did not affect the learning of the other training. Total retention of A-avoidance memory was demonstrated when A-avoidance training was given first, whereas DR-avoidance memory was significantly lost (716%) when the DR-avoidance training was given first. The retroactive forgetting of DR-avoidance memory is considered as retrograde amnesia rather than retroactive memory inhibition because it depends on the activity during A-avoidance training (number of attacks) and not the quantity of A-avoidance learning. The magnitude of the amnesic effect due to this distracting activity in the A-avoidance training appears to be remarkably similar to that reported in a previous work using nitrogen-induced anoxia as the amnesic factor.

Animals↗
PubMed1989

Effects of idebenone on memory impairment induced in ischemic and embolization models of cerebrovascular disturbance in rats.

Two rat models of memory impairment in passive avoidance learning induced by cerebrovascular disturbance, were established to estimate the effects of a cerebral metabolic enhancer, idebenone. Transient and global cerebral ischemia in rats, produced by 4-vessel occlusion for 200 s immediately after the acquisition trial of passive avoidance learning, shortened the latencies in the retention test trial performed 24 h later. This retrograde amnesia was reversed significantly by idebenone administered orally or intraperitoneally at the doses of 10 and 30 mg/kg before the retention test trial. Idebenone at a dose of 10 mg/kg, given intraperitoneally before or immediately after the ischemia, also markedly inhibited the appearance of amnesia. In the second model, permanent and cerebral hemisphere embolization produced by injecting 2,000 microspheres into the internal carotid artery, significantly impaired passive avoidance learning performed 7 days later. The repeated administration of idebenone (30 mg/kg, i.p.). once a day after the embolization, significantly improved the impairment of passive avoidance learning in the embolized rats. Furthermore, physostigmine and arginine-vasopressin as reference compounds improved the impairment of passive avoidance learning in these models. These findings suggest that idebenone ameliorates memory impairment induced by cerebral vascular disturbance in rats.

Administration, Oral↗
PubMedDate not supplied

[The effect of hormones from the peripheral endocrine glands on behavioral, learning and memory processes].

The present study was designed to explore the comparative influence of thyroid, adrenal, and gonadal hormones on the capability for learning, retention of memory traces and behavior in male rats under conditions of systemic administration of synthetic hormonal preparations. Behavior of animals was assessed during the active and passive avoidance learning, as well as in the open-field test. It was established that the increase in the level of corticosteroid, thyroid, or gonadal hormones did not affect the formation and retention of passive avoidance learning. Excess of corticosteroids increased behavioral activity but impaired the active avoidance learning and the following reproduction of the acquired reaction. Excess of gonadal hormones dramatically impaired the performance in the conditioned active avoidance test, and excess of thyroid hormones improved the active avoidance learning.

Adrenal Cortex Hormones↗
PubMed1987

Paraquat-induced, dose-dependent conditioned taste aversions and weight loss mediated by the area postrema.

Paraquat's (PQ) effect on feeding behavior in the rat was examined using a conditioned taste aversion (CTA) paradigm. CTA is a learned avoidance of tastes closely associated with prior illness. Male Sprague-Dawley rats trained to drink an instant breakfast solution were subsequently offered a novel-flavored solution and consumption was measured over 30 min. Following consumption of the novel solution, PQ (0.48-48.0 mumol/kg) was injected subcutaneously. Peak blood PQ concentrations were measured by serially sampling blood (0.15 ml) from an indwelling jugular cannula between 10 and 35 min after injection. Two days later, the rats were offered the same novel-flavored solution. Paraquat produced dose-dependent avoidance of the novel solution when injected subcutaneously. A PQ dosage of 2.7 mumol/kg or less did not alter consumption. The ED50 for CTA production of 13.0 mumol/kg was determined by log-probit analysis. The minimum effective dosage was 4.2 micron/kg. The doses examined did not produce overt clinical or histological signs of toxicity. Peak blood paraquat concentration was linearly related (r = 0.995) to dosage. Additionally when administered by gavage CTAs occurred only with a much larger PQ dosage (480 mumol/kg). Thermal lesions of a hindbrain circumventricular organ, the area postrema (AP), prevented PQ-induced CTAs despite repeated PQ injections. Additionally, weight loss following PQ exposure was also attenuated by AP lesions. CTAs were induced in these same AP-lesioned rats by oral administration of copper sulfate. This substance conditions taste aversions by activating vagal afferent neurons. The fact that copper sulfate-induced aversions were not blocked by lesions of the area posterema indicates that the lesioned rats are capable of forming CTAs when treated with a toxicant which does not act via the AP. These data indicate that PQ produces CTAs in a dose-dependent manner. Furthermore, PQ-induced CTAs and weight loss are mediated by the AP. The AP may contain receptors which detect xenobiotics, enabling animals to avoid future contact with these compounds.

Animals↗
PubMed1982

Effect of haloperidol and chlorpromazine on reversal learning of normal and striatectomized rats in a Y-maze.

Haloperidol (0.05-0.1 mg/kg) and chlorpromazine (0.5-1.0 mg/kg) improved reversal learning avoidance responses in a Y-maze, decreased intersessional fluctuations of errors and decreased the number of spontaneous exits from a correctly selected chamber. After bilateral lesions of the striatum this effect disappeared. Brain lesions also attenuated the ability of neuroleptics to suppress amphetamine-induced stereotypy and and accompanying defects in avoidance responses. The improvement of avoidance behavior by neuroleptics may be related to the reduction of spatial preference caused by functional asymmetry between the bilateral nigro-striatal systems.

Amphetamine↗
PubMedDate not supplied

Maternal age as a factor in determining the reproductive and behavioral outcome of rats prenatally exposed to ethanol.

Nulliparous Long-Evans rats were bred at one of four different ages and assigned to one of three treatment groups within each age condition. Maternal ages were 9, 18, 32, and 36 weeks. Treatment groups were ethanol (E), administered by gavage as 8 g/kg in two divided doses on days 10-14 of gestation, pair-fed (PF) controls, administered as an isocaloric sucrose solution by gavage on days 10-14 of gestation, and ad lib fed controls (C). All offspring were surrogate fostered shortly after delivery to untreated recently parturient dams. Litter sizes were standardized to 8 on the day of birth. Offspring were assessed longitudinally for growth, mortality, and behavior (olfaction, locomotor activity, maze learning, avoidance acquisition and startle). Approximately 85% of the 36 week old dams did not produce viable litters. In the remaining maternal age conditions, ethanol delayed offspring olfactory orientation and increased locomotor activity, the latter dissipating after 50-60 days of age. These ethanol-related effects occurred independent of maternal age condition. Maternal age, independent of ethanol, was a factor which reduced litter size and offspring weight up to 50 days, but produced few effects on behavior. The combination of maternal age and prenatal ethanol interacted to increase pregnancy loss (oldest maternal age), reduce offspring weight up to day 99 (oldest and middle maternal age), alter olfactory orientation performance (oldest and middle maternal age), reverse the typical ethanol-induced increase in activity for males in the figure-8 test (oldest maternal age group), shift the pattern of open-field activity, and change errors in a complex water maze. Not all of these interactions turned out to be specific to the ethanol X old maternal age condition. Several of the interactions occurred in both the old and middle maternal age conditions. The only effect of old maternal age that interacted strongly with ethanol was in their combined effects on reproduction. Here the combination of the two factors increased maternal mortality, the number of early pregnancy losses, and the number of litters where all members were dead or resorbed. It was concluded that short-term prenatal ethanol combined with advanced maternal age produces additive interactions on pregnancy success without affecting longer-term outcomes, while young maternal age showed no clear detrimental effects compared to the middle maternal age reference group.

Aging↗
PubMed1998

Oral toxicity of bis(2-ethylhexyl) phthalate during pregnancy and suckling in the Long-Evans rat.

Bis(2-ethylhexyl) phthalate (DEHP) is a compound widely used in plastics technology to impart flexibility to rigid polymers. We sought to determine whether the oral exposure of female rats to DEHP during gestation and suckling produces alterations in the litter. Female rats were exposed to different concentrations of DEHP suspended in drinking water (32.5 and 325 microl/litre) from day 1 of pregnancy to day 21 after delivery. Pup body weight gain and kidney, liver and testes weight was measured at different times (21, 28, 35, 42 and 56 days) after birth. Plasma concentrations of DEHP and histopathological alterations in kidneys, liver and testes were also studied. In addition, the ability of female pups (1 month of age) to perform a learned avoidance test, the 'beam walking' test, was evaluated. Perinatal exposure to DEHP produced no statistically significant changes in the body weight gain of offspring. Conversely, it produced a significant decrease in kidney and testes relative weight (organ/body weight) with a significant increase in relative liver weight. Signs of histological damage in kidneys, liver, and particularly testes, were observed. Pups exposed perinatally to the highest concentration of DEHP elicited a significant increase in the time necessary to perform the beam walking test.

Administration, Oral↗
PubMed2006

Cognitive inflexibility after prefrontal serotonin depletion is behaviorally and neurochemically specific.

We have previously demonstrated that prefrontal serotonin depletion impairs orbitofrontal cortex (OFC)-mediated serial discrimination reversal (SDR) learning but not lateral prefrontal cortex (PFC)-mediated attentional set shifting. To address the neurochemical specificity of this reversal deficit, Experiment 1 compared the effects of selective serotonin and selective dopamine depletions of the OFC on performance of the SDR task. Whereas serotonin depletions markedly impaired performance, OFC dopamine depletions were without effect. The behavioral specificity of this reversal impairment was investigated in Experiment 2 by examining the effect of OFC serotonin depletion on performance of a modified SDR task designed to distinguish between 3 possible causes of the impairment. The results showed that the reversal deficit induced by prefrontal serotonin depletion was not due to a failure to approach a previously unrewarded stimulus (enhanced learned avoidance) or reduced proactive interference. Instead, it was due specifically to a failure to inhibit responding to the previously rewarded stimulus. The neurochemical and behavioral specificity of this particular form of cognitive inflexibility is of particular relevance to our understanding of the aetiology and treatment of inflexible behavior apparent in many neuropsychiatric and neurodegenerative disorders involving the PFC.

5,7-Dihydroxytryptamine↗
PubMedDate not supplied

Recalling an aversive experience by day-old chicks is not dependent on somatic protein synthesis.

Long-term memory is dependent on protein synthesis and inhibiting such synthesis following training results in amnesia for the task. Proteins synthesized during training must be transported to the synapse and disrupting microtubules with Colchicines, and hence, blocking transport, results in transient amnesia. Reactivating memory for a previously learned avoidance triggers a biochemical cascade analogous to that following the initial training and renders the memory labile once more to protein synthesis inhibitors. However, the reminder-induced cascade differs in certain key features from that following training. Here we show that in a one-trial passive avoidance task in chicks, in contrast with initial consolidation following training, memory following a reminder is not impaired by Colchicine. We conclude that recall after a reminder does not require synaptic access to somatically synthesized proteins in this task. Our results support the hypothesis that in the chick, a reminder may instead engage local protein synthesis at the synapse, rather than in the soma.

Amnesia↗
PubMed1985

Arginine vasopressin, stress, and memory.

Arginine vasopressin (AVP) has been shown to have several non-renal actions including the potentiation of learned avoidance behavior in rats and improvement in cognitive functioning in humans. Research in our laboratory has confirmed these behavioral effects in rats using both peripheral and central injection of AVP. We have begun to examine the physiological basis for these effects. Peripheral administration of a vasopressor AVP antagonist reversed the prolongation of extinction produced by peripherally administered AVP in both active and passive avoidance, but also reversed the aversive unconditioned effects of AVP. However, central administration of the vasopressor AVP antagonist reversed peripheral effects of AVP only at doses shown to act peripherally to reverse vasopressor effects of AVP. An osmotic stress in doses known to liberate endogenous AVP mimicked the behavioral effects of exogenously administered AVP, and this stress effect was reversed by the AVP antagonist. These results support our hypothesis of separate but parallel AVP systems in the pituitary and brain with a role in behavioral adaptation to certain types of stress.

Animals↗