A neural model for conditioned avoidance learning.
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Glucose was tested alone or in combination with two stimulant drugs, amphetamine and nicotine, in mice of the CD-1 strain subjected to five daily shuttle-box training sessions. Pretraining intraperitoneal administration of glucose (50 or 100 mg/kg) had no effect, while amphetamine and nicotine, given alone, significantly improved avoidance acquisition at a dose of 0.5 mg/kg, but not 0.025 mg/kg. Significant improvement of avoidance learning was also produced by a combination of glucose with the lower dose of amphetamine or nicotine. This enhancing action, produced by a combination of glucose and stimulant drugs, at doses ineffective by themselves, might be due to a concomitant cholinergic and dopaminergic activation, induced by glucose and stimulant drugs, respectively.
A wide range of cognitive-behavioral sequelae, including memory deficits, results from hard metal disease in humans. Cobalt is a common component in the manufacture of hard metals and is a biologically active, toxic substance. This study examined the effects of cobalt exposure in rats. Results showed decreased exploratory behavior and a trend for higher-dose subjects to show decreased passive avoidance learning. No significant differences in active maze learning were found. These results indicate the value of further explorations of the cognitive-behavioral effects of cobalt exposure and suggest a number of methodological cautions.
Prolonged isolation in mice is known to induce several behavioral changes, among which impairment of learning was also reported. On the other hand, alcohol is known to have either stimulant or depressant effects on behavior. Further, alcohol effect is also known to depend on strain-linked characteristics and on emotional ground of animals. Since prolonged isolation may differently change the emotional setting of mice, according to the strain, the behavioral effects of alcohol on avoidance learning, have been studied in two strains of male mice differentially housed. Evidences were obtained that ethanol can either improve or worsen learning performances according to the strain and the housing conditions adopted.
Two experiments assessed the effects of 1) combined subicular complex and posterior cingulate cortical lesions on training-induced neuronal activity (TIA) in the anterior ventral (AV) and medial dorsal (MD) thalamic nuclei; 2) hippocampal (Ammon's horn and dentate gyrus) lesions on TIA in cingulate cortex and in the AV and MD thalamic nuclei. The rabbits acquired a conditioned avoidance response (CR), stepping in an activity wheel upon hearing a 0.5-s tone (CS+), in order to prevent a foot-shock scheduled 5 s after tone onset. No response was required after a different, safety-predictive tone (CS-). In experiment 1 the combined subicular and cingulate cortical lesions enhanced thalamic TIA during acquisition and increased CR incidence in the first session of acquisition. These results confirmed the hypothesis that subicular and cingulate cortical efferents are not essential for thalamic TIA or for avoidance learning. Hippocampal lesions (experiment 2) also enhanced thalamic TIA. However, unlike subicular lesions, hippocampal lesions enhanced posterior cingulate cortical TIA as well, especially during extinction training. Hippocampal lesions did not affect CR performance. The results suggested that subicular excitatory efferents are responsible for incrementing cingulate cortical TIA, which is viewed as subserving associative attention. Activity from hippocampus downregulates the cue-elicited neuronal activity of the cingulo-thalamic circuits by suppressing the excitatory influence of the subiculum. The hippocampal influence reduces cingulo-thalamic cue-elicited activation in particular circumstances, such as the onset of CR extinction, when an expected reinforcer is omitted.
Retention of one-trial passive avoidance training was compared in diabetic and nondiabetic rats. Also compared were corticosterone concentrations associated with both training and retention testing, catecholamine excretion related to training, and regional brain catecholamine concentrations accompanying retention testing. Diabetic rats showed significantly better retention for the task than did nondiabetic rats. Associated with retention differences, diabetic rats had higher epinephrine excretion and nondiabetic rats had lower excretion after footshock training relative to baseline measures. Norepinephrine excretion was elevated in diabetics both in baseline measurement and during the 24 hr following footshock training. No differences were found in baseline or stimulated corticosterone concentration between diabetic and nondiabetic rats. Diabetic rats had higher concentrations of norepinephrine (NE) and dopamine (DA) and lower 3,4-dihydroxyphenylacetic acid/dopamine (DOPAC/DA) ratios in hypothalamus and higher NE in brain stem and amygdala than did nondiabetics, although both diabetic and nondiabetic rats had reduced DA and NE following retention testing. The results indicate that there are biochemical alterations in diabetes that may have important behavioral impact.
Aftetr one-trial passive-avoidance training, indepelenet groups of rats tested promptly after training or at successive 6-hour intervals displayed a repetitive pattern of high then low retention scores. These results suggest that some physiological rhythm may interact with retention performance.
The roles of different forebrain structures in memory formation in the chick were investigated using restricted radio-frequency lesions. Young chicks will spontaneously peck at a small bright bead. If the bead has been coated with a distasteful substance, the chicks learn not to peck a similar bead on subsequent presentation. Thus, in a single trial chicks learn not to peck at an aversive stimulus. Bilateral lesions of the intermediate part of the medial hyperstriatum ventrale (IMHV) prevented the acquisition of this 1-trial passive-avoidance learning task. However, neither bilateral lesions of the lateral cerebral area (LCA) nor sham operation affected learning. IMHV has previously been shown to be critically involved in the learning process of imprinting in the chick. The present experiment demonstrates that the role of IMHV in learning is not restricted to imprinting. The function of IMHV in imprinting has been suggested to be concerned with the recognition of objects. In the present study sham-operated and LCA-lesioned chicks recognized the visual characteristics of the training bead and did not avoid a bead of a different color in the test. We propose that IMHV-lesioned chicks fail to learn the task because they are unable to recognize the visual characteristics of the training bead and consequently cannot make the association between the bead and the unpleasant taste.
The error-related negativity (ERN) is a response-locked brain potential generated when individuals make mistakes during simple decision-making tasks. In the present study, we examined ERN under conditions of reward and punishment, among participants who scored extremely low or high on the socialization scale of the California Psychological Inventory (CPI). Participants completed a forced-choice task, and were rewarded for correct responses in half the trials, and punished for incorrect responses in the remaining trials. A significant interaction between socialization (SO) and condition revealed that low-SO participants produced smaller ERNs during the punishment task than during the reward task, whereas high-SO participants produced similar ERNs in both conditions. Reaction time and electromyogram data essentially bolster the interpretation that the ERN effects reflect differences in error salience for high-SO and low-SO participants, and are consistent with the avoidance-learning deficits seen in psychopathy.
Daily injections of cocaine administered to pregnant rabbits (Oryctolagus cuniculus) throughout gestation were associated with neural and behavioral changes during development and in adulthood, including altered neuron structure and function in areas receiving dopaminergic projections and retarded Pavlovian eyeblink conditioning with low-salient conditional stimuli. Studies of discriminative avoidance learning have shown changes in learning-related cingulothalamic neuronal activity, but no behavioral learning impairment in cocaine-exposed offspring. Here, low-salient stimuli were used during discriminative avoidance conditioning. Impairments early in behavioral acquisition were found, as well as alterations of anterior cingulate and medial prefrontal cortical, medial dorsal thalamic, and amygdalar neuronal response profiles and learning-related neuronal activity. These results elucidate the neural processes, impaired by prenatal cocaine, that support conditioning with low-salient stimuli.
Despite cumulative evidence showing the detrimental effect of psychosocial stress on the learning/memory functions in dementia diseases, the precise neurobiological mechanisms behind such an effect remain unclear. Mice of the senescence-accelerated mice prone 10 (SAMP10) strain, a neurodegenerative dementia model, were chronically exposed to social isolation stress from the age of 5 weeks. At the age of 12 weeks, conditioning memory and spatial memory were evaluated by one-trial passive avoidance and Y-maze tests, respectively. Chronic social isolation stress significantly reduced conditioning memory but did not affect spatial memory. Although further behavioral tasks using an elevated plus maze and a pain threshold test exhibited stress-induced analgesia, an analysis of covariance excluded the possibility that such analgesia might contribute to the stress-induced impairment of conditioning memory. In addition, endocrinological and immunohistochemical analysis revealed that isolation stress elevated the serum corticosterone levels and inhibited the increase in c-Fos expression in the central amygdaloidal nucleus (CeA) that is required for conditioning memory during passive avoidance learning. In conclusion, chronic social isolation stress exacerbated conditioning memory in SAM mice, probably through a glucocorticoid-mediated decrease in neural activation in the CeA.
The serotonergic deficits induced by 3,4-methylenedioxyethamphetamine (MDEA, "eve"), were examined and compared with 3,4 methylenedioxymethamphetamine (MDMA, "ecstasy"). A single dose of MDEA (10, 20, or 40 mg/kg IP) induced a dose-related hyperthermia, but only the highest dose significantly reduced 5-HT content and 5-HT transporter density in the frontal cortex and in the hippocampus 7 days later. Long-term serotonergic deficits were much more marked when MDEA was given repeatedly (40 mg/kg IP., b.i.d., for 4 consecutive days). Single or repeated administration of MDEA induced no change on 5-HT1A receptor density in the frontal cortex, brain stem, or hippocampus, although 3 h after both treatments plasma corticosterone levels were significantly increased. MDEA (5-20 mg/kg, IP) produced significant retention deficits in a passive-avoidance learning task. Conversely, 7 days after the repeated administration of MDEA (40 mg/kg b.i.d., for 4 consecutive days) no effect on passive-avoidance performance was observed unless rats were treated again with another dose of MDEA (20 mg/kg IP) 30 min before the training trial. The 5-HT1A receptor antagonist, WAY 100635, prevented the impairment in retention performance induced by 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), but not by MDEA or MDMA, indicating that the effect of these amphetamine derivates was not mediated by 5-HT1A receptor activation. The results suggest the risk of serotonergic dysfunction associated with MDEA abuse in humans.