Visual snake aversion in Octodon degus and C57BL/6 mice

Animal Cognition - Phobia against spiders or snakes is common in humans, and similar phobia-like behaviors have been observed in non-human animals. Visual images of snakes elicit phobia in humans,...     

Excitotoxic lesions restricted to the dorsal CA1 field of the hippocampus impair spatial memory and extinction learning in C57BL/6 mice

Recent studies in patients with hippocampal lesions have indicated that the degree of memory impairment is proportional to the extent of damage within the hippocampus. Particularly, patients with damage restricted to the CA1 field demonstrate moderate to severe anterograde amnesia with only slight retrograde amnesia. Comparable results are also seen in other species such as non-human primates and rats; however, the effect of selective damage to CA1 has not yet been characterized in mice. In the present study, we investigated the effects of excitotoxic (NMDA) lesions of dorsal CA1 on several aspects of learning and memory performance in mice. Our data indicate that dorsal CA1 lesioned mice are hyperactive upon exposure to a novel environment, have spatial working memory impairments in the Y-maze spontaneous alternation task, and display deficits in an 8-arm spatial discrimination learning task. Lesioned mice are able to acquire an operant lever-press task but demonstrate extinction learning deficits in this appetitive operant paradigm. Taken together, our results indicate that lesions to dorsal CA1 in mice induce selective learning and memory performance deficits similar to those observed in other species, and extend previous findings indicating that this region of the hippocampus is critically involved in the processing of spatial information and/or the processing of inhibitory responses.     

Differential effects of localized lesions of n. accumbens on morphine- and amphetamine-induced locomotor hyperactivity in the C57BL/6J mouse.

Mice of the C57BL/6J strain became hyperactive to increasing doses of morphine sulfate. This response was similar to locomotor hyperactivity induced by amphetamine. Lesions and chemical blockade of posterior n. accumbens abolished amphetamine-induced hyperactivity and reduced but did not abolish the morphine response. These experiments demonstrate that the response to the two drugs is mediated by overlapping but noncongruent neural systems.     

Digital measurement of operant disk press force maintained in CD-1, BALB/c, and C57BL/6 mice

Force of disk press responses by inbred (C57BL/6 and BALB/c) and outbred (CD-1) mice were measured with a PC/DOS-based system, which allowed for continuous measurement of pressing, as well as for control of reinforcer presentation on the basis of response-force dimensions. Photobeam-based measurement of mouse entry into a hopper where reinforcers were presented provided additional information about anticipatory and consumatory behavior in relation to environmental stimuli leading up to reinforcer delivery Disk pressing was generated and measured with the use of an analog-to-digital interface with all three mouse strains. The strains differed in the physical and temporal characteristics of the disk press, as well as in the behavioral chain leading to reinforcer presentation. These measurement methods appear well suited for quantitating functional behavioral differences occasioned by genetic variations in mice.     

Behaviors of Swiss-Webster and C57/BL/6N sin mice in a fear/defense test battery

When confronted by an approaching threat stimulus (experimenter or laboratory rat), Swiss-Webster mice show initial flight, followed by freezing and defensive vocalization and biting, the latter only when escape is blocked. These defense patterns resemble those of the wild rat, suggesting that mice of this strain do not show the reductions in flight and defensive threat/attack that are typical of laboratory rats. C57/BL/6N Sin strain mice showed fewer avoidances to an approaching predator, as well as reduced vocalization and defensive biting, a pattern more similar to that of laboratory rats. As with rats, female mice appeared to be more defensive to a predator. They showed greater reactivity to dorsal contact and more frequent defensive biting and jump attacks than males of the same strains. These patterns of defensive behaviors suggest that, although strain differences in defense are substantial, laboratory mice are suitable for, and may offer several advantages in, the study of the genetic, endocrine, and pharmacological basis of antipredator defense. © 1995 Wiley-Liss, Inc.     

Age-related impairment in the 250-millisecond delay eyeblink classical conditioning procedure in C57BL/6 mice

In this study we tested 4-, 9-, 12-, and 18-month-old C57BL/6 mice in the 250-msec delay eyeblink classical conditioning procedure to study age-related changes in a form of associative learning. The short life expectancy of mice, complete knowledge about the mouse genome, and the availability of transgenic and knock-out mouse models of age-related impairments make the mouse an excellent species for expanding knowledge on the neurobiologically and behaviorally well-characterized eyeblink classical conditioning paradigm. Based on previous research with delay eyeblink conditioning in rabbits and humans, we predicted that mice would be impaired on this cerebellar-dependent associative learning task in middle-age, at ~9 months. To fully examine age differences in behavior in mice, we used a battery of additional behavioral measures with which to compare young and older mice. These behaviors included the acoustic startle response, prepulse inhibition, rotorod, and the Morris water maze. Mice began to show impairment in cerebellar-dependent tasks such as rotorod and eyeblink conditioning at 9 to 12 months of age. Performance in hippocampally dependent tasks was not impaired in any group, including 18-month-old mice. These results in mice support results in other species, indicating that cerebellar-dependent tasks show age-related deficits earlier in adulthood than do hippocampally dependent tasks.     

Age differences in acquisition and retention of one-way avoidance learning in C57BL/6NNia and autoimmune mice

Acquisition and 48-h retention of a step-up active avoidance response were studied in separate age groups of C57BL/6NNia mice (aged 1.5, 3.5, 6, 12, or 26 months) and five strains of genetically autoimmune mice differing in life span. The C57BL/6NNia mice showed no change in ability to acquire the avoidance response between 1.5 and 3.5 months, but showed a steady decline in that ability thereafter. Mouse strains with early-onset autoimmune disorder (NZB/B1NJ, MRL/MpJ-lpr, and BXSB/MpJ) showed declines in acquisition capability between 1.5 and 3.5 months of age, whereas mouse strains with mild, late-onset autoimmune disorder (MRL/MpJ- + and NZBWF1/J) showed stable or improved acquisition during that period. Both the C57BL/6NNia and NZB/B1NJ mice showed age-dependent declines in 48-h retention performance by 12 months of age. These findings suggested that while 48-h retention performance deficits were most related to chronological age, avoidance acquisition deficits were related to development of autoimmunity.     

Nicotine enhances contextual fear conditioning in C57BL/6J mice at 1 and 7 days post-training

Nicotine has been demonstrated to enhance learning processes. The present experiments extend these results to examine the effects of nicotine on acquisition and consolidation of contextual and cued fear conditioning, and the duration of nicotine's enhancement of conditioned fear. C57BL/6 mice were trained with two pairings of an auditory CS and a foot shock US. Multiple doses of nicotine were given before or immediately after training and on testing day (0.0, 0.050, 0.125, 0.250, and 0.375 mg/kg, i.p). Freezing to both the context and auditory CS was measured 24h after training and again 1 week after training. Mice did not receive nicotine for the 1-week retest. Nicotine (0.125 and 0.250 mg/kg) given on both training and testing days enhanced freezing to the context at 24h. In addition, elevated freezing to the context was seen 1 week post-training in mice previously treated with 0.125 and 0.250 mg/kg nicotine. Thus, nicotine-treated mice did show elevated levels of freezing when retested 1 week later, even though no nicotine was administered at the 1-week retest. Mice that received nicotine on training day or testing day only and mice that received nicotine with mecamylamine, a nicotinic receptor antagonist, were not different from saline-treated mice. In addition, post-training administration of nicotine did not enhance fear conditioning. The present results indicate that nicotine enhancement of contextual fear conditioning depends on administration of nicotine on training and test days but results in a long-lasting enhancement of memories of contextual fear conditioning that remains in the absence of nicotine.     

Nicotine Produces a Within-Subject Enhancement of Contextual Fear Conditioning in C57BL/6 Mice Independent of Sex

Nicotine enhances learning including contextual fear conditioning. The present study extends previous work on nicotine and conditioned fear to examine the nature of nicotine's enhancement of contextual fear conditioning and sex differences in contextual fear conditioning in C57BL/6 mice using a within-subjects design. Mice were trained by pairing of an auditory stimulus of 80 dB, 6 cps train of broad-band clicks conditioned stimulus (CS) with a 2 sec., 0.35 mA shock unconditioned stimulus (US). Twenty-four hours later mice were tested for freezing in the original context, and one hour later mice were retested in the same context. A 0.5 mg/kg dose of nicotine was given either for three conditions: (1) before training, testing, and retesting; (2) before training and retesting; and (3) before retesting only. The use of a within-subjects design allowed for testing if nicotine would produce state-dependent deficits in contextual fear conditioning. Nicotine did enhance contextual fear conditioning in the groups that received nicotine for both training and testing. Nicotine, however, did not alter freezing when given on training but not testing or testing but not training. No sex differences, however, existed for conditioning or for nicotine's effects on conditioning. These results suggest that nicotine enhanced acquisition and retrieval processes but did not produce state-dependent deficits when administered just for training or just for testing.     

Nicotine produces a within-subject enhancement of contextual fear conditioning in C57BL/6 mice independent of sex

Nicotine enhances learning including contextual fear conditioning. The present study extends previous work on nicotine and conditioned fear to examine the nature of nicotine’s enhancement of contextual fear conditioning and sex differences in contextual fear conditioning in C57BL/6 mice using a within-subjects design. Mice were trained by pairing of an auditory stimulus of 80 dB, 6 cps train of broad-band clicks conditioned stimulus (CS) with a 2 sec., 0.35 mA shock unconditioned stimulus (US). Twenty-four hours later mice were tested for freezing in the original context, and one hour later mice were retested in the same context. A 0.5 mg/kg dose of nicotine was given either for three conditions: (1) before training, testing, and retesting; (2) before training and retesting; and (3) before retesting only. The use of a within-subjects design allowed for testing if nicotine would produce state-dependent deficits in contextual fear conditioning. Nicotine did enhance contextual fear conditioning in the groups that received nicotine for both training and testing. Nicotine, however, did not alter freezing when given on training but not testing or testing but not training. No sex differences, however, existed for conditioning or for nicotine’s effects on conditioning. These results suggest that nicotine enhanced acquisition and retrieval processes but did not produc state-dependent deficits when administered just for training or just for testing.     

Sexual Behavior of C57BL/10 Mice and its Relation to Early Social Experience

Unexpectedly, imitation of value judgments (design preferences) by male and female third and sixth graders (N = 366) generally did not result from exposure to adult film models (Ms). As expected, the variable of identification was more sensitive to the experimental manipulation of M's characterological traits than the measure of imitation. As expected, children identified with an honest as opposed to dishonest M; however, dominance versus submission had no such effect, suggesting that power related theories are far from adequate in explaining identification. In third grade, children viewed leadership strictly in terms of dominance, while, unexpectedly, in sixth they viewed leadership in terms of character (honesty). Other unexpected significant results also were heuristic, suggesting that several dependent variables not previously emphasized in the experimental modeling literature with children merit greater attention: negative imitation (negativism), negative identification (disaffiliation), and the effects of characterological and physical appearance variables on both identification and imitation.     

Effect of prior exposure to a lithium- and an amphetamine-paired flavor on the acoustic startle response in rats

The experiments reported here evaluated the hypothesis that an amphetamine-paired flavor elicits conditioned fear-arousal, whereas a lithium-paired flavor elicits conditioned nausea-disgust by examining the effect of prior flavor exposure on an acoustic startle reaction (ASR). Exposure to a lithium-paired flavor by intraoral infusion, either immediately prior to a startle session (Experiment 1) or during a startle session (Experiments 2 and 3), resulted in a blunted ASR. In contrast, intraoral infusion of an amphetamine-paired flavor resulted in a potentiated ASR. The blunted ASR produced by exposure to a lithium-paired flavor dramatically reversed to a potentiated ASR when rats were pretreated with the antiemetic drug ondansetron prior to the saccharin-lithium pairing (Experiment 3). The findings shed light on a mechanism by which rewarding drugs produce conditioned taste avoidance in rats.     

Acute stress facilitates trace eyeblink conditioning in C57BL/6 male mice and increases the excitability of their CA1 pyramidal neurons

The effects of stress (restraint plus tail shock) on hippocampus-dependent trace eyeblink conditioning and hippocampal excitability were examined in C57BL/6 male mice. The results indicate that the stressor significantly increased the concentration of circulating corticosterone, the amount and rate of learning relative to nonstressed conditioned mice, and the excitability of CA1 hippocampal pyramidal neurons. Behaviorally, there was no effect of the stressor on control mice that received unpaired presentations of the tone and periorbital shock, i.e., neither stressed nor nonstressed control mice showed an increase in conditioned responding that was above baseline levels. Biophysically, the stressor significantly decreased the amplitude of the post-burst afterhyperpolarization (AHP) and decreased spike frequency accommodation relative to cells from nonstressed control mice. The effect was significant for mice that were stressed either 1 h or 24 h earlier. The results suggest that the stressor increases the excitability of hippocampal pyramidal neurons and that the mechanism underlying this increase may contribute to the more rapid acquisition of hippocampally dependent eyeblink conditioning.     

Strain and sex differences on olfactory discrimination learning in C57BL/6J and DBA/2J inbred mice (Mus musculus)

In this study, the authors explored potential strain and sex differences in nonspatial cognitive ability. Beginning around 90 days of age, male and female C57BL/6J (C57) and DBA/2J (DBA) inbred mice (Mus musculus) were tested on a task of simple odor discrimination learning with 3 repeated reversals. Males learned the task more readily than females, and DBA mice learned the task more readily than C57 mice. All differences became evident after repeated testing. Similarity of perseveration measures indicated the differences were not due to inhibitory deficits. Instead, a phase analysis localized differences to a transitional period of reversal learning. Females increased transitional errors that more likely indicated adaptive sampling strategies than memory failures. C57 females used this strategy indiscriminately, but DBA females sampled as a function of environmental uncertainty.     

Acute starvation in C57BL/6J mice increases myocardial UCP2 and UCP3 protein expression levels and decreases mitochondrial bio-energetic function

Associations between uncoupling protein (UCP) expression and functional changes in myocardial mitochondrial bio-energetics have not been well studied during periods of starvation stress. Our aim was to study the effects of acute starvation, for 24 or 48 h, on combined cardiac mitochondrial function and UCP expression in mice. Isolated heart mitochondria from female mice starved for 48 h compared to that from mice fed revealed a significantly (p < 0.05) decreased adenosine diphosphate-to-oxygen ratio, a significantly increased proton leak and an increased GTP inhibition on palmitic acid-induced state 4 oxygen consumption (p < 0.05). These bio-energetic functional changes were associated with increases in mitochondrial UCP2 and UCP3 protein expression. In conclusion, our findings suggest that increased UCP2 and UCP3 levels may contribute to decreased myocardial mitochondrial bio-energetic function due to starvation.