1,721,093 research outputs found
Chronic exposure to a novel odor increases pups' vocalizations, maternal care, and alters dopaminergic functioning in developing mice
No full textThis study was designed to assess the stress effect of manipulation of the olfactory
environment in developing mice. In a first experiment it was found that mouse pups could be
stressed (as measured by an increase in ultrasonic calls) by removing the litter from the dam
for 15 min/day for the first 14 days of life and exposing them to a novel odor (clean bedding).
This stress procedure also produced a long-term modification in maternal behavior. The
stress response (ultrasounds) and the modification of maternal behavior were prevented ..
Impairments produced by amphetamine and stress on memory storage are reduced following a chronic stressful experience
No full textPost-training administration of the psychostimulant, amphetamine or post-trial exposure to restraint stress impaired retention of an inhibitory avoidance response in DBA/2 (DBA) mice. The effect of amphetamine was dose-dependent (1-3 mg/kg) whilst the effect of stress depended on restraint duration (15, 30, or 60 min). Both effects on retention performance appeared to be due to an effect on memory consolidation. In fact, they were observed when the drug and the stressor were experienced at short, but not long, periods of time after training, which is when the memory trace is susceptible to modulation. Moreover, these effects could not be ascribed to a rewarding or non-specific action of the two treatments on retention performance, as the latencies during the retention test of those mice that had not received a footshock during the training, were not affected by the post-training treatments. Administration of either D1(SCH23390) or D2 [(-)-sulpiride] dopamine (DA) receptor antagonists prior to amphetamine injection or stress exposure antagonized the impairing effects of both treatments. These data indicate that brain dopamine was involved in both cases. Finally, when mice were food restricted for 13 days than allowed free access to food for 24 h before training, either the effects of amphetamine or restraint stress were reduced. Food restricted mice did not differ from control for stepthrough latencies either on the training or the test days, indicating the absence of amnesic or otherwise impairing effects of the experimental procedure per se. Instead, the results indicated hyposensitization to the effects of amphetamine and stress on memory consolidation in food restricted animals
A classical genetic analysis of two apomorphine-induced behaviors in the mouse
No full textApomorphine (3 mg/kg) produced in C57BL/6 (C57) mice a clear-cut increase in locomotor activity and climbing behavior in comparison with saline, while in DBA/2 (DBA) mice it produced a clear-cut decrease in locomotion and a small reduction in climbing behavior. Genetic analysis involving F1 and F2 hybrids and the backcross populations (F1 x C57; F1 x DBA) indicated that apomorphine-induced locomotion and climbing are inherited through different modes of inheritance. With regard to climbing behavior the mean analysis of apomorphine parameters showed that the additive-dominance model fitted adequately, while this single model did not fit the locomotor activity data for which the best fitting model involved epistatic parameter. Moreover, a zero correlation between the two behaviors in the F2 generation resulted, indicating that no relationship exists between these apomorphine-induced behaviors under our experimental conditions. These results suggest that the horizontal locomotion and climbing are distinct behaviors controlled, at least in part, by different genetic factors related to different dopaminergic mechanisms
The Neurophysiology of Stereotypy II - The Role of Stress
No full textRepeated exposure to uncontrollable aversive situations can cause profound, long-term changes in brain organization – effects that Cabib argues could underlie a new, more biologically meaningful definition of ‘stress’. Such changes can occur even in adult animals whose brains are fully developed, and seem to fall into two classes. One type of change, readily seen in C57 mice, for instance, is that stressors come to elicit increasingly minimal dopamine response from the NAc. This seems caused by enhanced dopamine release by the prefrontal cortex (pFC), which inhibits striatal activation. It is also correlated with a decreased density of post-synaptic striatal D2 receptors (receptors which, as we saw in the previous chapter, act to inhibit the indirect pathway and thence enhance direct pathway activity). Behaviourally, this acts to increase learned helplessness (e.g. causes less active struggling and more passive floating in ‘forced swim’ tests); to reduce responsive-ness (including stereotypy) to dopamine agonists like amphetamine; and to re-duce cage stereotypies. The second possible stress-induced change, in contrast, causes stress-induced NAc dopamine responses to become increasingly pro-nounced with repeated exposure, due to a wane in prefrontal inhibitory control and an increase in the density of post-synaptic striatal D2 receptors (thence leading to increased direct pathway output)
Effects of defeat experiences on dopamine metabolism in different brain areas of the mouse
No full textAbstract Immediately after a single defeat experience, mice presented significant changes in
dopamine (DA) metabolism in frontal cortex (FC), nucleus accumbens septi (NAS),
tuberculum olfactorium (TO), septum (SEP), hypothalamus (HYP), amygdala (AMY), and
bulbus olfactorius (BO) but not in caudatus putamen (CP). In BO, NAS, and TO, where levels
of 3-methoxytyramine (3-MT) were detectable with our analytical methods, the increase of
this metabolite suggested an increased DA release. Repeatedly defeated mice (3 days) ..
Genotype-dependent effects of chronic stress on apomorphine-induced alterations of striatal and mesolimbic dopamine metabolism
No full textAfter 10 daily consecutive restraint experiences, DBA/2 (DBA) mice showed an increase of climbing behavior after injection of 0.25 mg/kg of the dopamine (DA) agonist apomorphine (APO), while no changes were observed following vehicle or 1 mg/kg of APO. By contrast, chronically stressed C57BL/6 (C57) mice showed a clear-cut decrease of climbing behavior at the dose of 0.25 mg/kg of APO and a similar, although less pronounced, effect of stress on the behavior of mice injected either with vehicle or with 1 mg/kg APO. The DA agonist at these same doses decreased 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT) concentrations in the caudatus putamen (CP) and nucleus accumbens septi (NAS) of both strains. Higher DOPAC, HVA and 3-MT concentrations were evident in stressed DBA mice receiving 0.25 mg/kg but not 1 mg/kg of APO, in both CP and NAS. Concerning C57 mice, lower concentrations of the 3 metabolites were present at both doses of APO in the NAS of stressed mice in comparison with non-stressed animals, while no significant stress-related effects were evident in the CP. Non-significant differences between control and stressed mice of both strains were evident as regards DA concentrations in CP and NAS. These results suggest that repeated stressful experiences lead to a hyposensitivity of DA presynaptic receptors in DBA mice while they produce a sensitization of mesolimbic DA presynaptic receptors possibly accompanied by down-regulation of postsynaptic DA receptors in the C57 strain
Stress, depression and the mesolimbic dopamine system
No full textThe present review was aimed at re-evaluating results obtained from animal models of depression based on experimental stressors in the light of the most recent data on the effects of stress on mesolimbic dopamine (DA) functioning. The data reviewed reveal that the effects of stressful experiences on behaviour and on mesoaccumbens DA functioning can be very different or even opposite depending on the behavioural controllability of the situation, the genetic background of the organism and its life history. Exposure to a single unavoidable/uncontrollable aversive experience leads to inhibition of DA release in the accumbens as well as to impaired responding to rewarding and aversive stimuli. Moreover, the data reviewed indicate a strong relationship between these neurochemical and behavioural effects and suggest that they could model stress-induced expression and exacerbation of some depressive symptoms such as anhedonia and feeling of helplessness caused by life events as well as syndromal depression provoked by traumatic experiences in humans. Repeated and chronic stressful experiences can reduce the ability of stressors to disrupt behaviour, induce behavioural sensitisation to psychostimulants and promote adaptive changes of mesolimbic DA functioning. Opposite neural and behavioural changes, however, can be promoted in specific environmental conditions (repeated variable stressful experiences) or in genetically predisposed individuals. Thus, depressive symptoms may not represent the necessary outcome of stress experiences but be promoted by specific environmental conditions and by a genetically determined susceptibility
THE D2 DOPAMINE RECEPTOR AGONIST LY171555 INDUCES CATALEPSY IN THE MOUSE
No full textThe dopamine agonist LY171555 (quinpirole), a specific D2 receptor agonist, induces catalepsy in mice at doses ranging from 0.3 to 10 mg/kg. The effects of an intermediate dose of this compound (1 mg/kg SC) were antagonized by 25 mg/kg of the selective D2 antagonist (-)-sulpiride (IP) injected 20 min before LY171555. SCH 23390, a selective D1 antagonist, administered (0.3 mg/kg IP) 20 min before LY171555 (1 mg/kg) enhanced the cataleptic effects of this compound. Finally, when the D1 dopamine receptor agonist SKF 38393 (20 mg/kg SC) was administered immediately beforehand, the cataleptic effects of 1 mg/kg of LY171555 were markedly reduced. These results suggest that there is a functional interaction between D1 and D2 dopamine receptors in the modulation of catalepsy
Genotype-dependent modulation of LY 171555-induced defensive behavior in the mouse
No full textThe selective D2 dopamine receptor agonist LY 171555 increased defensive behavior dose dependently, decreased social investigation and activity, and increased immobility in mice of the C57BL/6 (C57) strain interacting with non-aggressive mice of the same strain. In the same test situation, DBA/2 (DBA) mice did not present any increase in defensive behavior following injection of the same doses of LY 171555, while exhibiting a marked decrease in activity and increased immobility. Mice of the BALB/c strain were less responsive than C57 mice as far as defensive behavior was concerned, and showed decreased activity and social investigation and increased immobility. These results point to a major genetic role in the modulation of social behavior by D2 receptors
Different effects of repeated stressful experiences on mesocortical and mesolimbic dopamine metabolism
No full textThe effects of repealed stressful experiences (10 min restraint, daily) on the levels of dopamine and metabolites in the nucleus accumbens septi and frontal cortex were evaluated. In naive mice, restraint stress increased 3-4-dihydroxyphenylacetic acid, homovanillic acid, and 3-methoxytyramine levels in the nucleus accumbens and 3-4-dihydroxyphenylacetic acid levels in the frontal cortex. The effects of stress on 3-methoxytyramine and homovanillic acid levels in the nucleus accumbens septi disappeared within five days of daily restraint experiences and the increase in 3-4-dihydroxyphenylacetic acid levels was no longer evident by the 10th day. By contrast, the response of mesocortical dopamine system to restraint (increased 3-4-dihydroxyphenylacetic acid levels) was unaffected by either five or 10 days of exposure to the stressor. Moreover, 10 min of restraint were still able to increase 3-4-dihydroxyphenylacetic acid levels in the frontal cortex of mice repeatedly exposed (nine days) to 120 min restraint. These results indicate that the mesolimbic and the mesocortical dopamine systems adapt differently to repeated exposure to a stressor. Copyright (C) 1996 IBRO. Published by Elsevier Science Ltd
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