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The present work examined the generalizability of the anhedonia phenomenon (extinction-like responding with repeated neuroleptic treatment) by examining the effects of pimozide (PIM) on nondeprived rats lever pressing for a sucrose solution reward (32%) in an eight day dosing regime. The procedures used replicated the essential features of a previous study (Gramling et al. [10]) wherein the effects of PIM on rats licking directly a sucrose solution were assessed. Thirty nondeprived rats were trained to lever press on a CRF schedule for a 32% sucrose solution reward and then assigned to one of five treatment groups (N = 6). The treatment conditions included a no-reward group (EXT; vehicle injections), two pimozide (PIM) with reward conditions (either PIM 0.25 mg/kg + RWD or PIM 0.5 mg/kg + RWD), and a vehicle control group (RWD; vehicle injections). These four groups each received their respective injections and operant exposure for eight consecutive days. The fifth group was a home cage (HC) control condition wherein the rats were injected with 0.5 mg/kg PIM each test day but did not receive operant exposure until the fourth test day. The PIM treated rats exhibited a significant curvilinear pattern of responding on the rate measure across eight days of testing, whereas rats in the no-reward condition exhibited a significant downward linear trend across eight days of testing. Within-session analysis revealed that rats in the EXT group responded at significantly higher rates during the first five minutes of testing on the first test day compared to rats in the PIM 0.5 + RWD condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some effects of pimozide on nondeprived rats' lever pressing maintained by a sucrose reward in an anhedonia paradigm. 361 48

The present work examines the generalizability of the anhedonia phenomenon (extinction-like responding with repeated neuroleptic treatment) by examining rats' licking behavior, a response heretofore untested, in the anhedonia paradigm. Nondeprived rats learned to lick a sucrose solution (32%) and were then tested for eight consecutive days in either a no-reward condition (N = 8) or two pimozide (PIM) with reward conditions (N = 8 at each of these two doses: 0.5 and 1.0 mg/kg). PIM treated animals did not exhibit rates or patterns of responding equivalent to animals in the extinction condition. Instead of an across session decline in rate, PIM treated animals showed a trend towards recovery on the rate measure. Within session patterns of responding of PIM treated animals more closely resembled animals in a normally rewarded condition responding at a generally lower rate, than animals in an extinction condition. The experimental procedure included the the use of home cage control animals, replication of the intermittent dosing procedure, and tests for transfer effects; all of these failed to produce patterns of responding typically obtained in the anhedonia paradigm when the response is lever pressing. Median lick duration and median interlick interval (ILI) were both lengthened with PIM treatment relative to injection control and extinction conditions, suggesting that pimozide treatment creates a motoric deficit. Taken together these results emphasize the importance of neuroleptics' motor vis a vis anhedonic effects.
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PMID:Some effects of pimozide on nondeprived rats licking sucrose solutions in an anhedonia paradigm. 615 Apr 96

The present investigation assessed the propensity of an acute psychogenic stressor exposure to induce behavioral change in paradigms assessing fear/anxiety (acoustic startle) and motivation/anhedonia (intracranial self-stimulation) in CD-1 mice. In the acoustic startle paradigm, a 10-min exposure of 2-4 month old mice (young adult mice) to fox odor (2,5-dihydro-2,4,5-trimethylthiazoline; TMT) was associated with decreased acoustic startle relative to mice exposed to the control odor, butyric acid (BA), immediately and relative to both saline and BA exposure 24 h following odor exposure in the home cage. In contrast, a 2-min exposure of young adult mice to TMT was associated with an increase in startle relative to saline and BA during the immediate post-odor test session only. In young adult mice a 2-min and a 10-min exposure to BA resulted in a startle profile of mice reminiscent of saline-treated mice. In comparison to young adult mice, a 2-min exposure of mature adult mice (5-7 months old) to TMT enhanced startle for up to 48 h relative to both saline and BA, while a 10-min exposure of mature adult mice to TMT enhanced startle for 168 h post-odor exposure relative to saline-exposed mice only. However, the greatest increase in startle amplitude (i.e. 48 h) was acquired following the 2-min exposure of mature mice to TMT. Among mature adult mice, a 10-min exposure to BA in the home cage eventuated in enhanced startle relative to saline-exposed animals 168 h following odor exposure. In comparison, exposure of mice to 10 min of TMT depressed responding for VTA brain stimulation at the initial 80 Hz frequency, but was ineffective in elevating reward thresholds relative to mice merely exposed to saline. Mice assessed in the ICSS paradigm were approximately 2-4 months old at the time of surgery and 5-7 months old at the completion of testing. These data suggest that acute odor exposure may induce a fear gradient dependent upon the perceived stressor severity and that the resultant anxiety-like effects are dependent on the duration of odor exposure, age of the animals and the temporal interval between odor presentation and behavioral testing. Moreover, the anxiogenic properties of psychogenic stressors can be separated from their anhedonic effects. The implications of these data for clinical psychopathology are discussed.
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PMID:Exposure of mice to a predator odor increases acoustic startle but does not disrupt the rewarding properties of VTA intracranial self-stimulation. 1291 55

Depression in humans is associated with sleep abnormalities of three types: altered rapid eye movement (REM) sleep, fragmented sleep, and reduced delta sleep. In an animal model of depression, chronic exposure to mild stressors (CMS, e.g. periods of soiled cage, reversed light/dark cycle, grouped housing, food and/or water deprivation) causes behavioral and hormonal changes which, in humans, often are associated with depression. In the CMS model, a reduced sucrose intake has been defined as one of the core symptoms of depression, anhedonia, although this finding is not consistent among various laboratories. In the present study, we investigated if the CMS procedure, in our laboratory, would cause decreased sucrose intake and, also, give sleep changes similar to what is found in depressed patients. Exposure to CMS decreased sucrose intake in our rats. The largest effect was obtained after 2 weeks of the stress protocol. CMS rats spent more time in REM sleep and showed more fragmented sleep compared to their baseline recording, while there were no changes in the control rats. Increased sleep fragmentation in CMS rats was particularly evident by increased number of arousals, and increased REM sleep and slow-wave-sleep-1 (SWS-1) episodes. The duration of sleep stage episodes was decreased. The amount of slow-wave-sleep-2 (SWS-2) was not decreased, however SWS-2 in percent of total SWS was reduced. Correlation analysis showed that animals that had less consumption of sucrose spent more time in REM sleep and had increased number of REM sleep episodes. In this study, CMS appears to be a model of depression.
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PMID:Chronic mild stress affects sucrose intake and sleep in rats. 1503 87

It is known that stress can influence the sensitivity to rewarding stimuli. Previous observations revealed that socially stressed rats do not display an appetitive behavioural response in anticipation of a reward. A previous study showed that this insensitivity to rewards (anhedonia) could be restored by chronic administration of an antidepressant. Several lines of evidence exist for the role of dopamine in the mechanism of action of antidepressant treatments concerning their therapeutic effect on anhedonia. Therefore, it was hypothesized that regular activation of the reward system, that involves mesolimbic dopaminergic systems, could counteract the effect of social stress on reward-sensitivity. For this, it was investigated whether a treatment of regular reward announcements could prevent the development of anhedonia. This was confirmed by the result that socially stressed rats that received this treatment were able to display anticipatory behaviour which is characterized by increased activity after presentation of a stimulus that was previously associated with a sucrose reward. Surprisingly, a non-treated socially stressed group, that did not show an anticipatory response for sucrose, did display anticipatory behaviour for another type of reward (enriched cage). It seems that, although one might assume the existence of an anhedonic state based upon the absence of anticipatory activity towards a sucrose reward, this assumption cannot be generalised to other types of reward. It will be discussed whether this might be caused by the highly rewarding properties of the enriched cage which probably has a therapeutical efficacy of its own.
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PMID:Announced rewards counteract the impairment of anticipatory behaviour in socially stressed rats. 1592 44

Depression is strongly related to social behavior. We have previously shown that social behavior of rats is individually stable. The purpose of the present study was to compare the sensitivity of animals with different sociability to chronic variable stress (CVS). Four social interaction tests were performed with 60 single-housed male Sprague-Dawley rats. Twenty rats with the lowest and 20 with the highest average social activity time were selected as low sociability (LS) and high sociability (HS) rats, respectively. Both groups were further divided into control and stress groups with equal average body weight. The CVS procedure lasted for 3 weeks. The stressors applied were cold water and wet bedding, imitation of injection, stroboscopic light, movement restriction in a small cage, tail pinch with a clothespin, and strong illumination during the predicted dark phase. In HS-rats, but not in LS-rats, CVS reduced sucrose intake compared with baseline after 3 weeks, suggesting that HS-rats are more vulnerable to anhedonia elicited by CVS. LS-animals were more anxious in the social interaction and open field tests, but stress eliminated differences with HS-animals in the social interaction test and increased their activity in the forced swimming test. In LS-rats stress increased ex vivo dopamine levels and reduced 5-HT levels in the frontal cortex, suggesting that the increased behavioral activity after stress may be related to increased impulsivity. This study thus revealed that animals with high sociability trait are more vulnerable to anhedonia elicited by chronic stress in conditions of single housing.
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PMID:Rats with high or low sociability are differently affected by chronic variable stress. 1834 96

The main purpose of the present study was to evaluate whether REM sleep deprivation (RSD) influences the development of anhedonia in rats in a peripheral neuropathy model induced by sciatic nerve constriction injury (CCI). Anhedonia was measured by assessing daily water/sucrose intake. Four groups were assessed: control (CTRL), CCI, RSD, and CCI+RSD (n=8/group). Intake data were collected at baseline (mean of 3 days), on the 1st and 2nd days after a CCI or SHAM procedure, during 4 days of RSD, and during an additional 10 days (rebound period or equivalent in home-cage rats). Control rats spontaneously and progressively increased sucrose intake, reaching final daily volumes significantly greater than respective initial baseline amounts. RSD promoted an additional and immediate significant increase in sucrose intake during sleep deprivation days. The CCI group did not display a spontaneous, progressive increase in sucrose intake. When CCI was combined with RSD, the increase in sucrose intake induced by RSD was significantly lower than in animals submitted to RSD alone; the (CCI+RSD) group also failed to show a spontaneous and progressive increase in sucrose intake. The present findings indicate that animal model of chronic neuropathy exhibits reduced sucrose ingestion. Accordingly, this anhedonic condition that constitutes to the core manifestation of depressive states did not occur in response to a single episode of total RSD.
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PMID:Increased susceptibility to development of anhedonia in rats with chronic peripheral nerve injury: involvement of sleep deprivation? 1941 57

Chronic stress causes insensitivity to rewards (anhedonia) in rats, reflected by the absence of anticipatory behavior for a sucrose-reward, which can be reversed by antidepressant treatment or repeated announced transfer to an enriched cage. It was, however, not clear whether the highly rewarding properties of the enriched cage alone caused this reversal or whether the anticipation of this reward as such had an additional effect. Therefore, the present study compared the consequences of the announcement of a reward to the mere effect of a reward alone with respect to their efficacy to counteract the consequences of chronic stress. Two forms of synaptic plasticity, long-term potentiation and long-term depression were investigated in area CA1 of the hippocampus. This was done in socially stressed rats (induced by defeat and subsequent long-term individual housing), socially stressed rats that received a reward (short-term enriched housing) and socially stressed rats to which this reward was announced by means of a stimulus that was repeatedly paired to the reward. The results were compared to corresponding control rats. We show that announcement of enriched housing appeared to have had an additional effect compared to the enriched housing per se as indicated by a significant higher amount of LTP. In conclusion, announced short-term enriched housing has a high and long-lasting counteracting efficacy on stress-induced alterations of hippocampal synaptic plasticity. This information is important for counteracting the consequences of chronic stress in both human and captive rats.
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PMID:Announced reward counteracts the effects of chronic social stress on anticipatory behavior and hippocampal synaptic plasticity in rats. 1992 Nov 57

Previous research demonstrated excessive decreases in reward sensitivity and increases in harm avoidance in depressed individuals. These results straightly lead to a hypothesis that depressed patients should avoid novelty or express reduced novelty-seeking behavior. Nevertheless, literature in this regard is inconsistent. Furthermore, whether the potentially altered novelty-associated behavior is dependent on changed anxiety/fear or related to altered goal-directed approaching tendency is unclear. Here, we tested novel object-approaching behavior in a free-exploration paradigm in chronic mild stress (CMS)-induced anhedonic and stress-resistant rats respectively. Other CMS-induced, emotional behaviors were also examined in a battery of behavioral tests including novel cage, exploration, locomotor activity and elevated plus maze (EPM). We found that compared with controls, stress-resistant rats who consistently showed lower anxiety level in EPM (time in open arms) and, open-field (OF) test (time in central area) showed no sign of enhanced novel object approaching behavior. To the contrary, the anhedonic ones who did not express any sign of reduced anxiety showed paradoxically intensified novelty-approaching behavior. We concluded that reduced anxiety would not necessarily lead to enhanced novelty-seeking behavior; anhedonia coexists with anxiety-independent, increased novelty-seeking behavior. The salient paradox of coexistence of anhedonia and increased novelty-seeking behavior was critically discussed.
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PMID:Coexistence of anhedonia and anxiety-independent increased novelty-seeking behavior in the chronic mild stress model of depression. 2012 16

Considerable data demonstrate a high prevalence of depressive symptoms in cancer patients. This study introduces an experimental model to examine the effect of tumor on depressive-like behavior. Female C57BL/6 mice were injected i.p. with syngeneic ID8 ovarian carcinoma. Experiment 1 measured sucrose intake before and after tumor incubation to assess the effect of tumor on anhedonic depressive-like behavior. Experiment 2 examined effects of tumor and social housing on anhedonia and a second depressive-like behavior, tail suspension test (TST) immobility. Systemic proinflammatory and antiinflammatory cytokines were measured following each experiment. Additional behaviors assessed the specificity of tumor's effect on depressive-like behavior. Tumor caused a reduction in sucrose intake relative to baseline and control levels (P<.05). Moreover, individually-housed tumor-bearing mice exhibited a lower sucrose preference than group-housed tumor-bearing or control mice in either housing condition (P<.05). Although tumor-bearing mice exhibited less locomotion than controls (P<.001), there was no significant effect of tumor on TST immobility. Tumor caused higher levels of systemic proinflammatory and antiinflammatory cytokines and smaller body weight (P<.05), but appetite and motor capacity were not significantly affected. Statistical mediation analysis showed that circulating interleukin-6 partially mediated the effect between tumor and home cage locomotion (P<.01) but not between tumor and sucrose intake. It is concluded that tumor elicits anhedonic depressive-like behavior in a murine model of ovarian cancer. This may have important implications for etiology of depression in the clinical cancer setting.
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PMID:Cancer induces inflammation and depressive-like behavior in the mouse: modulation by social housing. 2118 30


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