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Behavioral and neuroendocrine consequences of social subjugation across adolescence and adulthood
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The Club pm. Real Life! Signs and Wonders pm. Influence Living pm. Vietnam: Rising Hope pm. Jonathan Bernis: Jewish Voice pm. Sister 2 Sister pm. Adventures of Donkey Ollie pm. Young Exployers pm. CBN NewsWatch pm. Four major findings were obtained. First, our results revealed that observer rats showed increased impulsive aggressive behavior only when they were passively exposed to aggressive situations chronically. Second, all accumbal regions, regardless of hemisphere, generally showed lower D2R density in the chronic exposure conditions than in the acute exposure conditions, and this effect further depended on whether or not the observer rats were exposed to aggression.
In particular, as compared with the nonaggression exposure control conditions, acute passive exposure to aggression increased D2R density in the AcbC, whereas chronic passive exposure to aggression downregulated D2R density in the AcbSh. These contrasting patterns may reflect that the AcbC and AcbSh actually have differential functions.
For example, Bassareo, De Luca, and Di Chiara found that, although dopaminergic activity levels in both AcbC and AcbSh are activated by novel appetitive stimuli, only dopamine response in the AcbSh is then habituated and reduced following repeated appetitive stimuli. However, once dopaminergic activity became habituated by repeated exposure to aggression, this might abruptly reduce D2R density in the AcbSh but not AcbC , as was seen in the CA group see Fig. Future research needs to test this hypothesis. Taken together, high dopamine release may be correlated with low D2R density in the AcbSh, suggesting that downregulated D2R may result from a compensatory function to maintain dopamine activity.
In the present study, chronic passive exposure to aggression may have produced effects on D2R similar to a long-term dose of psychostimulants, as indicated by the low D2R density in the CA group. The third major finding was that 5-HT1BR density in the BLA, but not in the other amygdaloid nuclei, was bilaterally upregulated in the observer rats exposed to aggression, and this finding was present regardless of exposure length.
The subregional difference in 5-HT1BR density might explain some features of aggressive behavior in observer rats. In contrast, passive exposure to aggression did not affect 5-HT1BR density in the MeA, and thus was presumably not related to self-defensive aggression or any fear-related aggression. Rather, passive exposure to aggression changed the structure of the BLA, which is involved in associative learning of emotions e. This suggests that exposure to aggression might initiate an emotional-learning process to make aggression accessible as the socio-behavioral repertoire.
Further studies should clarify this hypothesis. However, our follow-up, simple regression analysis within each subgroup showed that these identified associations did not remain significant in the condition of passive exposure to aggression. The positive association between impulsive aggression and D2R density in the AcbC was somewhat unexpected, because D2R density in the AcbC was actually lower in the CA group which exclusively showed increased aggression than in the AN and CN control groups.
Because these behavioral and neurochemical outcomes resulted from chronic passive exposure to aggression, we propose that the interaction effect between D2R in the AcbSh and 5-HT1BR in the BLA on impulsive aggression provides a neurobiological perspective on why observers exposed to aggression chronically are at high risk for being aggressive.
That is, chronic passive exposure to aggression downregulates D2R density in the AcbSh and upregulates 5-HT1BR density in the BLA among observers, and these neurochemical profiles are significantly associated with increased impulsive aggression. Our findings on the interaction between the AcbSh and BLA may have some implications in the social learning of aggression. This may reflect associative learning of aggression, such that observer rats learned to associate an aggressive social interaction and its consequence e.
Thus, low D2R in the AcbSh is related to high reward-seeking behavior. Furthermore, reduced D2R density could reflect a compensatory function for excessive dopamine release, which induces intrinsic rewards; although, to our knowledge, no studies have directly examined the relation between D2R and extracellular concentrations of dopamine, a number of separate studies on drug use have consistently shown that chronic use of psychostimulants results in low D2R density in the AcbSh Hemby, ; Kindlundh et al.
On the basis of these findings, in our paradigm, repeatedly observing aggressive circumstances might accumulatively activate dopamine release in the nucleus accumbens. Consequently, D2R binding in the AcbSh was reduced as a compensatory function. Nevertheless, the drawback of the compensatory reduction of D2R density is that postsynaptic sensitivity to dopamine neurotransmission could be blunted if presynaptic dopamine release recovered to baseline.
Accordingly, after being removed from chronic passive exposure to aggression, observer rats may experience blunted sensitivity to dopamine release i.
Nevertheless, the following study limitations need to be noted: Although our findings indicated the linkage among aggressive behavior, D2R density, and 5-HT1BR density, there is still uncertainty with respect to the causal relationship among them. Moreover, it is still unclear whether age differences play a part in vulnerability to chronic exposure to aggression. On average, the postnatal day P in our sample of observer rats was specifically 44 days at the beginning of our exposure paradigm and 64 days at the time of assessing aggressive behavior.
A replication of our results may depend on the timing of being exposed to aggression Mrug et al. More research will be needed to clarify the developmental vulnerability to chronic exposure to aggression. In summary, for the present study we used a novel rat paradigm to examine the behavioral and neurochemical effects of passive exposure to aggression. Within this paradigm, it was demonstrated that chronic passive exposure to aggression increased impulsive aggressive behavior and reduced D2R density in the AcbSh among observer rats; in contrast, these effects were not found in acute exposure to aggression.
Overall, we concluded that repeated observations of aggression promote a number of neurobiological effects by downregulating D2R density in the AcbSh and upregulating 5-HT1B in the BLA, whereby observers are inclined to show increased impulsive aggression. The authors report no conflicts of interests. MH and MH Skip to main content Skip to sections. Advertisement Hide. Download PDF. Neurochemical correlates of accumbal dopamine D 2 and amygdaloid 5-HT 1B receptor densities on observational learning of aggression.
Article First Online: 04 February To clarify the two questions above, the present study was designed to follow up on prior studies examining the effects of passive exposure to aggression. To achieve this goal, we developed a rat paradigm specifically tailored to test our hypothesis of observer-learned aggression Suzuki et al.
Therefore, in this paradigm, we administered acute or chronic exposure session s right before a behavioral assessment of aggression for an observer rat see Fig. Open image in new window.
Additional rats for inducing aggressive contexts Additional male Sprague-Dawley rats were inbred in our ACF and prepared to manipulate the aggressive or nonaggressive control contexts that observer rats were exposed to. As Fig. In addition, D2R density was examined in the nucleus accumbens of the observer rats. Main effects of exposure condition and hemisphere, as well as any other interactions, were not found in these analyses. In contrast, no main effects of exposure length and hemisphere, nor any interaction, were found.
We also performed a simple regression analysis within each group using Bonferroni corrections. In these analyses, none of the effects identified above remained significant, although this might have been due to reduced statistical power. Each line represents the slope for aggression on D2R density in the AcbSh while 5-HT1BR density in the BLA was held at either a high value centered around its mean plus one standard deviation , a middle value centered around its mean , or a low value centered around its mean minus one standard deviation.
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Quote by David R. Wommack: “Close-up violence -- it's like a tornado hittin”
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