Chronic passive exposure to aggression decreases D2 and 5-HT 1B receptor densities.

It has been recently reported that passive exposure to aggression induces aggressive behavior in a rodent model. However, it remains unclear whether this response is correlated with neurochemical changes that correspond either to stress-induced aggression or non-stressed, learned aggression. Stress-induced aggression has been shown to result in increased brain dopamine D(2) receptor and serum corticosterone levels. In contrast, learned aggression is probably associated with reward deficiency syndrome, characterized by low dopamine D(2) receptor levels, without stress effects (i.e., high corticosterone levels). We hypothesized that chronic passive exposure to aggression would produce learned aggression, represented by low levels of dopamine D(2) receptor binding but normal levels of stress hormone. The present study additionally focused on serum testosterone and serotonin 5-HT(1B) receptor density that has been associated with aggression/reward circuits. Hormonal results indicated that there were no differences between the "observer" rats that had been passively exposed to aggression and non-aggression for 10 min/day for 23 consecutive days. However, receptor binding autoradiography identified lower densities of dopamine D(2) receptors in the cortical-accumbal regions (shell of the nucleus accumbens and cingulate and motor cortices) and lower 5-HT(1B) receptor densities in the tegmental regions (ventral tegmental area, substantia nigra pars compacta, and periaqueductal gray) among observers exposed to aggression, compared to controls. Changes in dopamine D(2) receptor densities due to chronic exposure to aggression do not resemble those patterns reported for stress-induced aggressive behavior. Our evidence suggests that the development of aggressive behavior among passive observers occurs through a learned, and not a stress-induced, mechanism. (c) 2009 Elsevier Inc. All rights reserved.