Chronic passive exposure to aggression decreases D2 and 5-HT1B receptor densities

Abstract 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.