PubMed · 9585643
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S I Harrison. 1998. Developmental contributions to comorbidity?. https://doi.org/10.1097/00004583-199805000-00003
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This study examined localization of positive versus negative motivational functions mediated by GABA circuits within the accumbens shell. Microinjections of a GABA(A) agonist (0, 25, 75, and 225 ng/0.5 microl muscimol) in rostral shell sites elicited appetitive increases in eating behavior. In contrast, microinjections in caudal shell sites elicited defensive burying or paw-treading behavior. Rats whose microinjections landed bilaterally outside of the accumbens shell did not display either behavior. Defensive treading elicited by caudal shell muscimol microinjection appeared to be a negative motivated response to threat (similar in parameters and orientation to normal defensive burying of a threatening electrified shock prod). The nucleus accumbens shell thus appears functionally heterogeneous in coding motivational valence. The demonstration that muscimol elicits positive eating behavior from rostral shell versus negative defensive behavior from caudal shell suggests in particular that GABAergic substrates of positive and negative types of motivated behavior in the nucleus accumbens shell are segregated along a rostrocaudal gradient.
Lactating mice exhibit a dramatic increase in aggression, termed maternal aggression, only in association with the rearing and protection of their offspring. Previous work indicates that the neural mechanisms underlying maternal and male aggression are different in rodents. In this study, we sought to examine possible neural regions involved in the control of maternal aggression by combining behavioral testing with immunohistochemistry for both cFOS and pCREB, two indirect markers of neuronal activity. All lactating female mice were exposed to a male intruder for 20 min and those exhibiting maternal aggression were placed in one group and those that were non-aggressive were placed in a second group. Thus, the sensory stimuli were similar and the main difference between the two groups was the behavior. cFOS expression increased significantly in the claustrum, bed nucleus of the stria terminalis, medial preoptic nucleus, paraventricular nucleus, medial amygdala, and cortical amygdala in association with maternal aggression. In contrast, the number of pCREB-positive cells significantly increased only in the ventrolateral portion of the caudal periaqueductal gray and in the lateral septum in aggressive lactating mice. Due to large variance in the counts of pCREB-positive cells, the data were log transformed prior to statistical analysis. Thus, the sites of cFOS and pCREB increases do not overlap, but provide complementary indirect information on neural regions active during maternal aggression. These results complement previous studies of nitric oxide release during maternal aggression to create a possible map of the functional neural circuitry underlying maternal aggression.
The dopamine D2 receptor (D2) has been implicated in attention-deficit hyperactive disorder (ADHD) and aging. Two isoforms of D2 have been identified, termed D2L (long form) and D2S (short form). In this study, we investigated the role of D2L in offensive aggression, using mice lacking the dopamine D2L receptor (D2L-/-) as a model system and the resident-intruder test. We found that D2L-/- mice showed much lower levels of aggression than wild-type mice. Interestingly, offensive aggression also decreased as the age of the mice increased. These results suggest that both the D2L receptor and aging play roles in the modulation of offensive aggression. This finding may contribute to our understanding of the neurobiological basis of aggression.