Summary As an essential means to resolve conflicts, aggression is expressed by both sexes but often at a higher level in males than in females. Recent studies suggest that cells in the ventrolateral part of the ventromedial hypothalamus (VMHvl) that express estrogen receptor alpha and progesterone receptor (Esr1/PR) are essential for male but not female mouse aggression. In contrast, here we show an indispensable role of VMHvlEsr1+ cells in female aggression. This population is active when females attack naturally. Inactivation of these cells reduces female aggression whereas their activation elicits attack. Additionally, we found that female VMHvl contains two anatomically distinguishable subdivisions that show differential gene expression, projection and activation patterns after mating and fighting. These results support an essential role of the VMHvl in both male and female aggression and reveal the existence of two previously unappreciated subdivisions in the female VMHvl that are involved in distinct social behaviors.

There have been few studies of whether vitamin D insufficiency is linked with depression in healthy young women despite women’s high rates of both problems. Female undergraduates (n = 185) living in the Pacific Northwest during fall, winter, and spring academic terms completed the Center for Epidemiologic Studies Depression (CES-D) scale weekly for four weeks (W1–W5). We measured serum levels of vitamin D3 and C (ascorbate; as a control variable) in blood samples collected at W1 and W5. Vitamin D insufficiency (<30ng/mL) was common at W1 (42%) and W5 (46%), and rates of clinically significant depressive symptoms (CES-D ≥ 16) were 35–42% at W1–W5. Lower W1 vitamin D3 predicted clinically significant depressive symptoms across W1–W5 (β = −.20, p < .05), controlling for season, BMI, race/ethnicity, diet, exercise, and time outside. There was some evidence that lower levels of depressive symptoms in Fall participants (vs. Winter and Spring) were explained by their higher levels of vitamin D3. W1 depressive symptoms did not predict change in vitamin D3 levels from W1 to W5. Findings are consistent with a temporal association between low levels of vitamin D and clinically meaningful depressive symptoms. The preventive value of supplementation should be tested further.

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The creation of auditory threat Pavlovian memory requires an initial learning stage in which a neutral conditioned stimulus (CS), such as a tone, is paired with an aversive one (US), such as a shock. In this phase, the CS acquires the capacity of predicting the occurrence of the US and therefore elicits conditioned defense responses. Norepinephrine (NE), through β-adrenergic receptors in the amygdala, enhances threat memory by facilitating the acquisition of the CS-US association, but the nature of this effect has not been described. Here we show that NE release, induced by the footshock of the first conditioning trial, promotes the subsequent enhancement of learning. Consequently, blocking NE transmission disrupts multitrial but not one-trial conditioning. We further found that increasing the time between the conditioning trials eliminates the amplificatory effect of NE. Similarly, an unsignaled footshock delivered in a separate context immediately before conditioning can enhance learning. These results help define the conditions under which NE should and should not be expected to alter threat processing and fill an important gap in the understanding of the neural processes relevant to the pathophysiology of stress and anxiety disorders.

Norepinephrine (NE) plays a central role in the acquisition of aversive learning via actions in the lateral nucleus of the amygdala (LA) [1, 2]. However, the function of NE in expression of aversively-conditioned responses has not been established. Given the role of the central nucleus of the amygdala (CeA) in the expression of such behaviors [3-5], and the presence of NE axons projections in this brain nucleus [6], we assessed the effects of NE activity in the CeA on behavioral expression using receptor-specific pharmacology and cell-and projection-specific chemogenetic manipulations. We found that inhibition and activation of locus coeruleus (LC) neurons decreases and increases freezing to aversively conditioned cues, respectively. We then show that locally inhibiting or activating LC terminals in CeA is sufficient to achieve this bidirectional modulation of defensive reactions. These findings support the hypothesis that LC projections to CeA are critical for the expression of defensive responses elicited by conditioned threats.