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1. Thalamo-hippocampal pathway determines aggression and self-harm(Science Advances)

abstract
 Aggression and self-harm are maladaptive coping strategies that often occur in individuals with a history of early life trauma (ELT), yet their underlying neural mechanisms remain unclear. Here, we identify L-type calcium channel (LTCC)–expressing thalamic nucleus reuniens (RE) as a critical component regulating both behaviors. ELT-induced excessive LTCC activity in vesicular glutamate transporter 2 (vGlut2) RE neurons and its corresponding effects on persistent neuronal activation contribute to increasing susceptibility to aggression and self-harm. Activation of vGlut2 RE neurons projecting to ventral hippocampus (vCA1), but not medial prefrontal cortex, promotes these behaviors in control mice. Furthermore, we found that RE neurons modulate two distinct subsets of vCA1 neurons, with one projecting to the hypothalamus to drive aggression and another to the basal amygdala to mediate self-harm. Our findings uncover how LTCC functions in the RE-to-vCA1 neural pathway increase the risk of aggression and self-harm, highlighting potential therapeutic targets for mitigating destructive behaviors following early adversity.

2. IL-1R1-positive dorsal raphe neurons drive self-imposed social withdrawal in sickness

summary
 Sick animals exhibit behavioral changes that extend beyond physiological symptoms, such as appetite loss and hypoactivity, and include a decline in social interactions. While social isolation during sickness has been recognized to have the evolutionary benefit of staving off disease spread, the molecular and neural mechanisms underlying this response remain unclear. Cytokines—immune-derived signaling molecules—have emerged as neuromodulators impacting brain function during inflammation. Through behavioral screening, we identify a unique role for the cytokine interleukin-1β (IL-1β) in promoting social withdrawal during sickness. IL-1β directly modulates the activity of IL-1R1-expressing neurons in the dorsal raphe nucleus (DRN) (IL-1R1DRN). Activation of these neurons is sufficient to elicit social withdrawal, while their inhibition or genetic deletion of IL-1R1 rescues self-imposed social isolation during systemic inflammation. Our findings reveal a neural mechanism that actively promotes social disengagement in sick animals, highlighting the role of IL-1R1DRN neurons in driving these behavioral adaptations.