Department of Pharmacology, National Cheng-Kung University, Tainan 701, Taiwan.
Department of Pharmacology, National Cheng-Kung University, Tainan 701, Taiwan; Department of Biotechnology and Bioindustry Sciences, National Cheng-Kung University, Tainan 701, Taiwan.
Cell Rep. 2019 Jul 30;28(5):1195-1205.e3. doi: 10.1016/j.celrep.2019.07.005.
Impulsively aggressive individuals may suddenly attack others when under stress, but the neural circuitry underlying stress-provoked aggression is poorly understood. Here, we report that acute stress activates ventral hippocampus (vHip) neurons to induce attack behavior in post-weaning socially isolated mice. Chemogenetic inhibition of vHip neural activity blunts stress-provoked attack behavior, whereas chemogenetic activation promotes it. The activation of cell bodies in vHip neurons projecting into the ventromedial hypothalamus (VMH) induces attack behavior, suggesting that the vHip-VMH projection contributes to impulsive aggression. Furthermore, optogenetic inhibition of vHip glutamatergic neurons blocks stress-provoked attacks, whereas optogenetic activation of vHip glutamatergic neurons drives attack behavior. These results show direct evidence that vHip-VMH neural circuitry modulates attack behavior in socially isolated mice.
冲动攻击型个体在压力下可能会突然攻击他人，但压力诱发攻击行为的神经回路却知之甚少。在这里，我们报告急性应激激活腹侧海马（vHip）神经元，诱导断奶后社会隔离的小鼠产生攻击行为。vHip 神经元的化学遗传抑制会削弱应激引起的攻击行为，而化学遗传激活则会促进攻击行为。投射到腹内侧下丘脑（VMH）的 vHip 神经元胞体的激活会引起攻击行为，这表明 vHip-VMH 投射有助于冲动攻击。此外，vHip 谷氨酸能神经元的光遗传抑制阻止了应激引起的攻击，而 vHip 谷氨酸能神经元的光遗传激活则驱动了攻击行为。这些结果直接证明了 vHip-VMH 神经回路调节了社会隔离小鼠的攻击行为。
