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The article presents a study which explores how chronic pain–induced neuronal plasticity in the bed nucleus of the stria terminalis causes maladaptive anxiety . It mentions the use of a mouse model of neuropathic pain, and demonstrated neuronal plasticity in the bed nucleus of the stria terminalis (BNST), which plays a critical role in chronic pain–induced maladaptive anxiety.

Male animals may show alternative behaviors toward infants: attack or parenting. These behaviors are triggered by pup stimuli under the influence of the internal state, including the hormonal environment and/or social experiences. Converging data suggest that the medial preoptic area (MPOA) contributes to the behavioral selection toward the pup. However, the neural mechanisms underlying how integrated stimuli affect the MPOA-dependent behavioral selection remain unclear. Here we focus on the amygdalohippocampal area (AHi) that projects to MPOA and expresses oxytocin receptor, a hormone receptor mediating social behavior toward pups. We describe the activation of MPOA-projection AHi neurons in male mice by social contact with pups. Input mapping using the TRIO method reveals that MPOA-projection AHi neurons receive prominent inputs from several regions, including the thalamus, hypothalamus, and olfactory cortex. Electrophysiological and histologic analysis demonstrates that oxytocin modulates inhibitory synaptic responses on MPOA-projection AHi neurons. In addition, AHi forms the excitatory monosynapse to MPOA, and pharmacological activation of MPOA-projection AHi neurons enhances only aggressive behavior, but not parental behavior. Interestingly, this promoted behavior was related to social experience in male mice. Collectively, our results identified a presynaptic partner of MPOA that can integrate sensory input and hormonal state, and trigger pup-directed aggression. [ABSTRACT FROM AUTHOR]

In responses to looming objects, the praying mantis shows a defense behavior, which consists of retracting forelegs under the prothorax. The role of a looming-sensitive neuron in triggering this behavior was investigated by simultaneously recording the activity and behavioral responses of the neuron. The mantis initiated the defense behavior earlier in response to larger and slower looming stimuli. The time remaining to collision at defense initiation was linearly correlated with the ratio of the half-size of an approaching object to its speed (l/|v|), suggesting that the defense behavior occurred a fixed delay after the stimuli had reached a fixed angular threshold. Furthermore, the results suggested that high-frequency spikes of the looming-sensitive neuron were involved in triggering the defense behavior: the distribution of maximum firing rate for trials with defense was shifted to larger rates compared with trials without defense; the firing rate of the neuron exceeded 150 Hz ∼100 ms before the defense initiation regardless of stimulus parameters; when a looming stimulus ceased approach prematurely, high-frequency spikes were removed, and the occurrence of defense was reduced. [ABSTRACT FROM AUTHOR]