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Editor’s note iNature is China’s largest academic public account.
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iNature's innate defensive behavior triggered by environmental threats is very important to the survival of animals
.
In these behaviors, defensive attacks against threatening stimuli (such as predators) are usually the last line of defense
.
How the brain regulates defensive attacks is still poorly understood
.
On January 3, 2022, Cao Peng from the Beijing Institute of Life Sciences and Zhang Fan from Hebei Medical University jointly published a research paper entitled "Mechanically evoked defensive attack is controlled by GABAergic neurons in the anterior hypothalamic nucleus" in Nature Neuroscience.
Studies have shown that harmful mechanical forces in an unavoidable environment are the key stimulus that triggers defensive attacks in laboratory mice
.
Photoinhibition of vGAT+ neurons in the anterior hypothalamic nucleus (AHN) can eliminate mechanically induced defensive attacks
.
The vGAT+ AHN neuron encodes the strength of mechanical force and is governed by areas of the brain related to pain and aggression
.
The activation of these neurons triggers a bite attack on the predator while suppressing the ongoing behavior
.
The projection from vGAT+ AHN neurons to the gray matter around the aqueduct may be an AHN pathway involved in mechanically induced defensive attacks
.
Taken together, these data indicate that vGAT+AHN neurons encode harmful mechanical stimuli and regulate defensive aggression in mice
.
In response to environmental threats, humans and animals exhibit a series of innate defensive behaviors (for example, escape and defensive attacks)
.
These behaviors may occur as a function of the physical distance of the threat, as described in the classic model called the "predatory approach continuum"
.
This model is fully supported by behavioral research
.
For example, when the prey detects a predator cruising far away, freezing is usually the main form of defensive behavior after the prey encounters it
.
In response to an imminent visual stimulus that mimics approaching a predator, the prey quickly escapes to avoid capture
.
If the trapped prey is physically attacked by the predator, then defensive attacks are usually provoked as the last line of defense in the struggle for survival
.
Relative to the well-characterized freezing and escape neural circuits of different brain regions (hypothalamus, midbrain, thalamus), little is known about the brain mechanisms of sensory-triggered defensive attacks
.
The medial hypothalamic area (MHZ) is proposed to play a key role in defensive behavior, especially for predators
.
MHZ includes AHN, the dorsal medial part of the hypothalamic ventromedial nucleus (VMHdm), and the dorsal anterior papillary nucleus (PMD)
.
Neurons in VMHdm and PMD participate in defensive behaviors, such as freezing and escape
.
A previous study showed that hamsters threatened by live snakes had a significant increase in c-Fos expression in AHN, indicating that AHN neurons may be involved in the defensive attack against predators
.
In this study, the role of AHN neurons in encoding threat-related sensory information and regulating mice's defense against attacks was explored
.
The study shows that harmful mechanical forces in an unavoidable environment are the key stimulus that triggers defensive attacks in laboratory mice
.
Photoinhibition of vGAT+ neurons in the anterior hypothalamic nucleus (AHN) can eliminate mechanically induced defensive attacks
.
The vGAT+ AHN neuron encodes the strength of mechanical force and is governed by areas of the brain related to pain and aggression
.
The activation of these neurons triggers a bite attack on the predator while suppressing the ongoing behavior
.
The projection from vGAT+ AHN neurons to the gray matter around the aqueduct may be an AHN pathway involved in mechanically induced defensive attacks
.
Taken together, these data indicate that vGAT+AHN neurons encode harmful mechanical stimuli and regulate defensive aggression in mice
.
Xie Zhiyong, Gu Huating, and Huang Meizhu of Cao Peng Laboratory of Beijing Institute of Life Sciences are the co-first authors of the research paper
.
Other members of the laboratory (Cheng Xinyu, Shang Congping, Tao Ting, Li Dapeng) also made important contributions to the research
.
The Zhang Zhibin laboratory of the Institute of Zoology of the Chinese Academy of Sciences, the Zhang Fan laboratory of Hebei Medical University, the Tang Zongxiang laboratory of Nanjing University of Traditional Chinese Medicine, and the Zhancheng Laboratory of Beijing Institute of Biological Sciences also participated in this project and made important contributions
.
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