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Responsible Editor | Since the outbreak of the new crown epidemic, the social isolation adopted by Enzyme Beauty to prevent the spread of the virus has caused serious inconvenience to our study, work and life, and even harmed people's mental health.
The negative effects of social isolation have made us more and more aware of the importance of social activities and the need to intervene in social disorders in neuropsychiatric diseases.
Therefore, it is particularly urgent to clearly analyze the neural mechanisms behind social behavior.
The basal forebrain is a group of nerve nuclei located on the front ventral side of the bilateral cerebral hemispheres.
Traditionally, the basal forebrain has been regarded as a nucleus enriched with cholinergic neurons.
Correspondingly, previous studies have focused on cholinergic neurons and found that they play an important role in brain functions such as learning, memory, sleep and wakefulness.
In fact, in addition to cholinergic neurons, the basal forebrain also contains a large number of other types of neurons, such as glutamatergic excitatory neurons and GABAergic inhibitory neurons.
Previous studies have found that the structure and function of the basal forebrain of autistic patients have abnormal changes.
Considering that social disorder is the core clinical symptom of autism, it is of great scientific significance to explore whether and how the basal forebrain regulates social behavior.
Recently, the team of Professor Xu Han from the School of Brain Science and Brain Medicine of Zhejiang University/Second Affiliated Hospital of School of Medicine published a research paper entitled Basal forebrain mediates prosocial behavior via disinhibition of midbrain dopamine neurons in PNAS online, revealing for the first time the basal forebrain (basal forebrain).
forebrain, BF) The neural circuit mechanism that regulates social behavior.In order to answer the above scientific questions, members of the research team used Fiber Photometry technology to first detect the activities of different neuron types in the basal forebrain of mice during social interaction, and found that the somatostatin (SST) positive inhibitory neurons occurred in social interaction.
When is strongly activated.
When SST neurons were inhibited by optogenetic methods, the sociality of experimental mice was significantly reduced, indicating that SST neurons are necessary for normal social behavior.
What kind of neural circuits do SST neurons function through? Virus traces showed that SST neurons are closely anatomically connected to the ventral tegmental area (VTA) and the lateral habenular nucleus (LHb).
Interestingly, optogenetic inhibition of the BF SST to VTA projection pathway significantly reduced the sociality of mice, while inhibition of the BF SST to LHb projection pathway had no effect.
Therefore, the neural projection pathway from BF SST neurons to VTA is the key to regulating social behavior.
Previous studies have shown that sociality of mice is positively correlated with the activity of nerve endings in the nucleus accumbens (NAc) of dopamine neurons in the ventral tegmental area.
So, how does the activity of SST neurons enhance the activity of dopamine neurons in VTA, and lead to an increase in the release of dopamine (DA) in NAc, thereby producing social-promoting behavioral effects? Considering that SST neurons are inhibitory neurons, the researchers speculate that SST neurons may be local GABAergic neurons that act on VTA to inhibit dopamine neurons.
Consistent with this assumption, patch clamp recordings of isolated brain slices found that compared with VTA dopamine neurons, SST neurons and VTA GABA neurons have a higher probability of forming synaptic connections and stronger synaptic efficacy.
In vivo dopamine probe detection further found that after inhibiting the projection of SST neurons to VTA, the release of DA in NAc in mice was significantly reduced during social interaction, thus confirming the hypothesis of de-inhibition.
These experimental results show that BF SST neurons inhibit VTA GABAergic neurons and de-inhibit dopamine neurons, thereby producing social-promoting behavioral effects (see figure below).
These new discoveries not only deepen the understanding of the neural mechanisms of social behavior, but also provide potential new targets for clinical intervention in the medical practice of social disorders.
Wang Jun, Li Jie and Yang Qian, members of the basal forebrain promotion of social behavior and its neural circuit mechanism, are the co-first authors of the paper, and Professor Xu Han is the corresponding author of the paper.
This research work was strongly supported by Professor Duan Shumin, Professor Wu Zhiying, and Professor Xu Zhenzhong of Zhejiang University, Professor Li Yulong of Peking University and Professor Xu Tianle of Shanghai Jiaotong University.
Original link: https://
The negative effects of social isolation have made us more and more aware of the importance of social activities and the need to intervene in social disorders in neuropsychiatric diseases.
Therefore, it is particularly urgent to clearly analyze the neural mechanisms behind social behavior.
The basal forebrain is a group of nerve nuclei located on the front ventral side of the bilateral cerebral hemispheres.
Traditionally, the basal forebrain has been regarded as a nucleus enriched with cholinergic neurons.
Correspondingly, previous studies have focused on cholinergic neurons and found that they play an important role in brain functions such as learning, memory, sleep and wakefulness.
In fact, in addition to cholinergic neurons, the basal forebrain also contains a large number of other types of neurons, such as glutamatergic excitatory neurons and GABAergic inhibitory neurons.
Previous studies have found that the structure and function of the basal forebrain of autistic patients have abnormal changes.
Considering that social disorder is the core clinical symptom of autism, it is of great scientific significance to explore whether and how the basal forebrain regulates social behavior.
Recently, the team of Professor Xu Han from the School of Brain Science and Brain Medicine of Zhejiang University/Second Affiliated Hospital of School of Medicine published a research paper entitled Basal forebrain mediates prosocial behavior via disinhibition of midbrain dopamine neurons in PNAS online, revealing for the first time the basal forebrain (basal forebrain).
forebrain, BF) The neural circuit mechanism that regulates social behavior.In order to answer the above scientific questions, members of the research team used Fiber Photometry technology to first detect the activities of different neuron types in the basal forebrain of mice during social interaction, and found that the somatostatin (SST) positive inhibitory neurons occurred in social interaction.
When is strongly activated.
When SST neurons were inhibited by optogenetic methods, the sociality of experimental mice was significantly reduced, indicating that SST neurons are necessary for normal social behavior.
What kind of neural circuits do SST neurons function through? Virus traces showed that SST neurons are closely anatomically connected to the ventral tegmental area (VTA) and the lateral habenular nucleus (LHb).
Interestingly, optogenetic inhibition of the BF SST to VTA projection pathway significantly reduced the sociality of mice, while inhibition of the BF SST to LHb projection pathway had no effect.
Therefore, the neural projection pathway from BF SST neurons to VTA is the key to regulating social behavior.
Previous studies have shown that sociality of mice is positively correlated with the activity of nerve endings in the nucleus accumbens (NAc) of dopamine neurons in the ventral tegmental area.
So, how does the activity of SST neurons enhance the activity of dopamine neurons in VTA, and lead to an increase in the release of dopamine (DA) in NAc, thereby producing social-promoting behavioral effects? Considering that SST neurons are inhibitory neurons, the researchers speculate that SST neurons may be local GABAergic neurons that act on VTA to inhibit dopamine neurons.
Consistent with this assumption, patch clamp recordings of isolated brain slices found that compared with VTA dopamine neurons, SST neurons and VTA GABA neurons have a higher probability of forming synaptic connections and stronger synaptic efficacy.
In vivo dopamine probe detection further found that after inhibiting the projection of SST neurons to VTA, the release of DA in NAc in mice was significantly reduced during social interaction, thus confirming the hypothesis of de-inhibition.
These experimental results show that BF SST neurons inhibit VTA GABAergic neurons and de-inhibit dopamine neurons, thereby producing social-promoting behavioral effects (see figure below).
These new discoveries not only deepen the understanding of the neural mechanisms of social behavior, but also provide potential new targets for clinical intervention in the medical practice of social disorders.
Wang Jun, Li Jie and Yang Qian, members of the basal forebrain promotion of social behavior and its neural circuit mechanism, are the co-first authors of the paper, and Professor Xu Han is the corresponding author of the paper.
This research work was strongly supported by Professor Duan Shumin, Professor Wu Zhiying, and Professor Xu Zhenzhong of Zhejiang University, Professor Li Yulong of Peking University and Professor Xu Tianle of Shanghai Jiaotong University.
Original link: https://
