1. Non-selective neurons, which respond to both pain and itch stimuli indiscriminately.

2. Stimulus-specific neurons, which were selectively activated by either pain or itch stimuli.

Furthermore, using the dual-eGRASP technique—an advanced synaptic analysis method the research team discovered that stimulus-specific neurons in the ACC receive distinct synaptic inputs from the mediodorsal thalamus (MD). This finding indicates that pain and itch are processed by independent neuronal populations within the ACC, which receive differentiated synaptic inputs, providing fundamental insights into the neural mechanisms of pain and itch processing.

To further confirm the role of these neurons, the team used chemogenetic techniques to selectively deactivate either pain-specific or itch-specific neurons. The results showed suppressing pain neurons reduced pain perception without affecting itch, and vice versa. This discovery suggests that these neurons play a direct role in shaping how we experience pain and itch.

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A research team have uncovered the neural mechanisms underlying the processing of pain and itch in the anterior cingulate cortex (ACC). This study provides new insights into how the brain distinguishes between these two distinct sensory experiences.

Pain and itch are both unpleasant sensations, but they trigger different responses—pain often prompts withdrawal, while itching leads to scratching. Until now, scientists have struggled to understand how the brain processes these sensations separately, as they share overlapping neural pathways from the spinal cord to the brain.

Scientists at Wenzhou Medical University and Xiamen University have shown how autism symptoms in mice arise when a certain pair of competing nerve proteins falls out of equilibrium. The results of the team’s study, reported in PLOS Biology could point to potential therapeutic approaches for autism spectrum disorder (ASD). In their paper, titled “Mdfa2 deficiency leads to an aberrant activation of BDNF/TrkB signaling that underlies autism-relevant synaptic and behavioral changes in mice,” research leads Dongdong Zhao, PhD, at Wenzhou Medical University, and Yun-wu Zhang, PhD, at Xiamen University, and colleagues concluded that their findings “highlight a novel MDGA2-BDNF/TrkB-dependent mechanism underlying the synaptic function regulation, which may become a therapeutic target for ASD.”

Autism spectrum disorder is a complex neurodevelopmental disorder with its onset in early childhood, the authors noted. The disorder is characterized by reduced social interaction, increased stereotypic repetitive behavior, and altered cognition. “The prevalence of ASD has increased significantly in recent years, with approximately 1% of the world population considered to have the disorder,” the team noted. “Despite growing efforts devoted to this field, the etiology of ASD has yet to be fully elucidated.”

Previous research has linked certain genetic factors to ASD, including many associated with neuron activity, but it remains unclear exactly how these factors are related. “So far, identified genes only explain a portion of ASD occurrence,” the investigators continued. “Identifying additional ASD-associated genes and revealing the underlying mechanisms should provide new insights into the pathogenesis of ASD and its treatment strategies.”