Separate anterior paraventricular thalamus projections differentially regulate sensory and affective aspects of pain
Selomon Assefa Mindaye,
Wei-Hsin Chen,
Shih-Che Lin,
Yong-Cyuan Chen,
Mohamed Abbas Abdelaziz,
Yi-Shiuan Tzeng,
Arthur Chun-Chieh Shih,
Shih-Yu Chen,
Shi-Bing Yang,
Chien-Chang Chen
Affiliations
Selomon Assefa Mindaye
Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Cheng Kung University and Academia Sinica, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Wei-Hsin Chen
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Corresponding author
Shih-Che Lin
Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Taiwan University and Academia Sinica, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Yong-Cyuan Chen
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Mohamed Abbas Abdelaziz
Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Cheng Kung University and Academia Sinica, Taipei, Taiwan; Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Yi-Shiuan Tzeng
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Arthur Chun-Chieh Shih
Institute of Information Sciences, Academia Sinica, Taipei, Taiwan
Shih-Yu Chen
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Shi-Bing Yang
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan
Chien-Chang Chen
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan; Corresponding author
Summary: The experience of pain is complex, involving both sensory and affective components, yet the underlying neural mechanisms remain elusive. Here, we show that formalin-induced pain behaviors coincide with increased responses in glutamatergic neurons within the anterior paraventricular nucleus of the thalamus (PVA). Furthermore, we describe non-overlapping subpopulations of PVAVgluT2 neurons involved in sensory and affective pain processing, whose activity varies across different pain states. Activating PVA glutamatergic neurons is sufficient to induce mechanical hypersensitivity and aversion behaviors, whereas suppression ameliorates formalin-induced pain. Furthermore, we identify the segregation of PVAVgluT2 projections to the bed nucleus of the stria terminalis (BNST) and nucleus accumbens (NAc), each influencing specific aspects of pain-like behavior. This finding provides an important insight into the mechanism of distinct components of pain, highlighting the pivotal role of PVA in mediating different aspects of pain-like behavior with distinct circuits.
