The spino-parabrachio-amygdaloid pathway is critical for the manifestation of chronic pain.
The spino-parabrachio-amygdaloid pathway is critical for the manifestation of chronic pain.
复制标题
脊髓-旁臂肌-杏仁通路对于慢性疼痛的表现至关重要。
DOI:
10.1038/s41386-023-01745-7
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发表时间:
2024
期刊:
影响因子:
--
通讯作者:
Allen,HeatherN
中科院分区:
文献类型:
--
作者:
Nelson,TylerS;Allen,HeatherN
Pain is a complex phenomenon that elicits somatosensory and motor reflexive responses alongside enduring emotional and autonomic changes. Although pain serves as a protective mechanism to signal potential harm and encourage avoidance, it can also become persistent and pathological, disrupting regular functioning and quality of life. To effectively address chronic pain, it is imperative to increase our understanding of plasticity in the neural pathways that transmit nociceptive sensory information from peripheral nerve endings in the skin to higher-order brain areas facilitating cognition.Bernard and BessonLs pioneering work highlighted the crucial role of the spino-parabrachio-amygdaloid pathway in the ascending transmission of noxious somatosensory information [1]. Extracellular electrophysiological recordings in rats identified nociception-specific neurons in the parabrachial nucleus (PBN) that project to the central nucleus of the amygdala (CeA). PBN→ CeA neurons displayed broad receptive fields and graded responses to various noxious mechanical and thermal stimuli, consistently encoding the intensity of peripheral stimulation [1]. The PBN is a bilateral pontine brain structure that receives converging nociceptive information from peripheral nociceptors, spinal cord dorsal horn projection neurons, and other brainstem regions. The PBN then relays this ascending information to midbrain and forebrain regions for integration with emotional and cognitive inputs. The CeA is a bilateral almond shaped brain nucleus in the midbrain that is integral to processing and regulating emotional responses, particularly fear and anxiety. Thus, plasticity of PBN→ CeA neurons is hypothesized to be a central mechanism for maladaptive pain chronification and pain aversion [2].