VISCERAL PAIN

内脏疼痛导致恶性肿瘤和淋巴瘤患者的痛苦和功能障碍， 炎症状态。 人们对这种机制和神经系统知之甚少 内脏系统的疼痛比皮肤疼痛更严重。 虽然 脊髓丘脑束信号皮肤和内脏疼痛， 神经外科中线损伤后柱可以减轻骨盆 癌症疼痛，不影响皮肤感觉和疼痛。 假设1： 一条传递内脏膨胀疼痛信号的通路在 背柱 具体目标1是观察病变是否会降低 VPL神经元对结直肠伤害性扩张的反应。 假设2： 内脏伤害性通路是突触后背柱的一部分 通路 具体目标2是确定来源，目的地， 途径的肽含量。 解剖和电生理 实验计划记录对结肠直肠扩张的反应， 突触后背柱神经元和背柱核， 确定薄肌神经元的内脏反应是否通过 突触后背柱神经元，而不是直接初级传入 预测。 假设3：该通路也负责 发出内脏炎性疼痛的信号 具体目标3是点燃 结肠，并确定1）神经元的反应是否增强 内脏炎症后VPL神经元反应增强 通过中断通路的病变减少或防止; 3）相同 损伤阻止了脑干细胞群对c-FOS的染色。 假设 4是内脏炎性疼痛引起中枢敏感化。 具体目标4是研究致敏机制， 从内脏炎症通过确定1）氨基酸释放到 结肠炎时的背角; 2）如果背根反射 在结肠炎症期间发展; 3）如果可以减少致敏性 通过输注兴奋性氨基酸、GABA（A）或肽的拮抗剂 受体进入L 6-S1的背角;和4）肽基因 药理作用前后的调节和表达 操纵 长期目标是制定新的战略， 治疗内脏疼痛。

Visceral pain causes suffering and dysfunction in malignant and inflammatory states. Less is known about the mechanisms and neural systems involved in visceral than in cutaneous pain. Although the spinothalamic tract signals both cutaneous and visceral pain, a neurosurgical midline lesion in the dorsal column can relieve pelvic cancer pain, sparing cutaneous sensation and pain. HYPOTHESIS 1 is that a pathway that signals the pain of visceral distention ascends in the dorsal column. SPECIFIC AIM 1 is to see if a lesion reduces the responses of VPL neurons to noxious colorectal distention. HYPOTHESIS 2 is that the visceral nociceptive pathway is a part of the postsynaptic dorsal column pathway. SPECIFIC AIM 2 is to determine the source, destination, and peptide content of the pathway. Anatomical and electrophysiological experiments are planned to record responses to colorectal distention of postsynaptic dorsal column neurons and dorsal column nucleus and to determine if visceral responses of gracile neurons are signaled by postsynaptic dorsal column neurons rather than by direct primary afferent projections. HYPOTHESIS 3 is that the pathway is also responsible for signaling visceral inflammatory pain. SPECIFIC AIM 3 is to inflame the colon and to determine if 1) the responses of neurons become enhanced following visceral inflammation; 2) the enhanced responses of VPL neurons are reduced or prevented by a lesion interrupting the pathway; 3) the same lesions prevent brainstem cell groups from staining for c-FOS. HYPOTHESIS 4 is that visceral inflammatory pain causes central sensitization. SPECIFIC AIM 4 is to investigate mechanisms of the sensitization resulting from visceral inflammation by determining 1) the amino acids released into the dorsal horn during colon inflammation; 2) if dorsal root reflexes develop during colon inflammation; 3) if the sensitization can be reduced by infusing antagonists of excitatory amino acid, GABA(A) or peptide receptors into the dorsal horn at L6-S1; and 4) the peptide gene regulation and expression before and after the pharmacological manipulations. The long-term goal is to develop new strategies for therapy of visceral pain.