The transection of the inferior alveolar nerve (IANx) produces allodynia in the whisker pad (V2 division) of rats. Ectopic discharges from injured trigeminal ganglion (TG) neurons and thalamocortical reorganization are possible contributors to the sensitization of uninjured V2 primary and CNS neurons. To test which factor is more important, TG and ventroposterior medial nucleus (VPM) neurons were longitudinally followed before, during, and after IANx for up to 80 d. Spontaneous discharges and mechanical stimulation-evoked responses were recorded in conscious and in anesthetized states. Results show (1) a sequential increase in spontaneous activities, first in the injured TG neurons of the IAN (2-30 d), followed by uninjured V2 ganglion neurons (6-30 d), and then VPM V2 neurons (7-30 d) after IANx; (2) ectopic discharges included burst and regular firing patterns in the IAN and V2 branches of the TG neurons; and (3) the receptive field expanded, the modality shifted, and long-lasting after-discharges occurred only in VPM V2 neurons. All of these changes appeared in the late or maintenance phase (7-30 d) and disappeared during the recovery phase (40-60 d). These observations suggest that ectopic barrages in the injured IAN contribute more to the development of sensitization, whereas the modality shift and evoked after-discharges in the VPM thalamic neurons contribute more to the maintenance phase of allodynia by redirecting tactile information to the cortex as nociceptive.

译文

:下牙槽神经(IANx)横断会在大鼠的晶须垫(V2分区)中产生异常性疼痛。受损的三叉神经节(TG)神经元的异位放电和丘脑皮质重组可能是未受伤的V2原发神经元和CNS神经元致敏的原因。为了测试哪个因素更重要,在IANx之前,期间和之后,纵向追踪TG和后内侧内侧核(VPM)神经元长达80 d。在有意识和麻醉状态下记录自发放电和机械刺激诱发的反应。结果显示(1)自发活动依次增加,首先在IAN受伤的TG神经元中(2-30 d),其次是未受伤的V2神经节神经元(6-30 d),然后是VPM V2神经元(7-30) d)在IANx之后; (2)异位放电包括TG神经元IAN和V2分支的爆发和规则放电模式; (3)仅在VPM V2神经元中,感受野扩大,模态改变且持续放电。所有这些变化都出现在后期或维护阶段(7-30 d),而在恢复阶段(40-60 d)则消失了。这些观察结果表明,受伤的IAN的异位弹幕对致敏作用的贡献更大,而VPM丘脑神经元的形态改变和诱发的放电后,则通过将触觉信息重定向至伤害性皮层,从而对异常性疼痛的维持阶段做出了更大贡献。

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