Department of Anesthesia, Boston, Massachusetts, USA.
Nat Neurosci. 2010 Feb;13(2):239-45. doi: 10.1038/nn.2475. Epub 2010 Jan 10.
The perception of migraine headache, which is mediated by nociceptive signals transmitted from the cranial dura mater to the brain, is uniquely exacerbated by exposure to light. We found that exacerbation of migraine headache by light is prevalent among blind individuals who maintain non-image-forming photoregulation in the face of massive rod/cone degeneration. Using single-unit recording and neural tract tracing in the rat, we identified dura-sensitive neurons in the posterior thalamus whose activity was distinctly modulated by light and whose axons projected extensively across layers I-V of somatosensory, visual and associative cortices. The cell bodies and dendrites of such dura/light-sensitive neurons were apposed by axons originating from retinal ganglion cells (RGCs), predominantly from intrinsically photosensitive RGCs, the principle conduit of non-image-forming photoregulation. We propose that photoregulation of migraine headache is exerted by a non-image-forming retinal pathway that modulates the activity of dura-sensitive thalamocortical neurons.
偏头痛头痛的感知是由颅硬膜的伤害性信号传递到大脑介导的,其独特之处在于暴露于光线下会加剧。我们发现,在面对大量视杆/视锥细胞变性的情况下,盲人保持非成像光调节时,光会加剧偏头痛头痛。使用大鼠的单细胞记录和神经束追踪,我们在丘脑后发现了对硬脑膜敏感的神经元,其活动明显受到光的调节,其轴突广泛投射到感觉、视觉和联合皮层的 I-V 层。这种硬脑膜/光敏感神经元的细胞体和树突被来自视网膜神经节细胞(RGC)的轴突包围,主要来自内在光敏的 RGC,这是非成像光调节的主要途径。我们提出,偏头痛头痛的光调节是由调节硬脑膜敏感丘脑皮质神经元活动的非成像视网膜途径来实现的。