Light Evokes Melanopsin-Dependent Vocalization and Neural Activation Associated with Aversive Experience in Neonatal Mice
Light Evokes Melanopsin-Dependent Vocalization and Neural Activation Associated with Aversive Experience in Neonatal Mice
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DOI：
10.1371/journal.pone.0043787
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发表时间：
2012-09-13
期刊：
影响因子：
3.7
通讯作者：
Ahn, Andrew H.
中科院分区：
文献类型：
--
作者：
Delwig, Anton;Logan, Anne M.;Ahn, Andrew H.
表达黑视素的内在光敏视网膜神经节细胞（ipRGC）是新生小鼠眼中唯一有功能的光感受细胞。出生后第9天，在功能性视杆细胞和视锥细胞不存在的情况下，这些ipRGC介导对光源的强烈回避行为，称为负趋光性。为了确定这种行为是否与新生小鼠的厌恶体验有关，我们描述了光诱导的发声和参与厌恶和疼痛刺激处理的大脑区域神经元激活的模式。光诱发不同的黑视蛋白依赖的超声波发声相同的压力条件下发出的，如隔离从垃圾。相比之下，光并没有引起急性机械性疼痛引起的广谱呼叫。使用神经元激活的标记物，我们发现光诱导后丘脑中的即刻早期基因产物Fos，该脑区与光对硬脑膜的机械刺激的反应增强有关，并被认为是偏头痛恐惧症的基础。此外，光诱导中央杏仁核神经元中细胞外相关激酶（pERK）的磷酸化，这是一种与疼痛的厌恶方面的处理相关的细胞内信号。然而，光并没有激活Fos的表达在三叉神经脊束核尾侧，疼痛刺激的主要感受野的头部。我们的结论是，这些光诱发的发声和新生小鼠大脑激活的独特模式是一致的黑视素依赖性神经通路参与处理光作为一个令人厌恶的，但不是急性疼痛刺激。
Melanopsin-expressing intrinsically photosensitive retinal ganglion cells (ipRGCs) are the only functional photoreceptive cells in the eye of newborn mice. Through postnatal day 9, in the absence of functional rods and cones, these ipRGCs mediate a robust avoidance behavior to a light source, termed negative phototaxis. To determine whether this behavior is associated with an aversive experience in neonatal mice, we characterized light-induced vocalizations and patterns of neuronal activation in regions of the brain involved in the processing of aversive and painful stimuli. Light evoked distinct melanopsin-dependent ultrasonic vocalizations identical to those emitted under stressful conditions, such as isolation from the litter. In contrast, light did not evoke the broad-spectrum calls elicited by acute mechanical pain. Using markers of neuronal activation, we found that light induced the immediate-early gene product Fos in the posterior thalamus, a brain region associated with the enhancement of responses to mechanical stimulation of the dura by light, and thought to be the basis for migrainous photophobia. Additionally, light induced the phosphorylation of extracellular-related kinase (pERK) in neurons of the central amygdala, an intracellular signal associated with the processing of the aversive aspects of pain. However, light did not activate Fos expression in the spinal trigeminal nucleus caudalis, the primary receptive field for painful stimulation to the head. We conclude that these light-evoked vocalizations and the distinct pattern of brain activation in neonatal mice are consistent with a melanopsin-dependent neural pathway involved in processing light as an aversive but not acutely painful stimulus.