Department of Psychology, University of Nebraska at Omahagrid.266815.e, Omaha, Nebraska.
Department of Psychology, Eastern Michigan University, Ypsilanti, Michigan.
J Neurophysiol. 2021 Jun 1;125(6):2178-2190. doi: 10.1152/jn.00552.2020. Epub 2021 Apr 28.
The chorda tympani is a gustatory nerve that fails to regenerate if sectioned in rats 10 days of age or younger. This early denervation causes an abnormally high preference for NHCl in adult rats, but the impact of neonatal chorda tympani transection on the development of the gustatory hindbrain is unclear. Here, we tested the effect of neonatal chorda tympani transection (CTX) on gustatory responses in the parabrachial nucleus (PbN). We recorded in vivo extracellular spikes in single PbN units of urethane-anesthetized adult rats following CTX at P5 (chronic CTX group) or immediately prior to recording (acute CTX group). Thus, all sampled PbN neurons received indirect input from taste nerves other than the CT. Compared to acute CTX rats, chronic CTX animals had significantly higher responses to stimulation with 0.1 and 0.5 M NHCl, 0.1 and 0.5 M NaCl, and 0.01 M citric acid. Activity to 0.5 M sucrose and 0.01 M quinine stimulation was not significantly different between groups. Neurons from chronic CTX animals also had larger interstimulus correlations and significantly higher entropy, suggesting that neurons in this group were more likely to be activated by stimulation with multiple tastants. Although neural responses were higher in the PbN of chronic CTX rats compared to acute-sectioned controls, taste-evoked activity was much lower than observed in previous reports, suggesting permanent deficits in taste signaling. These findings demonstrate that the developing gustatory hindbrain exhibits high functional plasticity following early nerve injury. Early and chronic loss of taste input from the chorda tympani is associated with abnormal taste behaviors. We found that compared to when the chorda tympani is sectioned acutely, chronic nerve loss leads to amplification of spared inputs in the gustatory pons, with higher response to salty and sour stimuli. Findings point to plasticity that may compensate for sensory loss, but permanent deficits in taste signaling also occur following early denervation.
鼓索神经是一种味觉神经，如果在 10 天大或更小的大鼠中被切断就无法再生。这种早期去神经支配会导致成年大鼠对 NHCl 异常高的偏好，但新生儿鼓索神经切断对味觉后脑的影响尚不清楚。在这里，我们测试了新生儿鼓索神经切断（CTX）对旁臂核（PbN）味觉反应的影响。我们在戊巴比妥钠麻醉的成年大鼠中记录了活体细胞外棘波，这些大鼠在 P5 时接受了 CTX（慢性 CTX 组）或在记录前立即接受了 CTX（急性 CTX 组）。因此，所有被采样的 PbN 神经元都接收了除 CT 之外的味觉神经的间接输入。与急性 CTX 大鼠相比，慢性 CTX 动物对 0.1 和 0.5 M NHCl、0.1 和 0.5 M NaCl 和 0.01 M 柠檬酸的刺激反应显著更高。对 0.5 M 蔗糖和 0.01 M 奎宁刺激的反应在两组之间没有显著差异。慢性 CTX 动物的神经元也具有更大的刺激间相关性和显著更高的熵，这表明该组的神经元更有可能被多种味觉刺激激活。尽管慢性 CTX 大鼠的 PbN 中的神经反应高于急性切段对照，但味觉诱发的活动远低于以前的报告，这表明味觉信号存在永久性缺陷。这些发现表明，在早期神经损伤后，发育中的味觉后脑表现出很高的功能可塑性。早期和慢性丧失鼓索神经的味觉输入与异常的味觉行为有关。我们发现，与鼓索神经急性切断相比，慢性神经丧失导致味觉脑桥中保留输入的放大，对咸和酸刺激的反应更高。这些发现表明，这种可塑性可能补偿了感觉丧失，但在早期去神经支配后也会发生味觉信号的永久性缺陷。
