Neuroscience Training Program, Department of Psychiatry, University of Wisconsin-Madison, 7225 Medical Sciences Center, 1300 University Ave, Madison, WI 53706, USA.
Physiol Behav. 2011 Oct 24;104(5):796-803. doi: 10.1016/j.physbeh.2011.08.001. Epub 2011 Aug 6.
Stress is suggested to exacerbate symptoms and contribute to relapse in patients with schizophrenia and several other psychiatric disorders. A prominent feature of many of these illnesses is an impaired ability to filter information through sensorimotor gating processes. Prepulse inhibition (PPI) is a functional measure of sensorimotor gating, and known to be deficient in schizophrenia and sometimes in post-traumatic stress disorder (PTSD), both of which are also sensitive to stress-induced symptom deterioration. We previously found that a psychological stressor (exposure to a ferret without physical contact), but not footshock, disrupted PPI in rats, suggesting that intense psychological stress/trauma may uniquely model stress-induced sensorimotor gating abnormalities. In the present experiment, we sought to recreate the conditions where we found this behavioral difference, and to explore possible underlying neural substrates. Rats were exposed acutely to ferret stress, footshock, or no stress (control). 90 min later, tissue was obtained for Fos immunohistochemistry to assess neuronal activation. Several brain regions (prelimbic, infralimbic, and cingulate cortices, the paraventricular hypothalamic nucleus, the paraventricular thalamic nucleus, and the lateral periaqueductal gray) were equally activated following exposure to either stressor. Interestingly, the medial amygdala and dorsomedial periaqueductal gray had nearly twice as much Fos activation in the ferret-exposed rats as in the footshock-exposed rats, suggesting that higher activation within these structures may contribute to the unique behavioral effects induced by predator stress. These results may have implications for understanding the neural substrates that could participate in sensorimotor gating abnormalities seen in several psychiatric disorders after psychogenic stress.
压力被认为会加重精神分裂症和其他几种精神障碍患者的症状，并导致其病情复发。这些疾病的一个突出特征是，它们在通过感觉运动门控过程过滤信息方面存在障碍。前脉冲抑制（PPI）是感觉运动门控的一种功能测量方法，已知其在精神分裂症中存在缺陷，有时在创伤后应激障碍（PTSD）中也存在缺陷，这两种疾病都对应激引起的症状恶化敏感。我们之前发现，一种心理应激源（接触没有身体接触的雪貂）而不是足底电击，会破坏大鼠的 PPI，这表明强烈的心理压力/创伤可能独特地模拟应激引起的感觉运动门控异常。在本实验中，我们试图重现我们发现这种行为差异的条件，并探索可能的潜在神经基质。大鼠急性暴露于雪貂应激、足底电击或无应激（对照）。90 分钟后，获取组织进行 Fos 免疫组织化学，以评估神经元激活。几个脑区（额前皮质、下边缘皮质和扣带回皮质、室旁下丘脑核、室旁丘脑核和外侧中脑导水管周围灰质）在暴露于任一应激源后均被同等激活。有趣的是，在雪貂暴露的大鼠中，杏仁内侧核和背内侧中脑导水管周围灰质的 Fos 激活几乎是足底电击暴露的大鼠的两倍，这表明这些结构内的更高激活可能有助于由捕食者压力引起的独特行为效应。这些结果可能对理解神经基质有意义，这些神经基质可能参与几种精神障碍后心理应激引起的感觉运动门控异常。
