Dagnino-Subiabre Alexies, Muñoz-Llancao Pablo, Terreros Gonzalo, Wyneken Ursula, Díaz-Véliz Gabriela, Porter Benjamin, Kilgard Michael P, Atzori Marco, Aboitiz Francisco
Laboratory of Neurobiology and Behavior, Neuroscience Unit, Department of Biomedical Sciences, Faculty of Medicine, Universidad Católica del Norte, Coquimbo, Chile.
Behav Brain Res. 2009 Oct 12;203(1):88-96. doi: 10.1016/j.bbr.2009.04.024. Epub 2009 May 3.
Chronic stress induces dendritic atrophy in the inferior colliculus (IC, auditory mesencephalon) and impairs auditory avoidance conditioning. The aim of this study was to determine in Golgi preparations and in cued fear conditioning whether stress affects other auditory components, like the thalamic medial geniculate nucleus (MG) or the posterior thalamic nucleus (PO), in Sprague-Dawley rats. Chronic restraint stress produced a significant dendritic atrophy in the MG (stress: 407+/-55 microm; control: 808+/-120 microm; p<0.01) but did not affect auditory fear conditioning. The last result was in apparent contrast with the fact that stress impairs both the acquisition of auditory avoidance conditioned responses and the dendritic structure in two major nuclei of the auditory system. In order to analyze this disagreement, we investigated whether the stress-related freezing to tone occurring in the fear conditioning protocol corresponded to a conditioned or an unconditioned fear response, using changes in tone instead of light throughout conditioning trials. Chronic stress significantly enhanced visual fear conditioning in stressed animals compared to controls (stress: 58.9+/-8.42%, control: 23.31+/-8.01%; p<0.05), but this fear enhancement was related to unconditioned fear. Conversely, chronic stress did not affect the morphology of the PO (subserving both auditory and somatosensory information) or the corresponding auditory and somatosensory unconditioned responses (acoustic startle response and escape behavior). Our results suggest that the auditory conditioned stimulus can be processed in part independently of the IC and MG in the stressed animals, and sent to the amygdala via the PO inducing unconditioned fear. Comparable alterations could be produced in major depression.
慢性应激会导致下丘（IC，听觉中脑）的树突萎缩，并损害听觉回避条件反射。本研究的目的是在高尔基染色标本以及线索性恐惧条件反射实验中，确定应激是否会影响斯普拉格-道利大鼠的其他听觉成分，如丘脑内侧膝状体核（MG）或丘脑后核（PO）。慢性束缚应激导致MG出现显著的树突萎缩（应激组：407±55微米；对照组：808±120微米；p<0.01），但不影响听觉恐惧条件反射。最后这个结果与应激会损害听觉回避条件反射的习得以及听觉系统两个主要核团的树突结构这一事实明显矛盾。为了分析这种不一致性，我们在整个条件反射实验中使用音调变化而非光变化，研究恐惧条件反射实验中与应激相关的对音调的僵立反应是对应条件性恐惧反应还是非条件性恐惧反应。与对照组相比，慢性应激显著增强了应激动物的视觉恐惧条件反射（应激组：58.9±8.42%，对照组：23.31±8.01%；p<0.05），但这种恐惧增强与非条件性恐惧有关。相反，慢性应激不影响PO的形态（它同时处理听觉和躯体感觉信息）或相应的听觉和躯体感觉非条件反应（听觉惊吓反应和逃避行为）。我们的结果表明，在应激动物中，听觉条件刺激可以部分独立于IC和MG进行处理，并通过PO传递至杏仁核，引发非条件性恐惧。在重度抑郁症中可能会出现类似的改变。
