The present study in rats was conducted to identify brain regions affected by the interruption of vestibular transmission and to explore selected aspects of their functional connections. We analyzed, by positron emission tomography (PET), the regional cerebral glucose metabolism (rCGM) of cortical, and subcortical cerebral regions processing vestibular signals after an experimental lesion of the left laterodorsal thalamic nucleus, a relay station for vestibular input en route to the cortical circuitry. PET scans upon galvanic vestibular stimulation (GVS) were conducted in each animal prior to lesion and at post-lesion days (PLD) 1, 3, 7, and 20, and voxel-wise statistical analysis of rCGM at each PLD compared to pre-lesion status were performed. After lesion, augmented metabolic activation by GVS was detected in cerebellum, mainly contralateral, and in contralateral subcortical structures such as superior colliculus, while diminished activation was observed in ipsilateral visual, entorhinal, and somatosensory cortices, indicating compensatory processes in the non-affected sensory systems of the unlesioned side. The changes in rCGM observed after lesion resembled alterations observed in patients suffering from unilateral thalamic infarction and may be interpreted as brain plasticity mechanisms associated with vestibular compensation and substitution. The second set of experiments aimed at the connections between cortical and subcortical vestibular regions and their neurotransmitter systems. Neuronal tracers were injected in regions processing vestibular and somatosensory information. Injections into the anterior cingulate cortex (ACC) or the primary somatosensory cortex (S1) retrogradely labeled neuronal somata in ventral posteromedial (VPM), posterolateral (VPL), ventrolateral (VL), posterior (Po), and laterodorsal nucleus, dorsomedial part (LDDM), locus coeruleus, and contralateral S1 area. Injections into the parafascicular nucleus (PaF), VPM/VPL, or LDDM anterogradely labeled terminal fields in S1, ACC, insular cortex, hippocampal CA1 region, and amygdala. Immunohistochemistry showed tracer-labeled terminal fields contacting cortical neurons expressing the μ-opioid receptor. Antibodies to tyrosine hydroxylase, serotonin, substance P, or neuronal nitric oxide-synthase did not label any of the traced structures. These findings provide evidence for opioidergic transmission in thalamo-cortical transduction.

中文翻译：

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前庭补偿模型：丘脑病变后的神经可塑性。

在大鼠中进行了本研究，以鉴定受前庭传导中断影响的大脑区域，并探索其功能连接的选定方面。我们通过正电子发射断层扫描（PET）分析了在左后外侧丘脑核的实验性病变后，处理前庭信号的皮质和皮质下大脑区域的局部大脑葡萄糖代谢（rCGM），这是前庭输入到中枢的中继站皮质电路。在病变前和病变后天数（PLD）1、3、7和20时，对每只动物进行前庭电前庭刺激（GVS）的PET扫描，并比较每个PLD对rCGM的体素统计分析进行病变状态检查。病变后，在小脑（主要是对侧）中发现了GVS增强的代谢激活，以及在对侧皮质下结构（例如上丘）中，同侧视觉，内嗅和体感皮层中的激活减弱，这表明未病变侧未受影响的感觉系统中存在代偿过程。病变后观察到的rCGM变化类似于单侧丘脑梗死患者的变化，并且可以解释为与前庭补偿和置换相关的脑可塑性机制。第二组实验针对皮质和皮质前庭区域及其神经递质系统之间的连接。将神经元示踪剂注入处理前庭和体感信息的区域。注射入前扣带回皮层（ACC）或原代体感皮层（S1）腹侧后内侧（VPM），后外侧（VPL），腹外侧（VL），后侧（Po）和后背内侧核，背阔部分（ LDDM），蓝斑轨迹和对侧S1区域。注射到束旁核（PaF），VPM / VPL或LDDM顺向标记的S1，ACC，岛皮层，海马CA1区和杏仁核末端区域。免疫组织化学显示示踪剂标记的末端区域接触表达μ阿片受体的皮质神经元。酪氨酸羟化酶，5-羟色胺，P物质或神经元一氧化氮合酶的抗体未标记任何追踪的结构。这些发现为丘脑-皮层转导过程中的视蛋白传递提供了证据。