Otorhinolaryngology Department, Centro Hospitalar Universitário de S. João, EPE, Porto, Portugal; Unit of Anatomy, Department of Biomedicine, Faculty of Medicine, University of Porto, Porto, Portugal; CINTESIS@RISE, Faculty of Medicine, University of Porto, Porto, Portugal.
Unit of Anatomy, Department of Biomedicine, Faculty of Medicine, University of Porto, Porto, Portugal.
Physiol Behav. 2023 Jun 1;265:114171. doi: 10.1016/j.physbeh.2023.114171. Epub 2023 Mar 23.
Allergic rhinitis (AR) has been identified as a cause of olfactory dysfunction. Beyond the classic symptoms, AR has been associated with altered sleep patterns, a decline in cognitive performance and higher likelihood of depression and anxiety. The olfactory pathway has been postulated to be a possible link between nasal inflammation and central nervous system (CNS) modifications. Thus, we aimed to investigate the structural, functional and behavioral changes in the olfactory pathway and related areas in an animal model of AR.
AR was induced in adult Wistar rats by ovalbumin sensitization and challenge. Following olfactory and behavioral tests we investigated the synaptic structure of the olfactory bulb (OB), anterior olfactory nuclei (AON), piriform cortex and prefrontal cortex (PFC), by immunofluorescence detection of synaptophysin (Syn) and glutamatergic, GABAergic and dopaminergic neuronal markers.
We detected a significant decrease in Syn in the glomerular layer (GL) of OB and in the PFC of the AR group. Additionally, the optical density of GAD67 and VGLUT2 was reduced in the OB, AON and PFC, compared to controls. The behavioral tests demonstrated olfactory dysfunction and reduced male aggressiveness in AR rats, but we did not find any difference in the cognition and anxiety-like behavior.
We confirmed olfactory dysfunction in a rat model of AR and we identified modifications in synaptic activity by reduction of Syn optical density in the GL of the OB and in the PFC. This was accompanied by structural changes in glutamatergic and GABAergic activity in essential components of the olfactory pathway and PFC.
过敏性鼻炎（AR）已被确定为嗅觉功能障碍的原因。除了典型症状外，AR 还与睡眠模式改变、认知表现下降以及抑郁和焦虑的可能性增加有关。嗅觉通路被认为是鼻腔炎症和中枢神经系统（CNS）改变之间的可能联系。因此，我们旨在研究 AR 动物模型中嗅觉通路及相关区域的结构、功能和行为变化。
卵清蛋白致敏和激发诱导成年 Wistar 大鼠发生 AR。在嗅觉和行为测试后，我们通过免疫荧光检测突触蛋白（Syn）和谷氨酸能、GABA 能和多巴胺能神经元标志物，研究了嗅球（OB）、前嗅核（AON）、梨状皮层和前额叶皮层（PFC）的突触结构。
我们发现在 AR 组的 OB 的 GL 和 PFC 中 Syn 显著减少。此外，与对照组相比，OB、AON 和 PFC 中的 GAD67 和 VGLUT2 的光密度降低。行为测试表明 AR 大鼠存在嗅觉功能障碍和雄性攻击性降低，但我们在认知和焦虑样行为方面没有发现任何差异。
我们在 AR 大鼠模型中证实了嗅觉功能障碍，并通过降低 OB 和 PFC 中 GL 的 Syn 光密度，确定了突触活性的改变。这伴随着嗅觉通路和 PFC 中谷氨酸能和 GABA 能活性的结构变化。
