Doyle Wayne I, Meeks Julian P
Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas.
Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas
J Neurophysiol. 2017 Mar 1;117(3):1342-1351. doi: 10.1152/jn.00871.2016. Epub 2017 Jan 4.
Norepinephrine (NE) release has been linked to experience-dependent plasticity in many model systems and brain regions. Among these is the rodent accessory olfactory system (AOS), which is crucial for detecting and processing socially relevant environmental cues. The accessory olfactory bulb (AOB), the first site of chemosensory information processing in the AOS, receives dense centrifugal innervation by noradrenergic fibers originating in the locus coeruleus. Although NE release has been linked to behavioral plasticity through its actions in the AOB, the impacts of noradrenergic modulation on AOB information processing have not been thoroughly studied. We made extracellular single-unit recordings of AOB principal neurons in ex vivo preparations of the early AOS taken from adult male mice. We analyzed the impacts of bath-applied NE (10 μM) on spontaneous and stimulus-driven activity. In the presence of NE, we observed overall suppression of stimulus-driven neuronal activity with limited impact on spontaneous activity. NE-associated response suppression in the AOB came in two forms: one that was strong and immediate (21%) and one other that involved gradual, stimulus-dependent monotonic response suppression (47%). NE-associated changes in spontaneous activity were more modest, with an overall increase in spontaneous spike frequency observed in 25% of neurons. Neurons with increased spontaneous activity demonstrated a net decrease in chemosensory discriminability. These results reveal that noradrenergic signaling in the AOB causes cell-specific changes in chemosensory tuning, even among similar projection neurons. Norepinephrine (NE) is released throughout the brain in many behavioral contexts, but its impacts on information processing are not well understood. We studied the impact of NE on chemosensory tuning in the mouse accessory olfactory bulb (AOB). Electrophysiological recordings from AOB neurons in ex vivo preparations revealed that NE, on balance, inhibited mitral cell responses to chemosensory cues. However, NE's effects were heterogeneous, indicating that NE signaling reshapes AOB output in a cell- and stimulus-specific manner.
在许多模型系统和脑区中，去甲肾上腺素（NE）的释放与经验依赖性可塑性有关。其中包括啮齿动物的副嗅觉系统（AOS），该系统对于检测和处理与社会相关的环境线索至关重要。副嗅球（AOB）是AOS中化学感觉信息处理的第一个部位，接受来自蓝斑的去甲肾上腺素能纤维的密集离心神经支配。尽管NE的释放已通过其在AOB中的作用与行为可塑性相关联，但去甲肾上腺素能调制对AOB信息处理的影响尚未得到充分研究。我们在取自成年雄性小鼠的早期AOS离体标本中对AOB主神经元进行了细胞外单单位记录。我们分析了浴加NE（10μM）对自发活动和刺激驱动活动的影响。在NE存在的情况下，我们观察到刺激驱动的神经元活动总体受到抑制，对自发活动的影响有限。AOB中与NE相关的反应抑制有两种形式：一种是强烈且即时的（21%），另一种是逐渐的、依赖刺激的单调反应抑制（47%）。与NE相关的自发活动变化较为适度，在25%的神经元中观察到自发放电频率总体增加。自发活动增加的神经元在化学感觉辨别能力上表现出净下降。这些结果表明，AOB中的去甲肾上腺素能信号传导会导致化学感觉调谐的细胞特异性变化，即使在相似的投射神经元中也是如此。去甲肾上腺素（NE）在许多行为背景下在整个大脑中释放，但其对信息处理的影响尚不清楚。我们研究了NE对小鼠副嗅球（AOB）化学感觉调谐的影响。离体标本中AOB神经元的电生理记录显示，总体而言，NE抑制了二尖瓣细胞对化学感觉线索的反应。然而，NE的作用是异质性的，表明NE信号以细胞和刺激特异性的方式重塑了AOB的输出。
