Phillipps Hollian R, Hackwell Eleni C R, Sandovici Ionel, Constância Miguel, Grattan David R
Centre for Neuroendocrinology and Department of Anatomy, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Institute of Metabolic Science, Addenbrookes Hospital, Cambridge, UK.
J Neuroendocrinol. 2025 Sep;37(9):e70058. doi: 10.1111/jne.70058. Epub 2025 Jun 3.
During the post-partum period, new mothers are vulnerable to mood disorders. In adults, impairments in neurogenesis commonly associate with anxiety and depressive behaviors. Insulin-like growth factor 2 (IGF2) is expressed in the choroid plexus (CP) within the subventricular zone (SVZ) neurogenic niche, and global loss of IGF2 leads to increased anxiety. Previously, we have shown that Igf2 expression in CP tissue increases 6-fold during lactation but returns to baseline on suppression of prolactin present in lactation, suggesting it is induced by high levels of prolactin. To gain more insight into the role of prolactin-induced Igf2 expression in the CP, we have measured IGF2 levels in cerebrospinal fluid across reproductive states and developed mice in which Igf2 is conditionally removed from the CP. Using CP-derived IGF2 knockout mouse models, we have measured Prlr expression in CP tissue, SVZ mitogenesis, olfaction, and anxiety-like behavior using an elevated plus maze (EPM) and light/dark transition test (LDTT). Interestingly, we observed a reduction in Prlr expression in CP tissue in one of our Igf2 knockout mouse models, suggesting Igf2 may also act upstream to regulate Prlr expression in CP tissue. No changes were detected in SVZ proliferation rates between Igf2 knockout and controls. Using a buried food test (BFT), however, we show mice with conditional loss of Igf2 in the CP take longer to find a buried fruit loop as compared to controls, indicating olfaction deficits. Overall anxiety levels, however, were comparable between knockout and controls in the EPM and LDTT. Together, our findings reveal loss of CP-derived IGF2 leads to hyposmia in the absence of detectable changes to SVZ mitogenesis. We propose that CP-derived IGF2 may be acting directly in the olfactory bulb to elicit changes to improve olfaction, which may become particularly important during the post-partum period to facilitate mother-pup interactions.
在产后阶段,新妈妈容易患情绪障碍。在成年人中,神经发生受损通常与焦虑和抑郁行为有关。胰岛素样生长因子2(IGF2)在脑室下区(SVZ)神经发生微环境中的脉络丛(CP)中表达,IGF2的整体缺失会导致焦虑增加。此前,我们已经表明,CP组织中的Igf2表达在哺乳期增加6倍,但在抑制哺乳期存在的催乳素后恢复到基线水平,这表明它是由高水平的催乳素诱导的。为了更深入了解催乳素诱导的Igf2在CP中的作用,我们测量了不同生殖状态下脑脊液中的IGF2水平,并构建了Igf2在CP中被条件性敲除的小鼠。使用源自CP的IGF2基因敲除小鼠模型,我们通过高架十字迷宫(EPM)和明暗转换试验(LDTT)测量了CP组织中的Prlr表达、SVZ有丝分裂、嗅觉和焦虑样行为。有趣的是,我们在一个Igf2基因敲除小鼠模型中观察到CP组织中Prlr表达减少,这表明Igf2也可能在CP组织中Prlr表达的上游起调节作用。在Igf2基因敲除小鼠和对照组之间,SVZ增殖率没有检测到变化。然而,使用埋藏食物试验(BFT),我们发现与对照组相比,CP中Igf2条件性缺失的小鼠找到埋藏的水果圈所需的时间更长,这表明存在嗅觉缺陷。然而,在EPM和LDTT中,基因敲除小鼠和对照组的总体焦虑水平相当。总之,我们的研究结果表明,源自CP的IGF2缺失会导致嗅觉减退,而SVZ有丝分裂没有可检测到的变化。我们提出,源自CP的IGF2可能直接作用于嗅球,引发变化以改善嗅觉,这在产后阶段可能变得尤为重要,以促进母婴互动。