McLean Hospital, Harvard Medical School, Boston, MA, USA.
Department of Pharmacology and Physiology, University of Rochester, Rochester, NY, USA.
Neuropsychopharmacology. 2024 Nov;49(12):1839-1850. doi: 10.1038/s41386-024-01944-w. Epub 2024 Aug 5.
fMRI neurofeedback using autobiographical memory recall to upregulate the amygdala is associated with resting-state functional connectivity (rsFC) changes between the amygdala and the salience and default mode networks (SN and DMN, respectively). We hypothesize the existence of anatomical circuits underlying these rsFC changes. Using a cross-species brain parcellation, we identified in non-human primates locations homologous to the regions of interest (ROIs) from studies showing pre-to-post-neurofeedback changes in rsFC with the left amygdala. We injected bidirectional tracers in the basolateral, lateral, and central amygdala nuclei of adult macaques and used bright- and dark-field microscopy to identify cells and axon terminals in each ROI (SN: anterior cingulate, ventrolateral, and insular cortices; DMN: temporal pole, middle frontal gyrus, angular gyrus, precuneus, posterior cingulate cortex, parahippocampal gyrus, hippocampus, and thalamus). We also performed additional injections in specific ROIs to validate the results following amygdala injections and delineate potential disynaptic pathways. Finally, we used high-resolution diffusion MRI data from four post-mortem macaque brains and one in vivo human brain to translate our findings to the neuroimaging domain. Different amygdala nuclei had significant monosynaptic connections with all the SN and DMN ipsilateral ROIs. Amygdala connections with the DMN contralateral ROIs are disynaptic through the hippocampus and parahippocampal gyrus. Diffusion MRI in both species benefitted from using the ground-truth tracer data to validate its findings, as we identified false-negative ipsilateral and false-positive contralateral connectivity results. This study provides the foundation for future causal investigations of amygdala neurofeedback modulation of the SN and DMN through these anatomic connections.
使用自传体记忆回忆来上调杏仁核的 fMRI 神经反馈与杏仁核与突显和默认模式网络(分别为 SN 和 DMN)之间的静息状态功能连接(rsFC)变化有关。我们假设这些 rsFC 变化背后存在解剖学回路。使用跨物种大脑分割,我们在非人类灵长类动物中确定了与显示 rsFC 与左杏仁核的神经反馈前后变化的研究中的感兴趣区域(ROI)同源的位置。我们在成年猕猴的基底外侧、外侧和中央杏仁核核中注射了双向示踪剂,并使用明场和暗场显微镜来识别每个 ROI(SN:前扣带、腹外侧和岛叶皮质;DMN:颞极、额中回、角回、楔前叶、后扣带皮质、海马旁回、海马和丘脑)中的细胞和轴突末梢。我们还在特定 ROI 中进行了额外的注射,以验证杏仁核注射后的结果并描绘潜在的双突触途径。最后,我们使用来自四个死后猕猴大脑和一个体内人类大脑的高分辨率扩散 MRI 数据将我们的发现转化为神经影像学领域。不同的杏仁核核与所有 SN 和 DMN 同侧 ROI 均具有显著的单突触连接。杏仁核与 DMN 对侧 ROI 的连接通过海马和海马旁回进行双突触传递。两种物种的扩散 MRI 都受益于使用真实示踪剂数据来验证其发现,因为我们确定了假阴性同侧和假阳性对侧连接结果。这项研究为通过这些解剖连接进行杏仁核神经反馈调节 SN 和 DMN 的未来因果研究奠定了基础。