4.5 Article

Somatostatin Gene and Protein Expression in the Non-human Primate Central Extended Amygdala

期刊

NEUROSCIENCE
卷 400, 期 -, 页码 157-168

出版社

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2018.12.035

关键词

extended amygdala; threat processing; anxiety; central nucleus of the amygdala; bed nucleus of the stria terminalis

资金

  1. NIMH [R01MH081884, P50MH100031]
  2. NIMH T32 training grant [5T32MH018931]

向作者/读者索取更多资源

Alterations in central extended amygdala (EAc) function have been linked to anxiety, depression, and anxious temperament (AT), the early-life risk to develop these disorders. The EAc is composed of the central nucleus of the amygdala (Ce), the bed nucleus of the stria terminalis (BST), and the sublenticular extended amygdale (SLEA). Using a non-human primate model of AT and multimodal neuroimaging, the Ce and the BST were identified as key AT-related regions. Both areas are primarily comprised of GABAergic neurons and the lateral Ce (CeL) and lateral BST (BSTL) have among the highest expression of neuropeptides in the brain. Somatostatin (SST) is of particular interest because mouse studies demonstrate that SST neurons, along with corticotropin-releasing factor (CRF) neurons, contribute to a threat-relevant EAc microcircuit. Although the distribution of CeL and BSTL SST neurons has been explored in rodents, this system is not well described in non-human primates. In situ hybridization demonstrated an anterior-posterior gradient of SST mRNA in the CeL but not the BSTL of non-human primates. Triple-labeling immunofluorescence staining revealed that SST protein-expressing cell bodies are a small proportion of the total CeL and BSTL neurons and have considerable colabeling with CRF. The SLEA exhibited strong SST mRNA and protein expression, suggesting a role for SST in mediating information transfer between the CeL and BSTL. These data provide the foundation for mechanistic non-human primate studies focused on understanding EAc function in neuropsychiatric disorders. (C) 2018 IBRO. Published by Elsevier Ltd. All rights reserved.

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