{"id": "package:602b3bea-556c-4d79-a382-c7771a9bbada", "name": "dataset_description.xlsx", "self_uri": "https://services.scicrunch.io/sparc/drs/v1/objects/602b3bea-556c-4d79-a382-c7771a9bbada", "size": 15639, "created_time": "2023-12-22T19:20:35,469179Z", "updated_time": "2023-12-22T19:20:36,137001Z", "version": "1", "mime_type": "application/vnd.openxmlformats-officedocument.spreadsheetml.sheet", "checksums": [{"checksum": "0827a037c1e0bd060e63da6e1f3c05b971ccd287db4ef36eafbedbdd9ebc6ff7", "type": "sha256"}], "access_methods": [{"type": "s3", "access_url": {"url": "s3://prd-sparc-discover50-use1/362/files/dataset_description.xlsx"}, "region": "us-east-1"}], "dataset": {"id": "362", "doi": "DOI:10.26275/qdv4-0vx5", "title": "Chronic intermittent hypoxia remodels catecholaminergic innervation in mouse atria", "description": "Mapping the remodeling of tyrosine hydroxylase labeled axons in the flat-mount of whole left and right atria", "abstract": "Chronic intermittent hypoxia (CIH, a model for sleep apnea) is a major risk factor for several cardiovascular diseases (CVD). Autonomic imbalance (sympathetic overactivity and parasympathetic withdrawal) has emerged as a causal contributor of CIH-induced CVD. Previously, we showed that CIH remodels the parasympathetic pathway. However, whether CIH induces remodeling of the cardiac sympathetic innervation remains unknown. Mice (male, C57BL/6J, 2-3 months) were exposed to either room air (RA, 21% O2) or CIH (alternating 21% and 5.7% O2, every 6 min, 10h/day) for 8-10 weeks. Flat-mounts of their left and right atria were immunohistochemically labeled for tyrosine hydroxylase (TH, a sympathetic marker). Using a confocal microscope (or a Zeiss M2 Imager) and a Neurolucida 360 digitization and tracing system, we scanned both the left and right atria and quantitatively analyzed the sympathetic axon density in both groups. The segmentation data was mapped onto a 3D mouse heart scaffold using the NIH SPARC Scaffold Mapping tool. Our findings indicated that CIH significantly remodeled the TH-IR innervation of the atria by increasing its density at the sinoatrial node, the auricles, and the major veins attached to the atria (p <0.05, n=7). Additionally, CIH increased the branching points of TH-IR axons while decreasing the distance between varicosities. Abnormal patterns of TH-IR axons around intrinsic cardiac ganglia were also found following CIH. We postulate that the increased sympathetic innervation may further amplify the effects of enhanced CIH-induced central sympathetic drive to the heart. Our work provides an anatomical foundation for the understanding of CIH-induced autonomic imbalance."}}