A cardinal feature of the program project Is Its Integration of brainstem physiology and neuroanatomy at the regional, cellular, and subcellular levels as It relates to normal and abnormal homeostasis. Core B, the Neuroanatomy Core, provides high-quality, state-of-the-art neuroanatomy services to each of the individual projects, thereby facilitating completion of the program's Integrative specific alms. It Is a central resource that ensures consistent study design and execution In the neuroanatomic studies of the program project. Its centralization streamlines technical procedures, eliminates potential duplication, and facilitates Integration of neuroanatomic approaches across the projects. The core also facilitates the comparison and cross- fertilization between studies of human neuropathology and animal models. The Neuroanatomy Core B will continue to be based In the Department of Anesthesiology, Critical Care and Pain Medicine, Children's Hospital Boston, and to be directed by Dr. Kathryn Commons. She has a background in serotonin neurobiology and neuroanatomy, and the effects of nicotine upon serotonergic mechanisms, subjects germane to SIDS and the proposed specific alms of the program. Staffing Includes a highly expert and productive staff scientist. Core B resources Include the microscopy and technical resources of Dr. Commons'laboratory, supplemented by a network of supporting common resources at the division, department, hospital and university-wide level. Core B services Include consultations regarding optimal neuroanatomic procedures for individual specific aims, training In methodological approaches and techniques, and direct participation in the neuroanatomic aspects of Individual projects. Methods available in Core B include quantitative tissue receptor autoradiography, array tomography, multiple Immunolabeling, anterograde and retrograde tract-tracing, combined tract-tracing and Immunolabeling, quantitation and imaging of axonal terminals, and in situ hybridization. Core B also assists with refining study design, data summary and Interpretation and manuscript preparation. The core has a proven track record In neuroanatomic contributions to date In the current cycle, with several resulting publications, abstracts, and manuscripts in preparation. This progress represents a contribution to all of the individual projects. Furthermore, Core B has contributed to studies that span more than one project, thereby contributing to the active collaboration and synergism that characterizes this program project as a whole.

Public Health Relevance

The mission of the program project Is to elucidate the role of the brainstem and Interconnected brain regions in the sudden Infant death syndrome (SIDS), the leading cause of postneonatal infant mortality In the United States today. Neuroanatomy Core B provides a resource for state-of-the-art neuroanatomic services to the four projects of the program.

National Institute of Health (NIH)
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Research Program Projects (P01)
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Special Emphasis Panel (ZHD1-DSR-Z)
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Children's Hospital Boston
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Babb, Jessica A; Linnros, Sofia E; Commons, Kathryn G (2018) Evidence for intact 5-HT1A receptor-mediated feedback inhibition following sustained antidepressant treatment in a rat model of depression. Neuropharmacology 141:139-147
Dosumu-Johnson, Ryan T; Cocoran, Andrea E; Chang, YoonJeung et al. (2018) Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery. Elife 7:
Darnall, Robert A; Chen, Xi; Nemani, Krishnamurthy V et al. (2017) Early postnatal exposure to intermittent hypoxia in rodents is proinflammatory, impairs white matter integrity, and alters brain metabolism. Pediatr Res 82:164-172
Tenpenny, Richard C; Commons, Kathryn G (2017) What Gene Mutations Affect Serotonin in Mice? ACS Chem Neurosci 8:987-995
Cerpa, Veronica J; Wu, Yuanming; Bravo, Eduardo et al. (2017) Medullary 5-HT neurons: Switch from tonic respiratory drive to chemoreception during postnatal development. Neuroscience 344:1-14
Ehlinger, Daniel G; Commons, Kathryn G (2017) Altered Cav1.2 function in the Timothy syndrome mouse model produces ascending serotonergic abnormalities. Eur J Neurosci 46:2416-2425
Panzini, Chris M; Ehlinger, Daniel G; Alchahin, Adele M et al. (2017) 16p11.2 deletion syndrome mice perseverate with active coping response to acute stress - rescue by blocking 5-HT2A receptors. J Neurochem 143:708-721
Commons, Kathryn G; Cholanians, Aram B; Babb, Jessica A et al. (2017) The Rodent Forced Swim Test Measures Stress-Coping Strategy, Not Depression-like Behavior. ACS Chem Neurosci 8:955-960
Haynes, Robin L; Frelinger 3rd, Andrew L; Giles, Emma K et al. (2017) High serum serotonin in sudden infant death syndrome. Proc Natl Acad Sci U S A 114:7695-7700
Guo, Yue-Ping; Commons, Kathryn G (2017) Serotonin neuron abnormalities in the BTBR mouse model of autism. Autism Res 10:66-77

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