
Caroline Robinson
· Assistant Professor of MusicVerifiedUniversity of Michigan · Department of Organ
Active 2010–2024
About
Dr. Caroline Robinson joined the Department of Organ at the University of Michigan School of Music, Theatre & Dance as an assistant professor in the fall of 2024. She is an accomplished organist, pedagogue, church musician, and music collaborator with performance experience across the United States and internationally in England, Denmark, France, and Germany. Her performances have been broadcast on American Public Media’s Pipedreams, Pipedreams LIVE!, and Philadelphia’s WRTI’s Wanamaker Organ Hour. Robinson has been featured at conventions of the Organ Historical Society, the East Texas Pipe Organ Festival, and the American Guild of Organists, including performing at the 2022 National AGO Convention in Seattle. Her 2024-2025 performances will take her to notable venues such as the Gulangyu Organ Museum in China, the West Point Cadet Chapel, and St. Paul’s Cathedral in Pittsburgh, where she will also give masterclasses.
Research topics
- Medicine
- Internal medicine
- Psychiatry
- Psychology
- Neuroscience
- Psychotherapist
- Family medicine
- Demography
- Physical therapy
- Bioinformatics
- Environmental health
- Social psychology
- Pathology
- Gerontology
Selected publications
Experimental Neurobiology · 2024-02-29 · 3 citations
articleOpen accessSenior authorThe benefit of intranasal brain derived neurotrophic factor (BDNF) treatment on cognitive function in a neonatal postnatal day 7 (P7) mouse model of hypoxic ischemia (HI) was explored. Intranasal delivery is attractive in that it can promote widespread distribution of BDNF within both the brain and spinal cord. In this study we evaluated the effectiveness of intranasal BDNF to improve cognitive recovery following HI. HI is induced via ligation of the right carotid artery followed by a 45-minute exposure to an 8% oxygen/ 92% nitrogen mixture in an enclosed chamber. Male and female pups were subjected to a 2-hour hypothermia in a temperature-controlled chamber as a standard of care. A solution of saline (control) or recombinant human BDNF (Harlan Laboratories) was administered with a Gilson pipette at the same time each day for 7 days into each nasal cavity in awake mice beginning 24 hours after HI. We evaluated cognitive recovery using the novel object recognition (NOR) and western analysis to analyze neuro-markers and brain health such as synaptophysin and microtubule associated protein -2 (MAP2). The objective of this study was to evaluate the role and therapeutic potential of BDNF in neonatal HI recovery. Our results indicate that intranasal BDNF delivered within 24 hours after HI improved object discrimination at both 28 and 42 days after HI. Our results also demonstrate increased synaptophysin and MAP2 at day 42 in HI animals that received intranasal BDNF treatment compared to HI animals that were administered saline.
International Journal of Molecular Sciences · 2023-09-28 · 2 citations
articleOpen accessSenior authorCorrespondingAdequate perfusion of cerebral tissues, which is necessary for the preservation of optimal brain health, depends on insulin signaling within brain endothelial cells. Proper insulin signaling relies on the regulated internalization of insulin bound to the insulin receptor, a process which is disrupted by hyperinsulinemia via an unknown mechanism. Thus, the goal of this study was to characterize the impact of hyperinsulinemia on the regulation of molecular targets involved in cerebral blood flow and insulin receptor internalization into brain endothelial cells. The phosphorylation of molecular targets associated with cerebral blood flow and insulin receptor internalization was assessed in hyperinsulinemic brain endothelial cells. Insulin receptor uptake into cells was also examined in the setting of endocytosis blockade. Our data demonstrate that hyperinsulinemia impairs the activation of endothelial nitric oxide synthase. These data correspond with an impairment in clathrin-mediated endocytosis of the insulin receptor and dysregulated phosphorylation of key internalization effectors. We conclude that hyperinsulinemia alters the phosphorylation of molecular targets involved in clathrin-mediated endocytosis, disrupts signaling through the insulin receptor, and hinders the capacity for blood flow regulation by brain endothelial cells.
Brain stimulation · 2023-08-22 · 2 citations
letterOpen accessTranscutaneous auricular vagus nerve stimulation (taVNS) is an exciting non-invasive extension of traditional invasive cervical VNS. However, it is still unclear what vagus fibers taVNS engages and whether taVNS has measurable effects in reducing heart rate (HR) to assess parasympathetic nervous system activation. Ongoing research and clinical applications pairing VNS with activities promoting learning and stroke recovery are promising [1]. taVNS has also been used in newborns with hypoxic-ischemic (HI) brain injury and may improve their oromotor coordination during feeding [2].
Journal of Neuroscience Research · 2023-08-11 · 11 citations
articleOpen accessSenior authorCorrespondingObesity increases the risk for stroke and is associated with worse post-stroke outcomes; however, the mechanisms are poorly understood. Diet-induced obesity leads to insulin resistance and subsequently, brain insulin deficiency. The purpose of this study was to investigate the potential impact of brain insulin deficiency on post-stroke outcomes. To accomplish this, brain insulin levels were assessed in male C57BL/6J (B6) mice placed on either a standard diet or 54% kcal high-fat diet, a known model of insulin resistance. Mice were subjected to either a sham surgery (control) or 30-min middle cerebral artery occlusion to induce an ischemic stroke and administered either intranasal saline (0.9%) or intranasal insulin (1.75 U) twice daily for 5 days beginning on day 1 post-stroke. High-fat diet-induced brain insulin deficiency was associated with increased mortality, neurological and cognitive deficits. On the other hand, increasing brain insulin levels via intranasal insulin improved survival, neurological and cognitive function in high-fat diet mice. Our data suggests that brain insulin deficiency correlates with worse post-stroke outcomes in a diet-induced mouse model of insulin resistance and increasing brain insulin levels may be a therapeutic target to improve stroke recovery.
Figshare · 2023-01-01
datasetOpen accessSenior authorRaw data sets and images for flow cytometry and western immunoblotting. Microsoft Excel files with analysis also provided.
Figshare · 2023-01-01
datasetOpen accessSenior authorRaw data sets for hippoampal insulin levels, relative CSF:Insulin, blood glucose measurements, male and females post-stroke survival, modified neurological severity scores, pre and post stroke novel object location data, post-stroke weights, and blood flow.
Neural Plasticity · 2022 · 73 citations
Senior authorCorresponding- Medicine
- Neuroscience
- Bioinformatics
Ischemic stroke and traumatic brain injury (TBI) are among the leading causes of death and disability worldwide with impairments ranging from mild to severe. Many therapies are aimed at improving functional and cognitive recovery by targeting neural repair but have encountered issues involving efficacy and drug delivery. As a result, therapeutic options for patients are sparse. Neurotrophic factors are one of the key mediators of neural plasticity and functional recovery. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) serve as potential therapeutic options to increase neural repair and recovery as they promote neuroprotection and regeneration. BDNF and NGF have demonstrated the ability to improve functional recovery in preclinical and to a lesser extent clinical studies. Direct and indirect methods to increase levels of neurotrophic factors in animal models have been successful in improving postinjury outcome measures. However, the translation of these studies into clinical trials has been limited. Preclinical experiments have largely failed to result in significant impacts in clinical research. This review will focus on the administration of these neurotrophic factors in preclinical and clinical stroke and TBI and the challenges in translating these therapies from the bench to the clinic.
Diabetes and Vascular Disease Research · 2022-07-01 · 20 citations
articleOpen accessSenior authorCorrespondingInsulin receptors are internalized by endothelial cells to facilitate their physiological processes; however, the impact of hyperinsulinemia in brain endothelial cells is not known. Thus, the aim of this study was to elucidate the impact hyperinsulinemia plays on insulin receptor internalization through changes in phosphorylation, as well as the potential impact of protein tyrosine phosphatase 1B (PTP1B). Hippocampal microvessels were isolated from high-fat diet fed mice and assessed for insulin signaling activation, a process known to be involved with receptor internalization. Surface insulin receptors in brain microvascular endothelial cells were labelled to assess the role hyperinsulinemia plays on receptor internalization in response to stimulation, with and without the PTP1B antagonist, Claramine. Our results indicated that insulin receptor levels increased in tandem with decreased receptor signaling in the high-fat diet mouse microvessels. Insulin receptors of cells subjected to hyperinsulinemic treatment demonstrate splice variation towards decreased IR-A mRNA expression and demonstrate a higher membrane-localized proportion. This corresponded with decreased autophosphorylation at sites critical for receptor internalization and signaling. Claramine restored signaling and receptor internalization in cells treated with hyperinsulinemia. In conclusion, hyperinsulinemia impacts brain microvascular endothelial cell insulin receptor signaling and internalization, likely via alternative splicing and increased negative feedback from PTP1B.
Journal of Clinical and Translational Science · 2022-04-01
articleOpen accessOBJECTIVES/GOALS: Neonatal hypoxic-ischemic encephalopathy (HIE) is an acute neurologic syndrome where decreased blood flow and oxygen to the brain causes acute and chronic brain dysfunction. The only proven neuroprotective intervention for HIE is hypothermia treatment started within 6 hours of birth and 50% of survivors have long-term deficits. METHODS/STUDY POPULATION: Pre-clinical adult stroke studies demonstrated that vagus nerve stimulation (VNS) has anti-inflammatory effects and attenuates brain damage. Transcutaneous auricular VNS (taVNS) is safe and feasible in infants and may improve the motor skill of bottle feeding. We hypothesize that a combined hypothermia-taVNS treatment shortly after HIE birth will have neuroprotective effects, improve motor function, attenuate infarct volume inflammation compared to hypothermia alone. The HIE model includes ligation of the right common carotid artery in postnatal day 7 (P7) rats followed by 90min hypoxia (8% oxygen) and 2hr hypothermia. taVNS or sham taVNS was administered using a bipolar electrode placed on the auricular concha region for 30min, [30sec trains, 0.5msec duration, 20Hz frequency, followed by 4.5min breaks] RESULTS/ANTICIPATED RESULTS: Experimental groups include +HIE/+taVNS, +HIE/-taVNS, and -HIE/-taVNS. To assess motor function, grasping reflex and forelimb grip strength tasks were assessed prior to surgery through P10. Infarct volume was assessed at 72h after injury by staining coronal sections with cresyl-violet. Thirty-four rat pups underwent surgery with an 8.82% mortality rate. taVNS was well tolerated by the P7 rats when delivered below perceptual threshold (0.4-1.1mA). There was no difference in elementary motor function or infarct volume between any group. DISCUSSION/SIGNIFICANCE: Future studies will include 2.5hr hypoxia for a more severe brain injury and a -HIE/+taVNS control group. These initial pre-clinical studies in neonates are important in determining whether taVNS may translate as a treatment to improve outcomes after neonatal HIE.
Diabetes and cognitive dysfunction
Elsevier eBooks · 2022-05-21 · 10 citations
book-chapter
Recent grants
NIH · $586k · 2016
COBRE in Stroke Recovery Administrative Supplement: Equipment
NIH · $46.5M · 2014–2025
Molecular Mechanisms Underlying Obesity-related Memory Deficits
NIH · $1.8M · 2017–2022
Frequent coauthors
- 18 shared
Eva L. Feldman
Johns Hopkins University
- 12 shared
Patrick Kanju
Duke University
- 10 shared
Serena‐Kaye Sims
Medical University of South Carolina
- 7 shared
Alexus Williams
- 6 shared
John M. Hayes
University of Michigan–Ann Arbor
- 6 shared
Stephanie DiLucia
- 6 shared
Subramaniam Uthayathas
Howard University
- 5 shared
Anna Bakeman
University of Michigan–Ann Arbor
Awards & honors
- Laureate of the National Young Artists Competition in Organ…
- First prize from the 11th annual Albert Schweitzer Organ Fes…
- First prize from the 10th annual West Chester University Org…
- Semifinalist in the Dublin International Organ Competition (…
- Chosen as one of The Diapason’s “20 Under 30” promising youn…
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