About

Amber Ross is an Assistant Professor in the Department of Philosophy at the University of Florida, with a Ph.D. from UNC Chapel Hill obtained in 2013. Her areas of specialization include the ethics of artificial intelligence, philosophy of mind, and metaphysics. Her research focuses on the ethical implications of AI, particularly opaque AI systems, and the philosophical understanding of consciousness, mental fiction, and perception. Ross has contributed to discussions on the epistemological challenges facing phenomenal realism and the ethical considerations surrounding AI transparency. She has presented her work at various academic conferences, including the American Political Science Association Meeting and the Mind and Matter conference at the University of Helsinki. Her publications explore topics such as the ethical use of AI, multisensory perception, and the nature of conscious thought. Ross is actively engaged in philosophical research that intersects technology, consciousness, and ethics, and she teaches courses related to ethics, data, technology, and animal minds at UF.

Research topics

• Medicine
• Biology
• Composite material
• Neuroscience
• Chemistry
• Internal medicine
• Endocrinology
• Pathology
• Cell biology
• Nanotechnology
• Chemical engineering
• Materials science
• Immunology

Selected publications

• IP62-23 INFLUENCE OF RADIOLOGY AND GENOMICS ON EXTREME RECLASSIFICATION DURING SURVEILLANCE

  The Journal of Urology · 2026-04-27

  articleSenior author
  PublisherDOI

• Guanosine contributes to rapid purinergic regulation of dopamine during ischemia

  Purinergic Signalling · 2026-04-20

  articleOpen accessSenior author

  Purinergic modulation of neurotransmission is a primary strategy employed in rapid neuroprotection during and after ischemic stroke. While the contributions of adenosine and ATP to the purinome are well-documented, guanosine-based regulatory activity has remained under-investigated. In the ischemia-vulnerable CA1 region of the hippocampus, dopamine serves as both a neurotransmitter involved in long-term potentiation during memory acquisition and as a regulator focused on modulating glutamate activity. Dopamine has been suggested as a potential protective force against glutamate-induced excitotoxicity in early ischemia. Here, we investigate changes in dopamine signaling during ischemia and demonstrate that guanosine administration during injury has an immediate protective effect. We observe rapid suppression of dopamine release following ischemic insult that is completely restored with administration of a low micromolar dose of guanosine. Changes in dopamine signaling and short-term mRNA production further suggest that guanosine's rapid regulatory role may be partially achieved through the adenosine A1 and A2a receptors and that it facilitates dopamine reuptake through the dopamine transporter DAT. We present the first evidence that guanosine plays a rapid regulatory role in dopamine neurotransmission and that it may function as a broad facilitator of neurotransmitter reuptake, diversifying our understanding of the purinome in ischemia.

  PublisherOA PDFDOI

• Optimization of Subsecond Estradiol Detection through Analysis of Surface–Analyte Interactions

  ACS electrochemistry. · 2026-03-28

  articleOpen accessSenior authorCorresponding

  Subsecond neurochemical signaling is the fastest and one of the most diverse forms of intercellular communication employed along the neuro-immune-endocrine axis; consequently, spatiotemporally resolved approaches with high sensitivity and selectivity tailored to specific analytes are required for adequate monitoring. However, many existing electrochemical approaches are optimized solely towards catecholamine and indolamine detection, leaving a wide array of structurally diverse neuroregulators at a disadvantage with limited detection capability. Here, we use estradiola fast-signaling neurosteroid vital for neuroprotection that has proven difficult to detect with existing methodsas a model target analyte for optimizing direct electrochemical detection at carbon surfaces. We take a two-pronged approach to optimizing estradiol detection by examining the electrode-analyte interface from the perspective of both the carbon surface and the target molecule. We first establish the surface characteristics of diverse carbon fibers, then examine estradiol's electrochemical behavior at each surface. Finally, we determine the contributions of estradiol's structure to specific adsorption, elucidating subtle structural considerations to analyte-specific tailoring of carbon electrodes. By taking this multi-perspective approach, we develop a thorough understanding of the interactions between carbon sensing surfaces and estradiol for improved sensitivity and selectivity. Moreover, our approach is applicable to other neglected neurochemicals that have proven challenging to detect. This work creates a potentially broadly applicable roadmap for customizing direct monitoring at carbon surfaces through a tailored approach to optimizing the electrode-analyte interface.

  PublisherDOI

• Strategies to Mitigate Breast-related Adverse Events in Patients with High-risk Biochemically Recurrent Prostate Cancer Receiving Enzalutamide Monotherapy: Perspectives and Challenges

  European Urology Focus · 2025-12-19 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• Engineering localized injury: a 3D microfluidic platform approach for ex vivo tissue interrogation

  Analytical and Bioanalytical Chemistry · 2025-12-06

  articleOpen accessSenior author

  Over the years, interrogating and replicating biological events ex vivo and in vitro has proven to provide a breadth of knowledge into various mechanisms of diseases; however, there remains a challenge in understanding the onset of disease within tonic, localized environments over time. Microfluidics provides an alternative approach that can be coupled with many methods to better replicate specific localized and prolonged biological events. In this work, we introduce a novel 3D-printed device that significantly improves upon previous microfluidic approaches aimed at maintaining high spatial resolution and sustainment of delivery, ultimately enabling us to examine localized injuries within an ex vivo model with higher precision and control. This work focuses on focal ischemia; however, it should be noted that the device is applicable to any event that needs high spatial resolution and sustained fluidic delivery. We demonstrate that tissue remains viable on this platform and that we are capable of achieving exquisite fluidic control, not affordable from standard lithographic techniques. Additionally, we incorporate real-time neurochemical monitoring to demonstrate rapid and robust changes in dopamine signaling at the site of focal ischemia, further validating our platform for localized injury studies. This device fills a critical gap in the existing literature by significantly improving upon the capabilities of localized tissue stimulation and further enhances our understanding of local physiological changes during ischemic events, providing a critical advance in biomedical tools for measuring at localized regions within tissue.

  PublisherOA PDFDOI

• α2-Adrenergic modulation of neuroimmune interactions differs between the spleen and mesenteric lymph nodes

  The Journal of Immunology · 2025-11-11

  articleSenior author

  The sympathetic nervous system modulates immune responses through the release of norepinephrine (NE), yet the dynamics of this signaling differ across lymphoid organs. In this study, we investigated how NE release and α2-adrenergic receptor (α2AR) modulation influence neuroimmune interactions in the spleen and mesenteric lymph nodes (MLNs), 2 secondary lymphoid tissues with distinct innervation patterns. Using fast-scan cyclic voltammetry (FSCV), we found that the spleen exhibited more frequent and higher-amplitude NE events than the MLNs, consistent with its denser sympathetic innervation. Pharmacological manipulation of α2ARs revealed that yohimbine hydrochloride, an α2AR antagonist, increased NE release in both organs, while dexmedetomidine hydrochloride, an α2AR agonist, suppressed it, often below detection thresholds. Complementary 3D immunohistochemistry demonstrated tissue- and cell type-specific changes in immune cell proximity to neuronal structures following adrenergic modulation, with T cells and B cells displaying distinct spatial reorganization. These findings highlight that α2AR signaling fine-tunes NE release and immune cell localization in a context-dependent manner, influenced by organ-specific architecture and innervation. Our results underscore the importance of dynamic local neuroimmune interactions in immune regulation and suggest potential therapeutic opportunities for targeting adrenergic signaling in inflammatory and autoimmune diseases.

  PublisherDOI

• Artificial Intelligence (AI)-Driven Screening of Equivocal Prostate Immunohistochemistry (IHC) Cases: Development and Validation of a Screening and Cancer Detection Framework

  Modern Pathology · 2025-10-04 · 1 citations

  articleOpen access
  PublisherOA PDFDOI

• Inhibition of PTPRS function does not affect the survival or regeneration of dopaminergic neurons but alters synaptic function in the nigrostriatal pathway

  Neurobiology of Disease · 2025-07-05

  articleOpen access

  Parkinson's Disease (PD) is characterized by midbrain dopaminergic (mDA) neuron degeneration in the ventral midbrain, contributing to debilitating motor symptoms. This study investigated whether Protein Tyrosine Phosphatase Receptor Sigma (PTPRS), a known inhibitor of axonal growth through chondroitin sulfate proteoglycan (CSPG) interaction, plays a role in mDA neuron survival, function, and regeneration in PD. Our data show that inhibition of PTPRS using intracellular sigma peptide (ISP) enhances human mDA neuron neurite outgrowth in vitro, suggesting an inhibitory role of this receptor in the differentiation of human embryonic stem cell (hESC)-derived mDA neurons in vitro. However, genetic deletion and pharmacological inhibition of PTPRS does not affect mDA neuron survival, axon density, or motor behavior in 6-OHDA unilateral partially lesioned mice. Similarly, mDA-specific deletion of Ptprs does not affect the basal behavioral measurement in cKO mice, including general locomotion and motor learning. Interestingly, however, Ptprs deletion led to a reduced response in the behavior sensitization to repeated methamphetamine (METH) exposure in cKO mice, suggesting a dampened response in synaptic function in cKO mice under these conditions. Ex vivo voltammetry recording in the striatum indeed shows altered parameters of dopamine (DA) release upon stimulation. These findings indicate that the inhibition of PTPRS function in human mDA neuron progenitors might be a promising strategy for enhancing neurite outgrowth or incorporation in host tissues in transplantation therapies. Finally, our data support that inhibition of PTPRS function in mDA neurons in adult mice in vivo could inhibit METH induced plasticity and behavioral sensitization. • Ptprs inhibition enhances neurite outgrowth of hES derived mDA neurons in vitro. • Ptprs ko in mDA neurons at E16.5 does not affect mDA neuron development or survival. • Ptprs inhibition doesn't stimulate mDA neurite sprouting in vivo post 6-OHDA lesion. • Ptprs ko in mDA neurons dampens behavioral methamphetamine sensitization. • Ptprs ko in mDA neurons modulates dopamine release.

  PublisherDOI

• Oligopeptides and Polypeptides Impact Norepinephrine Detection in Lymphoid Tissue

  ACS Chemical Neuroscience · 2025-09-11

  articleSenior authorCorresponding

  Detection of neurochemicals voltammetrically can be challenging in complex matrices like tissue. Norepinephrine (NE) is a neurotransmitter in the brain and is directly released by the sympathetic nervous system in the periphery. Fast-scan cyclic voltammetry (FSCV) is an electrochemical technique previously used to detect NE from sympathetic neurons in lymphoid tissues. Mesenteric lymph nodes present a unique challenge to FSCV due to their complex tissue matrix, which includes immune cells and neurons. These cells release various neuropeptides, cytokines, and other chemical signaling molecules, which can interfere with FSCV. Notably, Neuropeptide Y (NPY) from sympathetic neurons, and Substance P (SubP) and Calcitonin Gene-Related Peptide (CGRP) from sensory neurons are common peptides that are released locally near NE sites. These peptides are regulated by and interact with NE through complex neuronal circuits, potentially impacting FSCV NE detection. We demonstrate that increasing levels of each peptide alter voltammetric NE detection. We observed that the NE oxidation potential shifts with each peptide in vitro, and NE cyclic voltammograms exhibit unique peak broadening specific to NPY compared to SubP and CGRP, indicating that each peptide affects the carbon fiber microelectrode (CFME) differently. Overall, we show significant convolution of voltammetric NE peaks in the presence of peptides, providing evidence that future developments in materials to reduce protein fouling could significantly improve the robustness and accuracy of NE FSCV detection.

  PublisherDOI

• Purinergic Receptor P2Y1 Modulates Catecholamine Signaling in Murine Mesenteric Lymph Nodes

  ACS Chemical Neuroscience · 2025-02-24 · 4 citations

  articleOpen accessSenior authorCorresponding

  Neuroimmune communication is crucial for the body’s response to physiological challenges, homeostasis, and immune stress response. Adrenergic and purinergic neurotransmission in the sympathetic nervous system is vital for this communication. This study achieves the first co-detection of adenine-based purines and catecholamines in mesenteric lymph nodes via fast-scan cyclic voltammetry. Additionally, we reveal that manipulating an ATP receptor can impact catecholamine signaling in the lymph node for the first time. The G-protein-coupled receptor P2Y1, which controls intracellular Ca2+ levels, was targeted with the antagonist MRS2179. MRS2179 decreased catecholamine concentrations, increased inter-event times, and prolonged event durations. These results suggest that events became smaller, less frequent, and longer-lasting, possibly attributable to decreased intracellular Ca2+ levels. These findings indicate that ATP release in the lymph node can partially regulate norepinephrine signaling, providing mechanistic insight into sympathetic neuronal neurotransmitter control. A deeper understanding of more complicated neuroimmune mechanisms could potentially influence the development of therapeutic strategies in immunology and neurobiology.

  PublisherOA PDFDOI

Recent grants

• CAREER: Tunable Graphene Microelectrodes for Real-time Biological Sensing

  NSF · $675k · 2022–2026

Frequent coauthors

• Gordon S. Mitchell

  University of Florida

  20 shared

• Rebecca R. Pompano

  Carter Center

  17 shared

• Juliet V. Santiago

  University of Florida

  17 shared

• Elisa J. Gonzalez‐Rothi

  University of Florida

  17 shared

• Ashley Holland

  University of Florida

  17 shared

• Kristin Smith

  16 shared

• Alec K. Simon

  University of Florida

  16 shared

• Kelsey Stefan

  University of South Florida

  16 shared

Education

• Ph.D., Chemistry

  University of Virginia

  2014

• B.S., Chemistry

  Christopher Newport University

  2009

Awards & honors

• Research Fellowship, Center for Cognitive Studies, Tufts Uni…
• Horace Williams Fellowship, UNC Chapel Hill, 2004-2010
• Visiting Scholar Fellowship, University of Reading, UK, 2007…
• Graduate Student Opportunity Fund Grant, UNC Chapel Hill, 20…
• Scholars of Tomorrow Fellowship, UNC Chapel Hill, 2004-2005