Camron D. Bryant
· ProfessorVerifiedNortheastern University · Department of Pharmaceutical and Biomedical Sciences
Active 1999–2025
About
Camron D. Bryant is a Professor in the Department of Pharmaceutical and Biomedical Sciences at Bouvé College of Health Sciences, Northeastern University. His contact information includes the location X138 at 140 TF and the phone number 617-373-7663. The biography provided does not include specific details about his research focus, background, or key contributions.
Research topics
- Biology
- Computational biology
- Neuroscience
- Genetics
- Cell biology
- Evolutionary biology
- Psychiatry
- Medicine
- Psychology
- Cognitive science
Selected publications
Journal of Pharmacology and Experimental Therapeutics · 2025-03-22 · 1 citations
articleOpen accessSenior authorAddiction Neuroscience · 2025-06-15
articleOpen accessSenior authorCorresponding• We observed few significant FVB/N substrain differences in withdrawal-associated traits on Postnatal (P) day 7 and P14, which allowed us to combine FVB/N substrains to improve our statistical power to detect the effects of morphine withdrawal on additional spectrotemporal properties of USVs • All morphine-withdrawn FVB/N substrains showed altered USV syllable profiles during spontaneous morphine withdrawal (16 h) on P7 and P14. • We observed syllable sequences unique to FVB/N saline-treated controls and morphine-withdrawn pups on P7 and P14. • Morphine-withdrawn pups displayed altered length, power, and frequency properties of USVs compared to saline-treated controls on P7 and P14. • Multiple withdrawal traits correlated with increased USV emissions and acoustic features on P7 and P14. Concomitant with the opioid epidemic, there has been a rise in pregnant women diagnosed with opioid use disorder and infants born with neonatal opioid withdrawal syndrome (NOWS). NOWS refers to withdrawal signs following cessation of prenatal opioid exposure that comprise neurological, gastrointestinal, and autonomic system dysfunction. A critical indicator of NOWS severity is excessive, high-pitched crying. However, NOWS evaluation is mostly subjective, and additional cry features may not be easily recognized during clinical assessment. Thus, there is a need for more objective measures of NOWS severity. We used a third trimester-approximate opioid exposure paradigm to model NOWS traits in genetically similar inbred substrains of FVB/N mice (NJ, NCrl, NHsd, and NTac). Pups were injected twice daily from postnatal day 1 (P1) to P14 with morphine (10 mg/kg, s.c.) or saline (20 microliters/g, s.c.). Because there were very few minor substrain differences in spontaneous withdrawalinduced ultrasonic vocalization (USV) profiles, we collapsed across substrains to evaluate the effects of morphine withdrawal on additional USV properties. We identified syllable sequences unique to morphine-withdrawn and saline-control FVB/N pups on P7 and P14. We also observed an effect of spontaneous morphine withdrawal on the acoustic properties of USVs on P7 and P14. Some withdrawal traits correlated with acoustic properties of USVs in morphine-withdrawn FVB/N pups on P7 and P14. This in-depth investigation of mouse USV features during spontaneous neonatal opioid withdrawal has implications for predicting neonatal opioid withdrawal severity in mice and applying objective approaches to understanding cries in human infants suffering from NOWS.
Progress in Neuro-Psychopharmacology and Biological Psychiatry · 2025-12-24 · 1 citations
articleOpen accessSenior authorCorrespondingNeuroscience · 2025-02-04 · 1 citations
articleOpen accessJournal of Neuroscience · 2025-03-31 · 3 citations
articleOpen accessThere is a high rate of comorbidity between binge eating (BE) and binge drinking (BD) behaviors, suggesting a common neuropathology. Recently, phosphodiesterase 4B ( PDE4B ) was identified as a pleiotropic gene associated with comorbid alcohol use disorder (AUD) and anorexia nervosa with BE in a genome-wide association study, implicating PDE4B as a potential contributor to shared genetic risk between these disorders. Here, we developed a novel mouse model of comorbid BE and BD in C57BL/6NJ mice in which mice underwent 10 d of BE, followed by 10 d of BD. Females exhibited cross-sensitization from BE to BD, which was apparent on the first day of ethanol access, whereas cross-sensitization emerged in males over multiple trials of BD. Accordingly immunoblotting of the nucleus accumbens tissue indicated a female-selective increase in PDE4B protein expression that was apparent on both the first and last day of BD in mice with a prior BE history. Acute pretreatment with the selective PDE4B inhibitor A33 (1.0 mg/kg) reduced the expression of cross-sensitization to BD in females on Day 1, and this effect was maintained during a 5 d A33 treatment regimen. The 5 d A33 treatment regimen also reduced expression of cross-sensitization to BD that had emerged in males over repeated sessions. These results provide preclinical, functional validation of PDE4B as a driver of food–ethanol cross-sensitization in a novel model for BE and BD comorbidity and support PDE4B in the shared genetic risk for these behavioral pathologies and as a target for pharmacotherapeutic intervention in comorbid AUD and BE behaviors.
OmNI: a modular open-source framework for interactive multi-omics data integration and visualization
NAR Genomics and Bioinformatics · 2025-11-28 · 1 citations
articleOpen accessAbstract Omics Notebook Interactive (OmNI) is an R-based, open-source, and modular framework engineered for streamlined multi-omics data integration and analysis across diverse data types, incorporating interactive visualizations at each processing step. OmNI performs differential expression analysis utilizing customizable linear models, accommodating various covariates and complex experimental designs. For cross-omic layer integration, OmNI employs a modified S-score statistic, ensuring sensitive detection of differential features. The framework also integrates network and metabolomics data, offering detailed insights into regulatory mechanisms through comprehensive enrichment analysis using multiple pathway databases. Outputs include interactive HTML reports, CSV/TSV files, and Cytoscape-compatible objects. OmNI is readily deployable in both local and high-performance computing environments, enabling scalable data processing. Acknowledging the public health concerns of opioids, we performed TMT18-based deep proteome and phosphoproteome analysis of brains from genetically diverse collaborative cross diversity outbred (CC/DO) founder mouse strains exposed to fentanyl to demonstrate OmNI’s capabilities. The integrative S-score uniquely identified differential signaling and interaction hubs conserved across all strains and revealed strain-specific molecular neuro-responses to fentanyl. OmNI is freely available for download at https://github.com/gracerhpotter/OmNI and is also accessible via a web interface at https://emili-laboratory.shinyapps.io/omni/.
Long-read whole-genome sequencing of SHR rat substrains with distinct substance use phenotypes
Mammalian Genome · 2025-12-22
articleOpen accessThe Spontaneously Hypertensive Rat (SHR) is a widely used model for hypertension and, more recently, for neuropsychiatric disorders such as ADHD and Substance Use Disorder (SUD). Despite a common origin, SHR substrains from different vendors exhibit distinct behavioral phenotypes, particularly in models of SUD. This study characterizes the genomic landscape of two such substrains, SHR/NCrl and SHR/NHsd, using high-fidelity long-read sequencing to identify genetic variants associated with their phenotypic divergence. We identified over 5.8 million variants shared by both substrains compared to the reference genome. These include high-impact variants in genes involved in blood pressure regulation, such as Ramp2 and Npy1r, providing a potential genetic basis for their hypertensive phenotype. We also discovered 17,618 high-confidence variants unique to each substrain. From these, we selected 500 high-quality SNP markers suitable for genetic mapping studies, such as Reduced Complexity Crosses (RCCs). Computational predictions indicated moderate-impact variants in genes involved in neuroplasticity and synaptic function. Notably, the SHR/NHsd substrain carries unique missense variants in Ptpro and Tenm2, genes linked to glutamatergic synapses and SUD-related pathways. In contrast, the SHR/NCrl substrain has unique variants in genes such as Wwc1 and Pcdh10, which are involved in synaptic plasticity and neurotransmission. These findings provide a critical genomic resource for dissecting the heritable components of SUD-related behaviors.
Genes Brain & Behavior · 2025-01-13 · 1 citations
articleOpen accessSenior authorCorrespondingOpioid use disorder is heritable, yet its genetic etiology is largely unknown. C57BL/6J and C57BL/6NJ mouse substrains exhibit phenotypic diversity in the context of limited genetic diversity which together can facilitate genetic discovery. Here, we found C57BL/6NJ mice were less sensitive to oxycodone (OXY)-induced locomotor activation versus C57BL/6J mice in a conditioned place preference paradigm. Narrow-sense heritability of OXY-induced locomotor activity traits ranged from 0.22 to 0.31, implicating suitability for genetic analysis. Quantitative trait locus (QTL) mapping in an F2 cross identified a chromosome 1 QTL explaining 7%-12% of the variance in OXY locomotion and anxiety-like withdrawal in the elevated plus maze. A second QTL for EPM withdrawal behavior on chromosome 5 near Gabra2 (alpha-2 subunit of GABA-A receptor) explained 9% of the variance. To narrow the chromosome 1 locus, we generated recombinant lines spanning 163-181 Mb, captured the QTL for OXY locomotor traits and withdrawal, and fine-mapped a 2.45-Mb region (170.16-172.61 Mb). Transcriptome analysis identified five, localized striatal cis-eQTL transcripts and two were confirmed at the protein level (KCNJ9, ATP1A2). Kcnj9 codes for a potassium channel (GIRK3) that is a major effector of mu opioid receptor signaling. Atp1a2 codes for a subunit of a Na+/K+ ATPase enzyme that regulates neuronal excitability and shows functional adaptations following chronic opioid administration. To summarize, we identified two candidate genes underlying the physiological and behavioral properties of opioids, with direct preclinical relevance to investigators employing these widely used substrains and clinical relevance to human genetic studies of opioid use disorder.
bioRxiv (Cold Spring Harbor Laboratory) · 2024-07-04 · 2 citations
preprintOpen accessSenior authorCorrespondingRationale: Opioid use during pregnancy can lead to negative infant health outcomes, including neonatal opioid withdrawal syndrome (NOWS). NOWS comprises gastrointestinal, autonomic nervous system, and neurological dysfunction that manifest during spontaneous withdrawal. Variability in NOWS severity necessitates a more individualized treatment approach. Ultrasonic vocalizations (USVs) in neonatal mice are emitted in isolation as a stress response and are increased during opioid withdrawal, thus modeling a negative affective state that can be utilized to test new treatments. Objectives: We sought to identify the behavioral and USV profile, brainstem transcriptomic adaptations, and role of kappa opioid receptors in USVs during neonatal opioid withdrawal. Methods: We employed a third trimester-approximate opioid exposure model, where neonatal inbred FVB/NJ pups were injected twice-daily with morphine (10mg/kg, s.c.) or saline (0.9%, 20 ul/g, s.c.) from postnatal day(P) 1 to P14. This protocol induces reduced weight gain, hypothermia, thermal hyperalgesia, and increased USVs during spontaneous morphine withdrawal. Results: , which contributes to withdrawal-induced dysphoria. The kappa opioid receptor (KOR) antagonist, nor-BNI (30 mg/kg, s.c.), significantly reduced USVs in FVB/NJ females, but not males during spontaneous morphine withdrawal. Furthermore, the KOR agonist, U50,488h (0.625 mg/kg, s.c.), was sufficient to increase USVs on P10 (both sexes) and P14 (females only) in FVB/NJ mice. Conclusions: We identified an elevated USV syllable, Complex 3, and a female-specific recruitment of the dynorphin/KOR system in increased USVs associated with neonatal opioid withdrawal severity.
Alcohol Clinical and Experimental Research · 2024-09-16 · 1 citations
articleOpen accessBACKGROUND: Adolescent sensitivity to alcohol is influenced by genetic background. Data from our laboratory suggested that adolescent C57BL/6J and DBA/2J inbred mice differed in susceptibility to alcohol-induced deficits in dorsal hippocampus-dependent contextual fear learning. METHODS: To investigate the biological underpinnings of this strain difference, we examined dorsal hippocampus gene expression using RNA-sequencing after alcohol or saline administration followed by Pavlovian fear conditioning across male and female C57BL/6J and DBA/2J adolescents. RESULTS: Strains exhibited dramatic differences in dorsal hippocampus gene expression. Specifically, C57BL/6J and DBA/2J strains differed by 3526 transcripts in males and 2675 transcripts in females. We identified pathways likely to be involved in mediating alcohol's effects on learning, including networks associated with Chrna7, a gene encoding the nicotinic cholinergic receptor alpha 7 subunit, and Fmr1, a gene encoding the fragile X messenger ribonucleoprotein. CONCLUSIONS: These findings provide insight into the mechanisms underlying strain differences in alcohol's effects on learning and suggest that different biological networks are recruited for learning based on genetics, sex, and alcohol exposure.
Recent grants
NIH · $463k · 2018
NIH · $174k · 2017
NIH · $3.3M · 2020–2026
NIH · $296k · 2013
NIH · $50k · 2010
Frequent coauthors
- 57 shared
Jacob A. Beierle
Boston University
- 41 shared
Emily J. Yao
Boston University
- 33 shared
Andrew Emili
Boston University
- 29 shared
Julia L. Scotellaro
Boston Children's Hospital
- 25 shared
Martin T. Ferris
University of North Carolina at Chapel Hill
- 23 shared
Qiu T. Ruan
University School
- 23 shared
Julia C. Kelliher
Northeastern University
- 22 shared
Stanley I. Goldstein
Boston University
Labs
Pharmaceutical and Biomedical SciencesPI
Education
- 1995
Ph.D., Pharmacology
University of California, San Francisco
- 1992
M.S., Pharmacology
University of California, San Francisco
- 1990
B.S., Pharmacology
University of California, San Francisco
- Resume-aware match score
- Save to shortlist
- AI-drafted outreach
See your match with Camron D. Bryant
PhdFit ranks faculty by your research interests, methods, and publications — grounded in their actual work, not templates.
- Free to start
- No credit card
- 30-second signup