Articles by Angela N. Pierce in JoVE
Assessment of Perigenital Sensitivity and Prostatic Mast Cell Activation in a Mouse Model of Neonatal Maternal Separation Isabella M. Fuentes1, Angela N. Pierce1, Pierce T. O'Neil1, Julie A. Christianson1 1Anatomy and Cell Biology, University of Kansas Medical Center We are measuring perigenital mechanical sensitivity and mast cell activation in the prostate of male C57BL/6 mice that underwent an early life stress paradigm – neonatal maternal separation, in order to induce a preclinical model of chronic prostatitis/chronic pelvic pain syndrome.
Other articles by Angela N. Pierce on PubMed
Back Pain and Leg Complaints That Revealed Non-small Cell Carcinoma: a Case Study Journal of Chiropractic Medicine. Sep, 2011 | Pubmed ID: 22014908 The purpose of this case study is to describe the clinical presentation of a patient with a chief complaint of low back and leg pain with no prior diagnosis of lung cancer.
Stress and Chronic Pelvic Pain Progress in Molecular Biology and Translational Science. 2015 | Pubmed ID: 25744684 Chronic pelvic pain is the number one reason that patients suffering from irritable bowel syndrome, interstitial cystitis/painful bladder syndrome, vulvodynia, or chronic prostatitis/chronic pelvic pain syndrome seek medical attention. These syndromes generally have no associated pathology or identified underlying etiology, although dysfunction within the immune system, central nervous system, and peripheral nervous system has been identified. Due to the lack of pathology, chronic pelvic pain syndromes are often diagnosed by exclusion, and the high degree of comorbid symptomology among these and other functional pain disorders complicate identifying appropriate treatment strategies. Chronic stress exposure early in life has been shown to increase the likelihood of pelvic pain later in life, and acute stress exposure can induce or increase symptom severity. In this chapter, we describe the individual chronic pelvic pain syndromes and how stress influences the likelihood of diagnosis and the severity of symptoms experienced by patients.
Neonatal Vaginal Irritation Results in Long-term Visceral and Somatic Hypersensitivity and Increased Hypothalamic-pituitary-adrenal Axis Output in Female Mice Pain. Jun, 2015 | Pubmed ID: 26098441 Experiencing early life stress or injury increases a woman's likelihood of developing vulvodynia and concomitant dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. To investigate the outcome of neonatal irritation of the vagina (NVI), female mouse pups were administered intravaginal zymosan on postnatal days 8 and 10 and were assessed as adults for vaginal hypersensitivity by measuring the visceromotor response (VMR) to vaginal balloon distension (VBD). Western blotting and calcium imaging were performed to measure transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) in the vagina and innervating primary sensory neurons. Serum corticosterone, mast cell degranulation, and corticotropin-releasing factor receptor 1 (CRF1) expression were measured as indicators of peripheral HPA axis activation. Colorectal and hindpaw sensitivity were measured to determine cross-sensitization resulting from NVI. Adult NVI mice had significantly larger VMR during VBD than naïve mice. TRPA1 protein expression was significantly elevated in the vagina and calcium transients evoked by mustard oil (TRPA1 ligand) or capsaicin (TRPV1 ligand) were significantly decreased in DRG from NVI mice, despite displaying increased depolarization-evoked calcium transients. Serum corticosterone, vaginal mast cell degranulation, and CRF1 protein expression were all significantly increased in NVI mice, as were colorectal and hindpaw mechanical and thermal sensitivity. Neonatal treatment with a CRF1 antagonist, NBI 35965, immediately prior to zymosan administration largely attenuated many of the effects of NVI. These results suggest that NVI produces chronic hypersensitivity of the vagina, as well as of adjacent visceral and distant somatic structures, driven in part by increased HPA axis activation.