This Rodent Sensory Phenotyping Core is designed to provide state-of-the-art technologies, facilities and approaches for the measurement and modeling of pain- and itch-related behavior in rodents, and to ensure that any detected changes are specific to these sensations. The major objective is to provide the capacity to behaviorally phenotype pain and itch in rodents to and to support this, three specific aims are proposed Aim 1. Identify, validate, and optimize behavioral outcome measures indicative of pain- and itch-like sensory experiences in rodents.
Aim 2. Model clinical pain conditions in rodents.
Aim 3. Model itch in rodents. The Core will have access to new facilities at Children's Hospital Boston specifically designed for rodent behavioral phenotyping and equipped by funds from the Hospital for the proposed tests and outcome measures. The Core will provide a central focus for the four subprojects, linking the investigators and their research teams in determining in vivo behavioral correlates of their specific molecular and cellular studies.The Core will: i) Provide advice on experimental design;selection of the most appropriate model, outcome measure, choice and numbers of animals, habituation, controls, blinding, drug delivery, and pharmokinetic analyses, ii) Provide facilities for;behavioral measurements, surgery and housing, iii) Provide the equipment necessary to perform the behavioral experiments and analyze the data generated, iv) Advise on data analysis and interpretation, as well as ethical issues.
Pain is a major clinical problem whose scientific investigation relies heavily on preclinical studies in rodents. Central to these is the need to behaviorally phenotype pain.The Behavioral Core will strengthen our ability to use mouse and rat models of sensory diseases to their full potential, both to understand the neurobiological mechanisms responsible, and test new therapies.
|Vardeh, Daniel; Mannion, Richard J; Woolf, Clifford J (2016) Toward a Mechanism-Based Approach to Pain Diagnosis. J Pain 17:T50-69|
|Bean, Bruce P (2015) Pore dilation reconsidered. Nat Neurosci 18:1534-5|
|Talbot, SÃ©bastien; Abdulnour, Raja-Elie E; Burkett, Patrick R et al. (2015) Silencing Nociceptor Neurons Reduces Allergic Airway Inflammation. Neuron 87:341-54|
|Bourane, Steeve; Duan, Bo; Koch, Stephanie C et al. (2015) Gate control of mechanical itch by a subpopulation of spinal cord interneurons. Science 350:550-4|
|Ellis, Samantha; Kalinowski, Danuta S; Leotta, Lisa et al. (2014) Potent antimycobacterial activity of the pyridoxal isonicotinoyl hydrazone analog 2-pyridylcarboxaldehyde isonicotinoyl hydrazone: a lipophilic transport vehicle for isonicotinic acid hydrazide. Mol Pharmacol 85:269-78|
|Kahle, Kristopher T; Khanna, Arjun; Clapham, David E et al. (2014) Therapeutic restoration of spinal inhibition via druggable enhancement of potassium-chloride cotransporter KCC2-mediated chloride extrusion in peripheral neuropathic pain. JAMA Neurol 71:640-5|
|Jo, Sooyeon; Bean, Bruce P (2014) Sidedness of carbamazepine accessibility to voltage-gated sodium channels. Mol Pharmacol 85:381-7|
|Py, BÃ©nÃ©dicte F; Jin, Mingzhi; Desai, Bimal N et al. (2014) Caspase-11 controls interleukin-1Î² release through degradation of TRPC1. Cell Rep 6:1122-8|
|Duan, Bo; Cheng, Longzhen; Bourane, Steeve et al. (2014) Identification of spinal circuits transmitting and gating mechanical pain. Cell 159:1417-32|
|Prescott, Steven A; Ma, Qiufu; De Koninck, Yves (2014) Normal and abnormal coding of somatosensory stimuli causing pain. Nat Neurosci 17:183-91|
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