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Cortical Signature and Modulation of Pain

皮质特征和疼痛调节

基本信息

批准号：
10438580
负责人：
ZHIGANG HE
金额：
$ 79.54万
依托单位：
MASSACHUSETTS INSTITUTE OF TECHNOLOGY
依托单位国家：
美国
项目类别：
财政年份：
2018
资助国家：
美国
起止时间：
2018-09-30 至 2024-02-29
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10438580
关键词：
Ablation Acute Affect Affective Anterior Apical Area Attenuated Axon Behavior Brain Cell Nucleus Cells Cognitive Computer Analysis Data Dendrites Development Dimensions Dissection Efferent Pathways Electric Stimulation Electrodes Elements Esthesia Excision Face Fingers Forelimb Foundations Future Genetic Goals Head Headache Human Hypersensitivity Image Individual Injury Knowledge Label Light Link Literature Maps Massage Mechanics Motor Motor Cortex Movement Mus Neurons Nociception Operative Surgical Procedures Pain Pain Disorder Painless Pathway interactions Patients Pattern Perception Physiology Play Population Primary Lesion Process Reporting Research Rodent Role Sensory Slice Somatosensory Cortex Spinal Stimulus Tactile Techniques Testing Thalamic structure Time Tongue Touch sensation Trigeminal Neuralgia allodynia anatomical tracing base brain research central pain chronic neuropathic pain chronic pain chronic pain patient cingulate cortex cingulotomy dorsal horn extracellular imaging study in vivo in vivo calcium imaging inflammatory pain injured mechanical allodynia mechanical stimulus mouse model negative affect nerve injury nerve supply neural circuit neuroregulation optogenetics pain model pain perception pain processing pain relief pain sensation painful neuropathy pressure presynaptic programs relating to nervous system response sensory cortex somatosensory tissue injury virus genetics zona incerta

项目摘要

Cortical Signature and Modulation of Pain Abstract/Project Summary Pain perception contains two main dimensions: the sensory-discriminative and the affective-cognitive aspects. In this proposal, we will focus on the cortical signature and modulations of the sensory aspects of pain using mouse models. Pain can be largely divided into inflammatory or neuropathic pain. A common condition in both types of pain is mechanical allodynia: externally applied innocuous gentle touch becomes painful. Paradoxically, pain elicits self-initiated recuperative behaviors such as rubbing and massaging of the painful regions; and the mechanical stimuli from such self-generated behaviors generally relieve pain. The neural circuit mechanisms underlying the opposite effects of external versus self-applied mechanical stimuli in pain conditions remain poorly understood. Based on previous research as well as our preliminary studies, we hypothesize that corticospinal projecting neurons from primary somatosensory (S1) cortex facilitate mechanical hypersensitivity in pain models, whereas specific motor cortex projection neurons play key roles in suppressing tactile allodynia in self-initiated recuperative behaviors (such as licking and wiping in mice). We further hypothesize that the cortical pain signature can be read out from activity patterns of large populations of individual S1 neurons by comparing their activities in the painful versus non-painful or pain- relieved conditions. We will use a combination of viral-genetic labeling of specific cortical neurons, in vivo calcium imaging and in vivo multi-electrode extracellular recording in freely behaving mice, optogenetics- assisted slice physiology, opto/chemicogenetic manipulations, and computational analyses to test our hypotheses.

疼痛的皮质特征和调节