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High-probability grants
According to our matching algorithm, Min Zhuo is the likely recipient of the following grants.
Years |
Recipients |
Code |
Title / Keywords |
Matching score |
1997 — 2001 |
Zhuo, Min |
R29Activity Code Description: Undocumented code - click on the grant title for more information. |
Descending Biphasic Modulation in Persistent Pain
DESCRIPTION: (Applicant's Abstract) The long-term goal of this project is to explore the central mechanisms involved in persistent pain. The lack of understanding of central mechanisms has made persistent pain difficult to treat. Peripheral sensitization (increased sensitivity of primary afferent nociceptors) and central sensitization (enhanced nociceptive transmission in the spinal cord) contribute to persistent pain induced by tissue or nerve injury. However, descending influences from supraspinal structures on spinal sensory transmission during persistent pain haven't been investigated. The present proposal tests the hypothesis that descending biphasic (facilitatory and inhibitory) modulation from the rostromedial medulla (RMM) contribute to persistent pain by enhancing spinal sensory transmission. Single neurons in the RMM will be recorded to examine plastic changes of single neurons in the RMM during persistent pain induced by a subcutaneous injection of formalin into the receptive field. Changes in neuron activity in the RMM may effect spinal sensory transmission through descending biphasic modulation. Thus, responses of spinal neurons to noxious stimuli will be recorded to determine the effects of descending biphasic modulation from the RMM on spinal nociceptive transmission during persistent pain. In addition, responses of spinal neurons to non-noxious stimuli will be measured to test the effects of descending biphasic modulation from the RMM on spinal non-nociceptive transmission during persistent pain. Behavioral and pharmacological experiments will be carried out to characterize the effects of descending biphasic modulation on behavioral reflexes and spinal receptor(s) which mediate the effects during persistent pain. Electrophysiological, behavioral and pharmacological approaches will generate converging information about the role of descending influences on spinal plasticity before and during persistent noxious input. It is hypothesized that the RMM plays an important role in the induction and maintenance of spinal changes associated with persistent pain.
|
0.951 |
1999 — 2002 |
Zhuo, Min |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Serotonergic Regulation of Sensory Transmission
DESCRIPTION: (Applicant's Abstract) The long-term goal of this project is to investigate the regulatory effects of serotonin on fast sensory synaptic transmission in the spinal cord. Spinal nociceptive transmission receives the control of endogenous pain modulatory systems in the central nervous system. Descending serotonergic projecting pathways from the rostroventral medulla play important roles in the modulation of spinal nociceptive transmission. However, synaptic mechanisms of serotonergic inhibition and facilitation in the spinal cord are not completely understood. In this proposal, the regulation of spinal fast synaptic transmission by serotonin will be studied. To characterize AMPA and kainate receptor-mediated sensory synaptic transmission in the spinal dorsal horn, fast glutamatergic synaptic transmission between primary afferent fibers and spinal dorsal horn neurons will be examined using whole-cell patch-clamp recording techniques in spinal cord slices. Pharmacological receptor antagonists will be used to examine kainate receptor-mediated EPSCs. AMPA and kainate receptor-mediated currents will be also recorded from isolated or cultured dorsal horn neurons. To examine the role of kainate receptors in ascending sensory transmission, kainate receptor-mediated EPSCs induced by stimulation of afferent sensory fibers will be studied. Recordings from prelabeled spinothalamic tract cells will be also performed. Experiments will be carried out to investigate the effects of 5-HT on kainate receptor-mediated EPSCs and agonist-evoked currents. Finally, pharmacological experiments will be performed to study synaptic mechanisms for facilitation produced by 5-HT, in spinal slices, isolated or cultured neurons. The proposed studies will generate synaptic mechanisms for fast glutamatergic transmission as well as 5-HT regulation in the spinal cord. This information will be important for understanding central pain transmission and modulation.
|
0.951 |
2003 — 2006 |
Zhuo, Min |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. |
Synaptic Change in Cingulate Cortex After Amputation
DESCRIPTION (provided by applicant): The long-term goal of this project is to characterize excitatory synaptic transmission and plasticity in the anterior cingulate cortex (ACC) and explore their roles in cortical sensory responses after amputation. Understanding of these mechanisms may provide insights into pathophysiological changes in amputees, such as phantom limb sensation and phantom pain. Patients who have suffered amputation in a variety of clinical contexts, including trauma and cancer, often experience abnormal sensory experiences, including phantom limb sensation and phantom pain. It can happen at 24 hours after surgery and persists for months or years. Effective clinical prevention and treatment are not available, due to poor understanding of the mechanisms. Recent human studies demonstrate that cortical reorganization in forebrain areas, including the ACC, correlates with phantom pain in amputees. Little is known about synaptic mechanisms and possible changes in the ACC after amputation. Here, we plan to use both in vitro brain slices and in vivo animals to investigate long-lasting changes in the ACC after amputation. Four Specific Aims are proposed: To characterize synaptic transmission and plasticity in the ACC, electrophysiological recordings will be performed from ACC slices and the contribution of different glutamate receptors and L-type voltage-gated calcium channels to synaptic transmission and plasticity will be studied. To examine sensory responses in the ACC of anesthetized mice, intracellular recordings will be performed from ACC cells in anesthetized mice. Sensory responses to peripheral electrical shocks will be recorded and the cells will be labeled by intracellular injection of the dye biocytin. To study the physiological modulation of ACC after amputation, sensory responses to peripheral electrical shocks will be performed to detect long-lasting changes lasting hours after amputation. Late changes (weeks to months) after amputation will be also investigated. Finally, to explore the molecular mechanism contributing to amputation induced plastic changes; the contribution of calcium-dependent signaling molecules to amputation-induced plastic changes in the ACC will be studied. The proposed studies will characterize basic synaptic mechanisms in the ACC and determine the synaptic and molecular mechanisms for amputation related synaptic plasticity in the ACC. This information will provide a potential neuronal basis for understanding phantom limb sensation and phantom pain.
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