Authors
Rohini Kuner
Summary
Glutamatergic signaling mechanisms and intracellular calcium mobilization in the spinal cord are crucial for the development of nociceptive plasticity, which is associated with chronic pathological pain1,2. Long-form Homer proteins anchor glutamatergic receptors to sources of calcium-influx and -release at synapses3-5, which is antagonized by the short, activity-dependent splice variant Homer1a. Using this protocol Homer1a can be targeted to specific spinal segments in vivo. Using this method we have shown that Homer1 function is critically involved in pain plasticity and constitutes a promising therapeutic target for the treatment of chronic inflammatory pain.Further details
The protocol was published on Protocol Exchange in 2006. To see the entire protocol, click on the source link.Advertisement
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