Synaptic scaffolding protein Homer1a protects against chronic inflammatory pain.

Glutamatergic signaling and intracellular calcium mobilization in the spinal cord are crucial for the development of nociceptive plasticity, which is associated with chronic pathological pain. Long-form Homer proteins anchor glutamatergic receptors to sources of calcium influx and release at synapses, which is antagonized by the short, activity-dependent splice variant Homer1a. We show here that Homer1a operates in a negative feedback loop to regulate the excitability of the pain pathway in an activity-dependent manner.

Spinal upregulation of the nitric oxide synthase-interacting protein NOSIP in a rat model of inflammatory pain.

Nitric oxide and nitric oxide synthases are key players in synaptic plasticity events in the spinal cord, which underly the development of chronic pain states. To date, little is known about the molecular mechanisms regulating the activity of nitric oxide synthases in nociceptive systems. The present study was aimed at the immunohistochemical determination of the expression of a nitric oxide synthase-interacting protein (NOSIP) in the rat spinal cord and dorsal root ganglia and studying its regulation in states of nociceptive hypersensitivity in a rat model of post-inflammatory pain.