Neuron i e P D

D(Basbaum et al., 2009). The peripheral axons of these pseudou-nipolar neurons innervate tissues, such as skin, muscle, and visceral organs, to detect painful stimuli, whereas their central imaging with a trigeminal neuropathic pain model and detected robust neuronal hypersensitivity in injured and uninjured nerves in the skin, soma in trigeminal ganglion, and central terminals inaxons transmit these signals to secondary-order neurons in the spinal cord dorsal horn (in the case of DRG neurons) and the the spinal trigeminal nucleus. Strikingly, extensive TRPV1 hyper-activity was observed in central terminals innervating all dorsalgeminal ganglion, and central terminals in the spinal trigeminal nucleus. Extensive TRPV1 hyperactivity was observed in central terminals innervating all dorsal horn laminae. The central terminal TRPV1 sensitization was maintained by descending seroto-nergic (5-HT) input from the brainstem. Central blockade of TRPV1 or 5-HT/5-HT3A receptors atten-uated central terminal sensitization, excitatory pri-mary afferent inputs, and mechanical hyperalgesia in the territories of injured and uninjured nerves. Our results reveal central mechanisms facilitating central terminal sensitization underlying chronic pain