The main objective of this proposal is to characterize nociresponsive laminae I and V neurons in the mouse dorsal horn and to address the contribution of key contributors to pain and injury-induced alterations of nociceptive processing. Specifically, we will use in vivo extracellular recordings of these neurons to test the hypothesis that the cloned capsaicin/vanilloid receptor, VR1, is essential for selective modalities of pain sensation and that it contributes to injury-evoked thermal hyperalgesia relayed by neurons originating in both spinal laminae I and V. To specifically address the properties of nociresponsive projection neurons, in some experiments we will antidromically activate laminae I and V projection neurons from parabrachial nucleus and ventral posterior thalamus.
| Eckert 3rd, W A; Julius, D; Basbaum, A I (2006) Differential contribution of TRPV1 to thermal responses and tissue injury-induced sensitization of dorsal horn neurons in laminae I and V in the mouse. Pain 126:184-97 |
| Shields, Shannon D; Eckert 3rd, William A; Basbaum, Allan I (2003) Spared nerve injury model of neuropathic pain in the mouse: a behavioral and anatomic analysis. J Pain 4:465-70 |
