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Neuronal Hyperpolarization-Activated Pacemaker Channels Drive Neuropathic Pain
It is demonstrated that hyperpolarization-activated, cyclic nucleotide-modulated (HCN) "pacemaker" channels play a previously unrecognized role in both touch-related pain and spontaneous neuronal discharge originating in the damaged dorsal root ganglion.

Upregulation of dorsal root ganglion (alpha)2(delta) calcium channel subunit and its correlation with allodynia in spinal nerve-injured rats.
Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after tight ligation of the left fifth and sixth lumbar spinal nerves, a >17-fold, time-dependent increase in alpha(2)delta subunit expression in DRGs ipsilateral to the nerve injury is found, suggesting that DRG alpha( 2)Delta regulation may play an unique role in neuroplasticity after peripheral nerve injury.

Upregulation of Dorsal Root Ganglion α2δ Calcium Channel Subunit and Its Correlation with Allodynia in Spinal Nerve-Injured Rats
Using a rat neuropathic pain model in which gabapentin-sensitive tactile allodynia develops after tight ligation of the left fifth and sixth lumbar spinal nerves, a >17-fold, time-dependent increase in α2δ subunit expression in DRGs ipsilateral to the nerve injury is found, suggesting that DRG α2 δ regulation may play an unique role in neuroplasticity after peripheral nerve injury.

Regulation of Expression of the Sensory Neuron-Specific Sodium Channel SNS in Inflammatory and Neuropathic Pain
Examination of the levels of the transcript encoding the tetrodotoxin-resistant sodium channel SNS in dorsal root ganglion neurons in a range of inflammatory and neuropathic pain models in the rat found that SNS expression is little dependent on NGF even though SNS transcript levels dropped by more than 60% 7-14 days after axotomy.

Prolonged Alleviation of Tactile Allodynia by Intravenous Lidocaine in Neuropathic Rats
It is hypothesized that lidocaine would reduce tactile allodynia observed in a rat nerve injury model and effects after intravenous, intrathecal, and regional administration were compared to determine the site of drug action.

Selective Blockade of the Capsaicin Receptor TRPV1 Attenuates Bone Cancer Pain
It is shown that TRPV1 is present on sensory neuron fibers that innervate the mouse femur and that, in an in vivo model of bone cancer pain, acute or chronic administration of a TRP V1 antagonist or disruption of the TRPv1 gene results in a significant attenuation of both ongoing and movement-evoked nocifensive behaviors.
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