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This Article Full Text Full Text (PDF) All Versions of this Article: 579/3/849    most recent jphysiol.2006.126102v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Wang, X.-L. Articles by Pan, H.-L. Search for Related Content PubMed PubMed Citation Articles by Wang, X.-L. Articles by Pan, H.-L. Related Collections Alimentary

¹ Department of Anaesthesiology and Pain Medicine, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA
² Department of Anaesthesiology, The Third Hospital of Hebei Medical University, Shijiazhuang 050051, China

Hyperactivity of spinal dorsal horn neurons plays an important role in the development of diabetic neuropathic pain. However, little is known as to whether synaptic input to spinal dorsal horn neurons is altered in diabetic neuropathy. Also, the function of GABA_B receptors in the control of synaptic input to dorsal horn neurons in diabetes remains poorly understood. To determine the changes in synaptic input to dorsal horn neurons and the GABA_B receptor function in streptozotocin-induced diabetes, we performed whole-cell recording (GDP--S included in the internal solution) on lamina II neurons in rat spinal cord slices. The frequency of glutamatergic mEPSCs and the amplitude of monosynaptic EPSCs evoked from the dorsal root were significantly higher in diabetic than in control rats. On the other hand, the basal frequency and amplitude of GABAergic spontaneous IPSCs and mIPSCs and those of glycinergic spontaneous IPSCs and mIPSCs did not differ significantly between control and diabetic rats. The GABA_B agonist baclofen produced a significantly greater reduction in dorsal root-evoked EPSCs and the frequency of mEPSCs in control than in diabetic rats. However, the inhibitory effect of baclofen on GABAergic and glycinergic spontaneous IPSCs and mIPSCs was not significantly different in the two groups. These findings suggest that increased glutamatergic input from primary afferents to dorsal horn neurons may contribute to synaptic plasticity and central sensitization in diabetic neuropathic pain. Furthermore, the function of presynaptic GABA_B receptors at primary afferent terminals, but not that on GABAergic and glycinergic interneurons, in the spinal cord is reduced in diabetic neuropathy.

(Received 4 December 2006; accepted after revision 10 January 2007; first published online 11 January 2007)
Corresponding author H.-L. Pan: Department of Anaesthesiology and Pain Medicine, Unit 409, The University of Texas M. D. Anderson Cancer Center, 1400 Holcombe Blvd, Houston, TX 77030, USA.  Email: huilinpan{at}mdanderson.org