Activation of spinal d1/d5 receptors induces late-phase LTP of C-fiber-evoked field potentials in rat spinal dorsal horn.
Long-term potentiation (LTP) of C-fiber-evoked field potentials in spinal dorsal horn may be relevant to pathological pain. Our previous work has shown that the late phase of the spinal LTP is protein synthesis-dependent. Considerable evidence has accumulated that dopamine D1/D5 receptors are important for late-phase LTP in hippocampus. In this study, the role of D1/D5 receptors in LTP of C-fiber-evoked field potentials in spinal dorsal horn was evaluated in urethan-anesthetized Sprague-Dawley rats. We found the following. 1) Spinal application of SKF 38393, a D1/D5 receptor agonist, induced a slowly developed LTP of C-fiber-evoked field potentials, lasting for >10 h, and the effect was blocked by the D1/D5 antagonist SCH 23390, whereas a D2 receptor agonist (quinpirole) induced depression of C-fiber responses, lasting for 2 h. 2) The potentiation produced by D1/D5 receptor agonist occluded the late phase but not the early phase of the spinal LTP produced by tetanic stimulation. 3) SCH 23390 selectively depressed the late-phase LTP, when applied 40 min before tetanic stimulation. 4) The D1/D5 agonist-induced potentiation is blocked by the protein synthesis inhibitor anisomycin. 5) Activation of protein kinase A by spinal application of 8-Br-cAMP also induced spinal LTP, and the action occluded the potentiation induced by the D1/D5 receptor agonist. These results suggest that the spinal D1/D5 receptors participate in the protein synthesis-dependent late-phase LTP of C-fiber-evoked field potentials in spinal dorsal horn through the cAMP signaling pathway.
Yang
Hong-Wei
HW
Department of Physiology, Zhongshan Medical School of Sun Yat-sen University, Guangzhou, Peoples Republic of China .
Zhou
Li-Jun
LJ
Hu
Neng-Wei
NW
Xin
Wen-Jun
WJ
Liu
Xian-Guo
XG
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D000841:Anisomycin / Q000494:pharmacology; D001552:Benzazepines / Q000494:pharmacology; D003714:Denervation / Q000379:methods; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D017774:Long-Term Potentiation / Q000502:physiology*; D008297:Male; D036421:Nerve Fibers, Unmyelinated / Q000502:physiology*; D020671:Posterior Horn Cells / Q000502:physiology* / Q000528:radiation effects; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D017447:Receptors, Dopamine D1 / Q000502:physiology*; D050641:Receptors, Dopamine D5; D013116:Spinal Cord / Q000166:cytology; D013997:Time Factors
D001552:Benzazepines; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; C493607:Drd5 protein, rat; D011500:Protein Synthesis Inhibitors; D017447:Receptors, Dopamine D1; D050641:Receptors, Dopamine D5; D015124:8-Bromo Cyclic Adenosine Monophosphate; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; D000841:Anisomycin