title: Role of extracellular signal-regulated kinase in synaptic transmission and plasticity of a nociceptive input on capsular central amygdaloid neurons in normal and acid-induced muscle pain mice.
abstract: Application of phorbol 12,13-diacetate (PDA) caused marked enhancement of synaptic transmission of nociceptive parabrachio-amygdaloid (PBA) input onto neurons of the capsular central amygdaloid (CeAC) nucleus. The potentiation of PBA-CeAC EPSCs by PDA involved a presynaptic protein kinase C (PKC)-dependent component and a postsynaptic PKC-extracellular-regulated kinase (ERK)-dependent component. NMDA glutamatergic receptor (NMDAR)-dependent long-term potentiation (LTP) of PBA-CeAC EPSCs, which was also dependent on the PKC-ERK signaling pathway, was induced by tetanus stimulation at 100 Hz. In slices from mice subjected to acid-induced muscle pain (AIMP), phosphorylated ERK levels in the CeAC increased, and PBA-CeAC synaptic transmission was postsynaptically enhanced. The enhanced PBA-CeAC synaptic transmission in AIMP mice shared common mechanisms with the postsynaptic potentiation effect of PDA and induction of NMDAR-dependent LTP by high-frequency stimulation in normal slices, both of which required ERK activation. Since the CeAC plays an important role in the emotionality of pain, enhanced synaptic function of nociceptive (PBA) inputs onto CeAC neurons might partially account for the supraspinal mechanisms underlying central sensitization.
authors.affiliation: Institute of Zoology, National Taiwan University, Taipei 106, Taiwan.
authors.forename: Sin-Jhong
authors.initials: SJ
authors.lastname: Cheng
authors.forename: Chien-Chang
authors.initials: CC
authors.lastname: Chen
authors.forename: Hsiu-Wen
authors.initials: HW
authors.lastname: Yang
authors.forename: Ya-Ting
authors.initials: YT
authors.lastname: Chang
authors.forename: Shin-Wen
authors.initials: SW
authors.lastname: Bai
authors.forename: Chih-Cheng
authors.initials: CC
authors.lastname: Chen
authors.forename: Chen-Tung
authors.initials: CT
authors.lastname: Yen
authors.forename: Ming-Yuan
authors.initials: MY
authors.lastname: Min
mesh_terms: D000143:Acids / Q000009:adverse effects; D000344:Afferent Pathways / Q000502:physiology; D000679:Amygdala / Q000473:pathology*; D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018683:Excitatory Amino Acid Agents / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D005260:Female; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000503:physiopathology; D010146:Pain / Q000139:chemically induced / Q000473:pathology*; D010147:Pain Measurement; D018408:Patch-Clamp Techniques / Q000379:methods; D010703:Phorbol Esters / Q000494:pharmacology; D010766:Phosphorylation; D011984:Sensory Receptor Cells / Q000166:cytology / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D009435:Synaptic Transmission / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors; D017557:Ventral Tegmental Area / Q000187:drug effects / Q000502:physiology
chemical_list: D000143:Acids; D004791:Enzyme Inhibitors; D018683:Excitatory Amino Acid Agents; D010703:Phorbol Esters; D026941:Sodium Channel Blockers; C008874:phorbol-12,13-diacetate; D013779:Tetrodotoxin; D048049:Extracellular Signal-Regulated MAP Kinases