title: Low-threshold heat receptor in chick sensory neurons is upregulated independently of nerve growth factor after nerve injury.
abstract: In mammals, the cloned low-threshold heat receptor, vanilloid receptor subtype 1 (VR1), is involved in the genesis of thermal hyperalgesia after inflammation. However, there is evidence that VR1 is not involved in the thermal hyperalgesia that occurs after nerve injury. In search for other heat receptors which might be involved in this phenomenon, we previously demonstrated that chick dorsal root ganglion neurons, which are insensitive to capsaicin, respond to low-threshold heat. Here, we investigated whether expression of the low-threshold noxious heat receptor in chicks is regulated by nerve growth factor (NGF), as VR1 is in mammals. Heat (44 degrees C) responsiveness of isolated dorsal root ganglion neurons of chicks was investigated (i) under culture conditions for up to 4 days with and without NGF and (ii) after a tight ligation of the sciatic nerve for up to 6 days, using cobalt-uptake method. In every case, a significant upregulation in the proportion of heat-responsive neurons was observed. On the molecular level, there was an increase of chick VR1 mRNA level in dorsal root ganglion cells cultured for 3 days in medium lacking NGF. In rat dorsal root ganglion neurons cultured for 1-4 days without NGF, patch-clamp experiments revealed that after 1 day almost all neurons responding to heat also responded to capsaicin, whereas after 3-4 days, more than one-half of the heat-responsive neurons did not respond to capsaicin. These data suggest the existence of low-threshold heat receptors in chick dorsal root ganglion neurons, the expression of which is regulated independently of NGF.
authors.affiliation: Institute of Physiology, University of Würzburg, Röntgenring 9, 97070 Würzburg, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Wach
authors.forename: A
authors.initials: A
authors.lastname: Marín-Burgin
authors.forename: A
authors.initials: A
authors.lastname: Klusch
authors.forename: C
authors.initials: C
authors.lastname: Forster
authors.forename: S
authors.initials: S
authors.lastname: Engert
authors.forename: A
authors.initials: A
authors.lastname: Schwab
authors.forename: M
authors.initials: M
authors.lastname: Petersen
mesh_terms: D000818:Animals; D002211:Capsaicin / Q000494:pharmacology; D002478:Cells, Cultured; D002642:Chick Embryo; D002645:Chickens; D003035:Cobalt / Q000378:metabolism / Q000494:pharmacology; D005727:Ganglia, Spinal / Q000187:drug effects / Q000378:metabolism; D006930:Hyperalgesia / Q000378:metabolism / Q000503:physiopathology; D008026:Ligation / Q000379:methods; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D062559:NAV1.8 Voltage-Gated Sodium Channel; D020932:Nerve Growth Factor / Q000378:metabolism* / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009475:Neurons, Afferent / Q000187:drug effects; D018408:Patch-Clamp Techniques; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D011955:Receptors, Drug / Q000187:drug effects / Q000378:metabolism*; D012584:Sciatic Nerve / Q000293:injuries; D015222:Sodium Channels / Q000096:biosynthesis / Q000187:drug effects; D050916:TRPV Cation Channels; D013697:Thermosensing / Q000502:physiology; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology
chemical_list: D062559:NAV1.8 Voltage-Gated Sodium Channel; D012333:RNA, Messenger; D011955:Receptors, Drug; C568319:Scn10a protein, rat; D015222:Sodium Channels; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D003035:Cobalt; D020932:Nerve Growth Factor; D002211:Capsaicin