Dopamine exerts no acute effects on Kv1.3 in activated encephalitogenic T cells.
Apart from a central function in the extrapyramidal motor system, dopamine has been suggested to play a role in neuroimmune interactions. Particularly in diseases of the central nervous system, such as multiple sclerosis, alterations in dopamine homeostasis might have immunological consequences. We investigated potential effects of dopamine stabilized by ascorbic acid on specifically activated encephalitogenic T cells at the peak of activation. Those cells exhibited an upregulation of voltage-sensitive K+ channels which play a role in many neurotransmitter responses of lymphocytes and fulfilled a prerequisite to respond to dopamine, i.e. stable expression of mRNA for dopamine receptors DRD1, DRD2 and DRD3. However, whole-cell and perforated whole-cell recordings revealed no change in voltage-sensitive K+ currents. Moreover, T cell proliferation was not changed in the presence of dopamine. Previously reported dopamine effects on T cells may be explained by a comparatively lower activation of the cells under investigation, suggesting an activation dependence of dopamine effects that may not be mediated by K+ channels. Alternatively, the occurrence of dopamine degradation products under unprotected conditions may account for the changes reported. Nevertheless, care should be taken when using the dopamine-protecting anti-oxidant ascorbic acid, since we found that it markedly inhibited both K+ currents and lymphocyte proliferation at higher concentrations.
Strauss
Ulf
U
Neurobiological Laboratory, Department of Neurology, University of Rostock, Rostock, Germany. ulf.strauss@med.uni-rostock.de
Herbrik
Martin
M
Mix
Eilhard
E
Bajorat
Rika
R
Jung
Stefan
S
Gimsa
Ulrike
U
Rolfs
Arndt
A
D000255:Adenosine Triphosphate / Q000378:metabolism / Q000494:pharmacology; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism / Q000494:pharmacology; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D004298:Dopamine / Q000276:immunology / Q000378:metabolism / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology / Q000378:metabolism*; D051664:Kv1.3 Potassium Channel; D008213:Lymphocyte Activation / Q000187:drug effects* / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000276:immunology; D009103:Multiple Sclerosis / Q000276:immunology / Q000378:metabolism*; D015213:Neuroimmunomodulation / Q000187:drug effects / Q000276:immunology; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024642:Potassium Channels, Voltage-Gated / Q000187:drug effects* / Q000276:immunology; D012333:RNA, Messenger / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D011954:Receptors, Dopamine / Q000235:genetics; D043562:Receptors, G-Protein-Coupled / Q000187:drug effects / Q000276:immunology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
C496975:Kcna3 protein, rat; D051664:Kv1.3 Potassium Channel; D026902:Potassium Channel Blockers; D024642:Potassium Channels, Voltage-Gated; D012333:RNA, Messenger; D011954:Receptors, Dopamine; D043562:Receptors, G-Protein-Coupled; D000255:Adenosine Triphosphate; D001205:Ascorbic Acid; D011188:Potassium; D004298:Dopamine