Inhibition of pain behavior by GABA(B) receptors in the thalamic ventrobasal complex: effect on normal rats subjected to the formalin test of nociception.
The ventrobasal complex of the thalamus (VB) participates in the transmission and modulation of noxious information. Recent data suggested that GABA(B) receptors in the VB might be involved in the modulation of neuronal activity in response to chronic noxious input. However, in acute inflammatory pain, the role of GABA(B) receptors in the VB remains unknown. The formalin test of nociception was performed in rats stereotaxically injected in the VB contralateral to the formalin-injected paw, with saline (controls), baclofen (0.5 and 0.875 microg), a specific GABA(B) receptor agonist or CGP35348 (25 microg), a GABA(B) receptor antagonist. Control animals exhibited phase 1 (acute pain) and phase 2 (tonic pain) nociception-related activities as previously described. The higher dose of baclofen induced a significant decrease of all pain-related behaviors in both phases of the test and had no observable effects on the animals' motor function, while the lower dose could not reduce the total pain-related activities. Injection of CGP35348 prior to baclofen reduced the antinociceptive effect caused by baclofen during phase 2 in the paw-jerks and in total pain-related activities. CGP35348 alone had antinociceptive effects in both phases, though less pronounced than baclofen 0.875 microg in the total pain-related activities during phase 2. Data demonstrate that both the blockade and the activation of GABA(B) receptors in the VB of rats induce antinociception in acute and tonic pain. An important role for GABA(B) receptors on the thalamic processing of nociceptive input in the VB is suggested.
Potes
Catarina Soares
CS
Institute of Histology and Embryology, Faculty of Medicine and IBMC, University of Porto, 4200-319 Porto, Portugal.
Neto
Fani Lourença
FL
Castro-Lopes
José Manuel
JM
D000208:Acute Disease / Q000628:therapy; D000700:Analgesics / Q000494:pharmacology; D000818:Animals; D001418:Baclofen / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects / Q000502:physiology; D002908:Chronic Disease / Q000628:therapy; D004195:Disease Models, Animal; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology*; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009943:Organophosphorus Compounds / Q000494:pharmacology; D010146:Pain / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D010147:Pain Measurement / Q000187:drug effects; D017288:Pain Threshold / Q000187:drug effects / Q000502:physiology; D051381:Rats; D018080:Receptors, GABA-B / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D020651:Ventral Thalamic Nuclei / Q000187:drug effects / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000700:Analgesics; D018755:GABA Agonists; D018756:GABA Antagonists; D058786:GABA-B Receptor Agonists; D058788:GABA-B Receptor Antagonists; D009943:Organophosphorus Compounds; D018080:Receptors, GABA-B; D005680:gamma-Aminobutyric Acid; C066430:CGP 35348; D001418:Baclofen