Figure 7
NPS effects in the sample of amygdala neurons. Summary of data for the sample of CeA neurons tested in normal rats (n = 5 neurons; A) and in arthritic rats (6-8 h postinduction; n = 20 neurons, B and C). Bar histograms show average spikes/s (mean ± SE) as percent of predrug control values (set to 100%). Statistical analysis was performed on raw data. Background activity was measured as average firing rate over 3-5 min. For evoked “net” responses, background activity (15 s) was subtracted from the total activity during stimulation (15 s). (A) Stereotaxic application of NPS (100 μM, concentration in microdialysis probe; 20 min) into the ITC area had no effect under normal conditions. (B) NPS in the ITC inhibited background and evoked activity in arthritic rats significantly (n = 12 neurons; *,**,*** P < 0.05-0.001, Newman-Keuls posttests compared to predrug). Coapplication of a selective NPSR antagonist ([D-Cys(tBu)5]NPS, 1 mM, concentration in microdialysis probe; 20 min) into the ITC area reversed the effect of NPS significantly (n = 7 neurons; ##,### P < 0.01-0.001, Newman-Keuls posttests compared to NPS alone). (C) Nasal application of NPS inhibited background and evoked activity of CeA neurons significantly (n = 8 neurons; *** P < 0.001, Newman-Keuls posttests). Application of a selective NPSR antagonist (SHA68, 50 μM, concentration in microdialysis probe, 20 min) reversed the effect of NPS significantly (n = 6 neurons, ### P < 0.001, Newman-Keuls posttests).