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. Author manuscript; available in PMC: 2009 Jan 21.
Published in final edited form as: J Comp Physiol A Neuroethol Sens Neural Behav Physiol. 2007 Jun 6;193(7):715–728. doi: 10.1007/s00359-007-0227-9

Fig. 2.

Fig. 2

Inhibition of NO synthesis also modified the resting and odor-evoked activity of LNs. a-c Representative traces are shown for three LNs before, during, and after treatment with either 500 μM 7NI or 15 mM L-NAME (Table 1). Similarly to PNs, NOS inhibition in LNs resulted in: bursting (a n = 2; LN16; LN bursts were arrhythmic; compare to Fig. 1a), increased firing rates (b n = 3; LN19), and decreased firing rates (c n = 2; LN21) in different subsets of LNs. One LN had no change in activity when NO synthesis was blocked (Table 1). Changes in the RMP and action potential amplitude were also observed in bursting LNs (a n = 2). d The average resting firing activity was plotted as a percentage of baseline levels (± SEM) for each LN subset. e-g LN odor responses, like PN odor responses, were also abolished (e, h; LN22; n = 2; significance not measured, n < 4) and decreased (f, i; LN 21; n = 3), but also increased (g, j; LN23; n = 4; repeated measures ANOVA df = 2; F = 164; P < 0.0001; Tukey's post-hoc test: P < 0.001) after NO synthesis inhibition. Calibration a-c 20 mV and 250 ms; e-j 20 mV and 200 ms (gray bar)