In response to 1 nmol kg?1 CCK-8, dVGV afferent discharge rose to a peak of 170 �� 13% of pre-stimulus levels at 30 s, and the duration of the response (the time to 90% recovery) was 235 �� 46 s (n= 5). The decay half-time of the dVGV afferent response to CCK-8 at 1 nmol kg?1 was 86 s (95% confidence interval: 64 to 129 s, r2= 0.63, n= 6). In contrast, pVGV afferent activity increased to a peak of 140 �� 8% of pre-stimulus levels at 45 s and declined slowly thereafter. The duration of pVGV afferent excitation, 1164 �� 186 s (n= 5), was significantly longer than the dVGV afferent response (t test, P < 0.05). At lower doses of CCK-8, duration measurements of pVGV afferent activity were unreliable, due to the relatively small magnitude of the excitation compared with the level of variability in the firing rates. However, the aggregate AP24534 cost
data (Fig. 7) clearly demonstrate that even at the 100 and 300 pmol kg?1 dose, total pVGV afferent activity remained above baseline for more than 20 min post-stimulus. An exponential curve could not be fitted to the decay portion of pVGV afferent responses (r2 < 0.1, 95% confidence interval 30 s to +��, n= 6). In one pVGV recording, afferent inhibition, rather than excitation, was observed. Response profiles and durations In both dVGV and pVGV dual UNC2881
recordings, the temporal profile of CCK-8-evoked afferent excitation in each branch differed distinctively from that of the efferent responses in the same branch (Fig. 8A and
. Of interest, the temporal relationship of dVGV efferent to dVGV afferent activity bore a striking resemblance to that between dVGV efferent and pVGV efferent activity (Fig. 7A). This suggested that dVGV afferent activity might parallel pVGV efferent activity. Such a parallel was indeed observed (Fig. 8C and Supplemental Fig. S5). Linear regression of dVGV afferent vs. pVGV efferent STI571 supplier
responses yielded a coefficient of determination (r2) of 0.91 at the 1 nmol kg?1 dose and 0.88 for all doses combined, indicating a strong linear relationship between the two (slope = 1.7 �� 0.1 at 1 nmol kg?1 CCK-8). In contrast, r2 values for regressions of dVGV afferent vs. dVGV efferent responses were 0.31 at the 1 nmol kg?1 dose and 0.11 for all doses combined, and for pVGV afferent vs. pVGV efferent responses, r2 values were 0.46 at the 1 nmol kg?1 dose and 0.10 over all doses combined. Regression of pVGV afferent vs. dVGV efferent responses yielded r2 values of 0.22 both for the 1 nmol kg?1 dose and for all doses combined. Thus, only the dVGV afferent and pVGV efferent responses showed a strong linear relationship. The duration (time to 90% recovery) of dVGV afferent and pVGV efferent responses did not differ (unpaired t test, P < 0.05), while the duration of afferent activity in each branch differed significantly from the duration of efferent activity in the same branch (paired t test, P < 0.5) (Fig. 8D).