FIGURE 4.

Synaptic inhibition induced by muscarinic receptor activation by carbachol was attenuated in dentate cells from circadian-arrhythmic animals. Carbachol application decreased stimulus evoked inhibitory transmission (a1; n = 18 cells, p < .001), but increased spontaneous tonic inhibition (b1; p = .020). IPSPs are depolarizing because the intracellular electrode solution contained a high concentration of chloride (see methods). Representative traces of inhibitory responses are shown in panels (a1) and (b1). Box plots show median values and extend from the 25th to 75th percentiles; whiskers extend to minimum and maximum data points with individual values shown as circles. Stimulus-evoked IPSPs were significantly suppressed only in cells from ENT animals (a2; n = 8 ENT, n = 7 ARR); amplitudes are shown for individual cells from ENT (a3) and ARR (a4) animals. Frequency distributions of spontaneous IPSP intervals (b2) and amplitudes (b3) during the first 150 s of recording. Statistical comparisons were made with KS tests from cumulative frequency distributions of the data in panels (b2) and (b3). Carbachol increased the number of spontaneous IPSP events in both ENT (p = .001) and ARR (p = .003) groups. Cells from ARR animals had significantly more IPSP events before (control; p = .014) and during (carbachol; p = .003) drug application compared to ENT (b2). There were no significant differences (p > .05) in amplitudes (b3) of spontaneous ISPS events. *p < .05, **p < .001, n.s. (nonsignificant difference)