FIG. 4.
Epinephrine acts on α1-adrenoreceptors and increases the frequency of spontaneous glutamatergic EPSCs. A: Voltage-clamp recording from a PPG neuron at a holding potential (VH) of −70 mV demonstrating the effects of epinephrine on sEPSCs. B: Overlay of 15 consecutive 500 ms traces from the recording shown in A under control conditions (top) and in the presence of epinephrine (bottom). C: Overlay of 15 consecutive 500 ms traces under control conditions and in the presence of phenylephrine or clonidine, respectively, as indicated above each overlay. Phenylephrine, but not clonidine, led to an increase in sEPSC frequency. D: Mean normalized effects of epinephrine and selective α1- (phenylephrine) and α2- (clonidine, dexmedetomidine) adrenoreceptor agonists on sEPSC frequency. The mean sEPSC frequency in presence of the drug (freqD) as a fraction of the frequency in the absence of any drug (freqC) is plotted. The effect of epinephrine is blocked by the glutamate receptor antagonist kynurenic acid (Kyn) and by the α-adrenergic receptor antagonist yohimbine. Yohimbine also blocked the effect of phenylephrine. Kyn itself blocked the majority of sEPSCs. *P < 0.05, **P < 0.01, compared with control. Numbers of cells tested are given above the bars.