Noradrenergic modulation of somatosensory cortical neuronal responses to lontophoretically applied putative neurotransmitters

We examined the interaction of norepinephrine (NE) applied iontophoretically in small doses with the responsiveness of somatosensory cortical neurons to the putative neurotransmitter substances acetylcholine (ACh) and gamma-aminobutyric acid (GABA). Neuronal responses to microiontophoretic pulses (8- to 10-s duration at 45-s intervals) of ACh and GABA were examined before, during, and after NE iontophoresis. Computer-generated histograms used for quantitation of drug responses revealed a NE-induced enhancement of neuronal responsiveness to both ACh and GABA. NE differentially suppressed the spontaneous firing rate more than activity during ACh-induced excitation such that the excitatory response was enhanced relative to background discharge in 86% of the cells tested. In 13 of 35 cells tested, ACh responses were potentiated above control values. GABA-induced inhibition of cortical neuron spontaneous discharge was augmented during iontophoretic application of NE in 94% of the cells examined. Dopamine, even at doses sufficient to depress background firing rate, was not effective in facilitating responses to either ACh or GABA. These results are consistent with the hypothesis that a primary function of the central noradrenergic system is to enhance the efficacy of postsynaptically acting neurotransmitters.