Abstract
The effects of central noradrenergic activation on an auditory-evoked cortical response were studied using systemic administration of yohimbine (2 mg/kg intravenously. IV), a noradrenergic stimulant, in 13 anesthetized rats. To analyze changes of the response, surface and intracortical evoked potentials (EP) as well as extracellular single-unit recordings with tungsten microelectrodes were employed. It was noted that the initial-positive wave of the surface EP corresponded to unit firing responses in a restricted area of the auditory cortex, where the surface EP was largest and a polarity inversion of the intracortical EP was observed. The following effects were produced by yohimbine: 1) The initial-positive surface potential (n = 10) and corresponding intracortical potential with inverted polarity (n = 6) both showed an increase in amplitude and a decrease in peak latency; 2) the unit firing response (n = 10) tended to show an increase in peak frequency and a decrease in peak firing latency and 3) yohimbine produced an earlier ending of the firing period and in paired stimulation experiments (n = 7) it prolonged the period during which the second response was suppressed, indicating an augmentation of postexcitation inhibition. Later histological examination suggested that most of the units recorded were pyramidal cells. These findings indicate that chemical stimulation of the central noradrenergic system by yohimbine enhances both the initial excitatory and following inhibitory' processes in the auditory-evoked response of the cortical units (probably pyramidal cells), resulting not only in amplification of the response but also in advancement of the response phase. We proposed that this phase advance effect is an important aspect of noradrenergic function that contributes to an acceleration of information processing in the alert state.
Published Version
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