Blockade of epinephrine priming of the cerebral auditory evoked response by cortical cholinergic deafferentation.
The present study tested hypotheses derived from a neurobehavioral model of anxiety that posits an important role of the basal forebrain cholinergic system in the cortical processing of anxiety-associated stimuli and contexts. We hypothesized that visceral afferent activity induced by systemic administration of epinephrine would enhance the processing of auditory stimuli as evidenced by the cerebral auditory evoked response. We further predicted that selective lesions of the basal forebrain cortical cholinergic projection system would disrupt this processing, and would further block the effects of epinephrine. Results confirmed these hypotheses. Epinephrine was found to enhance the amplitude of the P70 component of the auditory evoked response in rats. Selective lesions of the basal forebrain corticopetal cholinergic projection, by intrabasalis infusions of 192 IgG saporin, delayed and reduced the amplitude of the P70 component, and blocked the potentiating effects of epinephrine on the auditory evoked response. The present results are consistent with the view that visceral afferent input may modulate cortical processing of sensory signals via the basal forebrain cholinergic system. These considerations emphasize the potential importance of ascending, bottom-up modulation of processing by telencephalic circuits that may impact on a wide range of behavioral functions.[1]References
- Blockade of epinephrine priming of the cerebral auditory evoked response by cortical cholinergic deafferentation. Berntson, G.G., Shafi, R., Knox, D., Sarter, M. Neuroscience (2003) [Pubmed]
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