Abstract 1651, Date 1:00 pm Monday, February 24, 2003 (24 hours) Session J3: Auditory Cortex: Cellular Mechanisms and Plasticity
Cholinergic Modulation of Auditory Evoked Potentials
Cherie R. Percaccio, Shilpa T. Mistry, Larry J. Cauller, Michael P. Kilgard
Optimal sound processing depends on a delicate balance of inhibition and excitation. We have previously demonstrated that housing conditions have a significant impact on the auditory evoked potential.   Diffuse neuromodulatory systems, such as acetylcholine, likely play an important role in modulating responses in the central auditory system.   To determine whether differences in cortical acetylcholine levels could explain our earlier enrichment effects, we compare auditory evoked responses from rats with lesions of the nucleus basalis and sham controls in two environments.       Adult Sprague Dawley rats (230-270 g) were chronically implanted with an epidural recording electrode over auditory cortex.   The immunotoxin 192 IgG-Saporin (or an inactive control) was injected into the ventricles.   After recovery, noise bursts and tones were delivered 125 times in random order with a 10s ISI and middle latency auditory evoked responses were recorded twice a week for 9 weeks.    The Pa component (25 ms latency) of the auditory evoked potential is typically small in uninjected and sham lesioned controls.   After lesion of the cholinergic nucleus basalis, the amplitude of the Pa component was substantially increased. These changes may be related to cholinergic deficits in autism and other neurological disorders, characterized by abnormal filtering of sensory stimuli. Damage to the cholinergic system will be confirmed with post-mortem acetylcholinesterase histochemistry.