Auditory elicitation of the P300 event-related evoked potential in the rat.

Auditory stimuli were used to elicit a P300 event-related evoked potential (ERP) in rat. Test conditions were comparable to those for eliciting ERP's in humans. A train of background tones with a randomly inserted target tone at a ten to one ratio were presented individually to ten unrestrained subjects in a baseline, a novel, and a trained condition. In the novel condition EEG's were averaged from subjects hearing both background and target stimuli for the first time. In the trained condition, subjects were previously trained using footshock in a shuttle box to discriminate the target tone. A statistical comparison of an ERP peak elicited at approximately 300 msec in both the novel and target condition compared with the baseline demonstrated the presence of the P300 in the rat.

Basal forebrain infusion of HC-3 in rats: maze learning deficits and neuropathology.

Ten adult male Sprague-Dawley rats were infused with hemicholinium (HC-3) using mini-osmotic pumps over a 14 day period through bilateral, chronically implanted cannulae in the nucleus basalis magnocellularis (nbm). Ten matched controls were infused in the same fashion with saline. HC-3 rats receiving implants demonstrated a significant deficit in maze-learning ability compared with individual and group performances before receiving the implants. In saline rats there was no significant difference in maze-learning ability before and after receiving implants. The HC-3 group receiving implants demonstrated a significant deficit in maze-learning ability compared with the saline control group. Serial sections through nbm from control and HC-3 rats indicated that all cannulae were located within infusion range of nbm. In HC-3 subjects, cholinergic cell bodies were destroyed with concurrent degeneration of terminal fields in cortex. Except for cannula insertion damage, the cholinergic neurotransmitter system appeared unharmed in controls. Stains for neuritic plaques and neurofibrillary damage were negative in both groups. The memory deficit in experimental subjects supported by the demonstrated destruction of nbm cholinergic neurons suggests that HC-3 may be useful in the development of an animal model for Alzheimer's Disease.