Memory for reward location is enhanced even though acetylcholine efflux within the amygdala is impaired in rats with damage to the diencephalon produced by thiamine deficiency.
A rodent model of diencephalic amnesia produced by thiamine deficiency (pyrithiamine-induced thiamine deficiency [PTD]) was implemented to assess both changes in behavior and acetylcholine (ACh) efflux in the amygdala across four training sessions of a delayed alternation task. Two versions of the delayed alternation task were used. In one version, when a correct alternation was made a unique reward was paired with each spatial location ([left arm-chocolate milk] or [right arm-rat chow]). This paradigm is called the differential outcomes procedure (DOP). In the second version of the task, correct delayed alternation resulted in the same rewards but randomized across location (Nondifferential Outcomes Procedure [NOP]). The PTD rats were impaired on the first session of delayed alternation testing. However, both control and PTD rats using the DOP performed significantly better on delayed alternation than rats trained with the NOP.This effect was driven primarily by the PTD rats in the DOP condition outperforming all other groups on sessions 2-4. Although ACh efflux in the amygdala increased during delayed alternation testing in all groups, the NOP-trained rats had a greater rise in training-related ACh release in the post-training period. This suggests that increased amygdalar cholinergic activation is more critical for processing spatial information than episodic reward information. These data correspond with the idea that cholinergic activation of the amygdala promotes processing in other neural systems.
Savage
Lisa M
LM
Behavioral Neuroscience Program, Department of Psychology, Binghamton University-SUNY, Binghamton, NY 13902, USA. lsavage@binghamton.edu
Guarino
Sabrina
S
D000109:Acetylcholine / Q000378:metabolism*; D000647:Amnesia / Q000209:etiology / Q000378:metabolism* / Q000473:pathology; D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D000963:Antimetabolites; D001245:Association Learning / Q000502:physiology; D001925:Brain Damage, Chronic / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D002799:Cholinergic Fibers / Q000378:metabolism / Q000473:pathology; D004027:Diencephalon / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D008297:Male; D018782:Maze Learning / Q000502:physiology*; D008568:Memory / Q000502:physiology*; D011340:Problem Solving / Q000502:physiology; D011745:Pyrithiamine; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012201:Reward; D013832:Thiamine Deficiency / Q000139:chemically induced / Q000150:complications / Q000473:pathology
D000963:Antimetabolites; D011745:Pyrithiamine; D000109:Acetylcholine