Presentation Details
| Latent Enhancement of Aversion Learning Following Benign Taste Experience Requires Basolateral Amygdala Activity Veronica Flores1, Jackson Chew1, Donald Katz2, Jian-You Lin2. 1Furman University, Greenville, SC, USA.2Brandeis University, Waltham, MA, USA |
Abstract
Conditioned taste aversion (CTA) trains an animal to dislike a particular taste that has been paired with malaise. Benign experience with a taste stimulus that will later be conditioned has long been known to reduce the strength of CTA learning. Our work has continuously replicated a related phenomenon wherein experience to “benign” taste stimuli conversely strengthens a later learned aversion to novel sucrose (latent enhancement [LE] of CTA) in Long Evans Rats. Our in-vivo electrophysiology studies have provided insight into this phenomenon suggesting that taste experience may increase discriminability/salience of the later portion of Gustatory Cortical (GC) responses that code for palatability of a novel taste – a result that could boost the associability of that taste and enhance learning. Given that palatability information has been shown to be relayed by the basolateral amygdala (BLA), we test the role of the BLA in LE of CTA using inhibitory designer receptors exclusively activated by designer drugs (iDREADDs) in 24 female Long Evans rats. iDREADDs were activated so to inhibit the BLA during taste experience sessions prior to CTA training toward novel sucrose. We collected in-vivo electrophysiological activity from GC during BLA-inhibited taste experience sessions and BLA-intact CTA learning. We predict that the previously noted enhancement GC response discriminability will be disrupted in the later portion of the taste response that reflects palatability when BLA is inhibited during taste experience. Our preliminary results support this prediction suggesting that the BLA is a vital part of the circuit responsible for integrating benign taste experience into later associative learning.
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No part of this publication may be reproduced, distributed, or transmitted in any form or by any means, including photocopying, recording, or other electronic or mechanical methods, without the prior written permission of the author.