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Baclofen acts in the central amygdala to reduce synaptic transmission and impair context fear conditioning

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Delaney, AJ, Crane, JW ORCID: 0000-0002-4601-0189, Holmes, M, Fam, J and Westbrook, RF 2018 , 'Baclofen acts in the central amygdala to reduce synaptic transmission and impair context fear conditioning' , Scientific Reports, vol. 8 , pp. 1-11 , doi: 10.1038/s41598-018-28321-0.

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Abstract

The two main sub-divisions of the Central amygdala (CeA), the lateral-capsular (CeA-LC) and the medial (CeA-M), contain extensive networks of inhibitory interneurons. We have previously shown that activation of GABAB-receptors reduces excitatory transmission between axons of the pontine parabrachial nucleus and neurons of the CeA-LC by inhibiting glutamate release from presynaptic terminals13. Here we have characterised GABAB-receptor activation on other excitatory and inhibitory projections within the CeA. Using whole-cell, patch-clamp recordings, we found that the GABAB-receptor agonist baclofen significantly reduced excitatory and inhibitory transmission from all tested inputs into the CeA-LC and CeA-M. In all but one of the inputs, reductions in transmission were accompanied by an increase in paired pulse ratio, indicating that presynaptic GABAB-receptors acted to reduce the release probability of synaptic vesicles. To examine the impact of GABAB-receptors in the CeA on contextual fear-conditioning, we infused baclofen into the CeA immediately prior to training. Compared to vehicle-infused rats, baclofen-infused rats displayed significantly less freezing both during the final stages of the training period and at test 24 hours later. The results of this study demonstrate that, by suppressing excitatory and inhibitory transmission, activation of presynaptic GABAB-receptors in the CeA inhibits the development of context conditioned fear.

Item Type: Article
Authors/Creators:Delaney, AJ and Crane, JW and Holmes, M and Fam, J and Westbrook, RF
Keywords: GABA-B, fear conditioning, central amygdala, baclofen, electrophysiology
Journal or Publication Title: Scientific Reports
Publisher: Nature Publishing Group
ISSN: 2045-2322
DOI / ID Number: 10.1038/s41598-018-28321-0
Copyright Information:

© 2018 The Authors. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/

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