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Psychopharmacology (Berl). 2012 Aug;222(4):645-61. doi: 10.1007/s00213-012-2665-5. Epub 2012 Mar 21.

Inactivation of the basolateral amygdala during opiate reward learning disinhibits prelimbic cortical neurons and modulates associative memory extinction.

Author information

1
Department of Anatomy and Cell Biology, The Schulich School of Medicine & Dentistry, University of Western Ontario, 468 Medical Science Building, London, ON N6A 5C1, Canada.

Abstract

RATIONALE:

Neurons within the basolateral amygdala (BLA) and prelimbic cortex (PLC) are involved in associative learning during morphine reward memory recall and extinction. However, the nature by which the BLA regulates PLC neuronal encoding of associative opiate reward learning is not presently understood.

OBJECTIVE:

The purpose of this study was to examine the functional effects of reversible inactivation of the BLA on behavioral and neuronal activity patterns in the PLC during either the acquisition or extinction phases of opiate reward memory processing.

METHODS:

Using a combination of in vivo neuronal population recordings in the rat PLC and pharmacological inactivation of the BLA during a place conditioning procedure, we examined the functional impact of BLA inactivation during the acquisition, recall, and extinction of opiate reward memory.

RESULTS:

Inactivation of the BLA caused an increase in the spontaneous firing and bursting activity of PLC neurons. Inactivation of the BLA during the acquisition phase of opiate reward conditioning caused a subsequent acceleration in the extinction of the previously learned opiate reward memory and behavioral aversions to morphine-paired environments. While BLA inactivation during extinction training led to a delay in extinction memory recall.

CONCLUSIONS:

Our findings demonstrate a functional link between the BLA and neuronal populations in the PLC specifically during the acquisition and extinction phases of opiate reward memory and suggest that BLA input to the PLC modulates the processing of opiate-related extinction memory.

PMID:
22430028
DOI:
10.1007/s00213-012-2665-5
[Indexed for MEDLINE]

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