Journal of Alzheimers Disease & Parkinsonism
Open Access

Research Article

Blockade of Lactate Transport in the Insular Cortex Impairs Reconsolidation, but not Retrieval, of Morphine-associated Memo ry and Prevents Subsequent Reinstatement

Yan Nie¹, He Ren², Jia-Rui Gu³, Chong-Ran Sun⁴, Yang Hui³, Yong-Bin Jing³ and En-You Li^1*

¹Department of Anesthesiology, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, PR China

²Radiology Department, Chongqin Hospital of Traditional Chinese Medicine, Chongqin City, PR China

³Harbin Medical University, Harbin, Heilongjiang Province, PR China

⁴Department of Neurosurgery, 2nd Affiliated Hospital of Zhejiang University Medical College, PR China

Corresponding Author:

Enyou Li
Department of Anesthesiology, The First Affiliated Hospital of Harbin Medical University
Harbin, Heilongjiang Province, PR China
Tel: 086-15996914018
E-mail: doctorPRC@hotmail.com

Received date: February 16, 2016; Accepted date: March 31, 2016; Published date: April 07, 2016

Citation: Nie Y, Ren H, Gu JR, Sun CR, Hui Y, et al. (2016) Blockade of Lactate Transport in the Insular Cortex Impairs Reconsolidation, but not Retrieval, of Morphine-associated Memory and Prevents Subsequent Reinstatement. J Alzheimers Dis Parkinsonism 6:227. doi:10.4172/2161-0460.1000227

Copyright: © 2016 Nie Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Drug-associated memories are critical for addictive behaviors, as these memories can trigger drug seeking and relapse by contextual cues. The transfer of lactate from astrocytes to neurons plays an important role in reward memory. Recently, studies have indicated that the insular cortex has a vital role in addictive procedure, which can be induced by contextual cues using both rat and human memory models. However, the neural locus in which the role of astrocyte–neuron lactate transport in long-term conditioning is required for reward memories is unclear. In investigating the involvement of insular astrocyte–neuron lactate transport in the processing of reward memory, using the conditioned place preference (CPP), we show that the local blockage of astrocyte–neuron lactate transport via the infusion of an inhibitor of glycogen phosphorylase (DAB) into the insular cortex impairs CPP expression of reconsolidation, but not extinction. Co-administering L-lactate and DAB confirmed that lactate could restore DABinduced memory deficit. The expression of c-fos in the insula cortex, the product of an immediate early gene, is also inhibited following memory reactivation. We found that the administration of DAB in the insula prior to reactivating the memory could inhibit the reconsolidation of reward memory, which could be reversed by the co-administration of DAB and L-lactate, and decrease the number of c-fos-positive cells. However, these treatments have no contribution to the extinction procedure, thereby indicating that the inhibitory contribution is reactivation dependent. Our results demonstrate that insular astrocyte–neuron lactate transport has a role in the processing of drug memory and that the blockage of insular astrocyte–neuron lactate transport could inhibit the reconsolidation of reward memory. This offers a novel therapeutic target to reduce the long-lasting conditioned responses to drug abuse.

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