A Conditioning-Strengthened Circuit From CA1 of Dorsal Hippocampus to Basolateral Amygdala Participates in Morphine-Withdrawal Memory Retrieval

Abstract

Conditioned context-induced retrieval of drug withdrawal memory contributes to drug relapse. The basolateral amygdala (BLA) is an important brain region that is involved in conditioned context-induced retrieval of morphine withdrawal memory. However, the upstream pathways of the activation of the BLA by conditioned context remains to be studied. The present results show that the CA1 of dorsal hippocampus is an upstream brain region of the activation of the BLA during conditioned context-induced morphine withdrawal memory retrieval; the indirect connection from the CA1 of dorsal hippocampus to the BLA is enhanced in mice with conditioned place aversion (CPA); the postrhinal cortex (POR) is a brain region that connects the CA1 of dorsal hippocampus and the activation of the BLA during conditioned context-induced retrieval of morphine-withdrawal memory. These results suggest that a conditioning-strengthened indirect circuit from the CA1 of dorsal hippocampus to the BLA through the POR participates in morphine withdrawal memory retrieval.

HIV-1 Tat and Morphine Differentially Disrupt Pyramidal Cell Structure and Function and Spatial Learning in Hippocampal Area CA1: Continuous versus Interrupted Morphine Exposure

“…The notion that Tat and morphine can independently impair spatial memory is consistent with the minimal behavioral interactions observed in the current study ( Zhu et al, 2011 ; Kitanaka et al, 2015 ; Kesby et al, 2016 ; Marks et al, 2016 ). Opioid-dependent individuals reportedly demonstrate hyper-connectivity in hippocampo-amygdalar memory circuits that may promote the recall of drug-associated cues ( Zhang et al, 2017 ; Ma et al, 2020 ). This hyperactive associative circuitry may counterbalance the general effects of Tat ( Basu and Siegelbaum, 2015 ; Roy et al, 2017 ; Sharifi et al, 2020 ).…”

Nucleus accumbens circuit disinhibits lateral hypothalamus glutamatergic neurons contributing to morphine withdrawal memory in male mice

“…The mechanisms underlying this increase in GABA release from NAcC D1-MSNs projecting to the LH following CPA memory expression remains unknown. We speculate that it may be related to contex-withdrawal association-induced strengthening of D1-MSNs projecting to the LH because in our previous study, we observed contex-withdrawal association-induced strengthening in other projection neurons 58 .…”

The role of hippocampus in memory reactivation: an implication for a therapeutic target against opioid use disorder

“…The hippocampus is often mentioned in studies for opioid withdrawal memory [49][50][51] and other types of aversive memory reactivation [52][53][54][55][56] (Table 1). Comprehensive presentation of the function of this brain region in memory reactivation comes from fear memory studies [24,57].…”

“…In particular, the induction of the immediate-early gene Arc in the DG was positively correlated with a higher aversion score in morphine-dependent animals [76], implying that the hippocampal DG participates in withdrawal memory reactivation. Recent studies have also revealed the role of hippocampal CA1 in withdrawal memory reactivation with some pharmacological and immunostaining methods [51]. However, how these hippocampal subregions engage in this process still requires further studies with advanced techniques in the neuroscience field.…”