ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2017
Reversal of Cocaine-Associated Synaptic Plasticity in Medial Prefrontal Cortex Parallels Elimination of Memory Retrieval.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Novel circUnc79 regulates morphine-induced reward memoryActa pharmaceutica Sinica. B · 2026Article
- Sex differences in noradrenergic regulation of the medial prefrontal cortex in mice.Biology of sex differences · 2025Article
- EcoHIV infection effects on cocaine seeking and neuroimmune responses in male mice depend on cocaine exposure pattern.Addiction neuroscience · 2025Article
- Remission from addiction: erasing the wrong circuits or making new ones?Nature reviews. Neuroscience · 2025Review
- Functional properties of corticothalamic circuits targeting paraventricular thalamic neurons.Neuron · 2024Article
- Distinct roles of excitatory and inhibitory neurons in the medial prefrontal cortex in the expression and reconsolidation of methamphetamine-associated memory in male mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Novel therapeutics in development for the treatment of stimulant-use disorder.Current opinion in neurobiology · 2024Review
- Vagus Nerve Stimulation (VNS) Modulates Synaptic Plasticity in the Infralimbic Cortex via Trk-B Receptor Activation to Reduce Drug-Seeking in Male Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Vagus nerve stimulation (VNS) modulates synaptic plasticity in the rat infralimbic cortex via Trk-B receptor activation to reduce drug-seeking.bioRxiv : the preprint server for biology · 2024Article
- Reinstatement of nicotine conditioned place preference in a transgenerational model of drug abuse vulnerability in psychosis: Impact of BDNF on the saliency of drug associations.Psychopharmacology · 2023Article
- A Novel CaMKII Inhibitory Peptide Blocks Relapse to Morphine Seeking by Influencing Synaptic Plasticity in the Nucleus Accumbens Shell.Brain sciences · 2022Article
- NMDA receptor-mediated synaptic transmission in prefrontal neurons underlies social memory retrieval in female mice.Neuropharmacology · 2022Article
- Blockade of β-Adrenergic Receptors by Propranolol Disrupts Reconsolidation of Drug Memory and Attenuates Heroin Seeking.Frontiers in pharmacology · 2021Article
- Toll-Like Receptor 4 Signaling and Drug Addiction.Frontiers in pharmacology · 2020Review
- The Projection From Ventral CA1, Not Prefrontal Cortex, to Nucleus Accumbens Core Mediates Recent Memory Retrieval of Cocaine-Conditioned Place Preference.Frontiers in behavioral neuroscience · 2020Article
- Dynamic CRMP2 Regulation of CaV2.2 in the Prefrontal Cortex Contributes to the Reinstatement of Cocaine Seeking.Molecular neurobiology · 2020Article
- Heterogeneity in the Paraventricular Thalamus: The Traffic Light of Motivated Behaviors.Frontiers in behavioral neuroscience · 2020Article
- Paraventricular Thalamus Projection Neurons Integrate Cortical and Hypothalamic Signals for Cue-Reward Processing.Neuron · 2019Article
- Effects of early life stress on cocaine conditioning and AMPA receptor composition are sex-specific and driven by TNF.Brain, behavior, and immunity · 2019Article
- Biphasic effect of abstinence duration following cocaine self-administration on spine morphology and plasticity-related proteins in prelimbic cortical neurons projecting to the nucleus accumbens core.Brain structure & function · 2019Article
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Abstract
Addiction is characterized by abnormalities in prefrontal cortex that are thought to allow drug-associated cues to drive compulsive drug seeking and taking. Identification and reversal of these pathologic neuroadaptations are therefore critical for treatment of addiction. Previous studies using rodents reveal that drugs of abuse cause dendritic spine plasticity in prelimbic medial prefrontal cortex (PL-mPFC) pyramidal neurons, a phenomenon that correlates with the strength of drug-associated memories in vivo. Thus, we hypothesized that cocaine-evoked plasticity in PL-mPFC may underlie cocaine-associated memory retrieval, and therefore disruption of this plasticity would prevent retrieval. Indeed, using patch clamp electrophysiology we find that cocaine place conditioning increases excitatory presynaptic and postsynaptic transmission in rat PL-mPFC pyramidal neurons. This was accounted for by increases in excitatory presynaptic release, paired-pulse facilitation, and increased AMPA receptor transmission. Noradrenergic signaling is known to maintain glutamatergic plasticity upon reactivation of modified circuits, and we therefore next determined whether inhibition of noradrenergic signaling during memory reactivation would reverse the cocaine-evoked plasticity and/or disrupt the cocaine-associated memory. We find that administration of the β-adrenergic receptor antagonist propranolol before memory retrieval, but not after (during memory reconsolidation), reverses the cocaine-evoked presynaptic and postsynaptic modifications in PL-mPFC and causes long-lasting memory impairments. Taken together, these data reveal that cocaine-evoked synaptic plasticity in PL-mPFC is reversible in vivo, and suggest a novel strategy that would allow normalization of prefrontal circuitry in addiction.
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