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Project Summary/Abstract Many methamphetamine (meth) addicts suffer cognitive impairments that may perpetuate the addiction cycle. Although, meth impacts several cognitive domains (e.g., attention, impulsivity, memory), the relationship between impaired cognitive function, addiction, and relapse is not well understood. Repeated meth use results in maladaptive brain changes in areas involved in recognition memory and relapse including cortical and subcortical structures. For example, the perirhinal cortex (PRH) is the primary neural substrate involved in recognition memory and directs the flow of information in and out of the parahippocampal structure. The medial prefrontal cortex (mPFC) mediates inhibitory control over behaviors like risk-taking and drug over-consumption; and, the nucleus accumbens (NA) regulates reward-related behaviors. Meth induced impairments in these areas result in memory deficits, loss of inhibitory control, and biased reward processing of drug-associated cues that precipitate a relapse episode. In this proposal, we will study the relationship between motivated drug taking, meth induced cognitive dysfunction, and relapse using a long access (LA) meth self-administration (SA) regimen that reliably establishes recognition memory deficits and results in robust relapse to drug seeking. Given that the PRH is the primary substrate involved in recognition memory, combined with our previous reports of a meth-induced dysregulation of glutamate physiology in this area, we hypothesis that meth impairs recognition memory through PRH projection neurons loss of communication with the mPFC. We also suggest that the pathway encompassing prelimbic (PL) and infralimbic (IL) outputs of the mPFC that project to the NAcore and NAshell are dysregulated by meth resulting in the reinstated responding to conditioned drug cues. As such these separate pathways, PRH-mPFC and mPFC-NA, suggest that recognition memory deficits and relapse are distinct domains of the addiction pathology. However, the PRH-NAcore is a relatively unexplored circuit and the behavioral relevance of this connection has not been determined. We hypothesize that this connection may be the unifying pathway between meth-induced recognition memory dysfunction and relapse. Our Specific Aims will determine whether meth causes functional changes within the pathways involved in recognition memory and cued reinstatement. Specific Aim 1 will test the hypothesis that meth causes functional changes within the PRH-mPFC circuitry that result in recognition memory deficits. Specific Aim 2 will test the hypothesis that functional changes within the mPFC-NA circuitry mediate cued reinstatement of meth seeking using a rodent model of reinstatement. Specific Aim 3 will determine the functional and behavioral relevance of the PRH-NAcore pathway. We hypothesize that this pathway is involved in recognition memory and relapse to meth seeking. Upon completion of our aims we will have a more complete understanding of the pathways involved in recognition memory and cued drug-seeking to better inform treatment approaches for meth addiction.
期刊论文(14)
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DOI: 10.1371/journal.pone.0034299
发表时间: 2012
期刊: PloS one
影响因子: 3.7
作者: [Schwendt M, Reichel CM, See RE]
通讯作者: See RE
DOI: 10.1016/j.neubiorev.2016.07.020
发表时间: 2016-10
期刊: NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
影响因子: 8.2
作者: [Bernheim, Aurelien, See, Ronald E., Reichel, Carmela M.]
通讯作者: Reichel, Carmela M.
DOI: 10.1093/ijnp/pyx058
发表时间: 2017-10-01
期刊: The international journal of neuropsychopharmacology
影响因子: --
作者: [Leong KC, Freeman LR, Berini CR, Ghee SM, See RE, Reichel CM]
通讯作者: Reichel CM
DOI: 10.1017/s1461145711000988
发表时间: 2012-08
期刊: The international journal of neuropsychopharmacology
影响因子: --
作者: [Reichel CM, See RE]
通讯作者: See RE
11
    Nitrergic interneurons and cue-induced cocaine seeking
    Nitrergic interneurons and cue-induced cocaine seeking
    Nitrergic interneurons and cue-induced cocaine seeking
    Contributions of Nitrergic Interneurons and NO Signaling in Cocaine Relapse
    国内基金
    海外基金
    层出镰刀菌氮代谢调控因子AreA 介导伏马菌素 FB1 生物合成的作用机理
    • 批准号:
      2021JJ40433
    • 项目类别:
      省市级项目
    • 资助金额:
      --
    • 批准年份:
      2021
    • 负责人:
      孙磊
    • 依托单位:
    寄主诱导梢腐病菌AreA和CYP51基因沉默增强甘蔗抗病性机制解析
    • 批准号:
      32001603
    • 项目类别:
      青年科学基金项目
    • 资助金额:
      24.0万元
    • 批准年份:
      2020
    • 负责人:
      段真珍
    • 依托单位:
    AREA国际经济模型的移植.改进和应用
    • 批准号:
      18870435
    • 项目类别:
      面上项目
    • 资助金额:
      2.0万元
    • 批准年份:
      1988
    • 负责人:
      史树中
    • 依托单位: