Inhibitory interneurons in fear conditioning and extinction
Inhibitory interneurons in fear conditioning and extinction
批准号:
7257816
负责人:
JASMEER P CHHATWAL
金额:
$3.6万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2004
资助国家:
美国
项目状态:
已结题
起止时间:
2004-08-01 至 2008-06-30
关键词:
AffectAmygdaloid structureBiological MarkersCREB1 geneCannabinoidsCell NucleusComplexDominant-Negative MutationExtinction (Psychology)FOS geneFrightImmediate-Early GenesImmunohistochemistryInterneuronsLabelLateralLearningLeftLocalizedMeasuresMediatingMemoryMitogen-Activated Protein KinasesNeuronsOutputPatternPlasticsPopulationRateRattusRecombinantsRodentSecond Messenger SystemsSystemTestingViral VectorWestern Blottingcell typeclassical conditioningconditioned feargenetic manipulationinhibitory neuronlearning extinctionpromoterreceptorreceptor expressionresponsesecond messengertranscription factortransmission process
中文摘要
描述(由申请人提供):经典恐惧条件反射中厌恶的CS-US配对的学习和恐惧反应的消除都严重依赖于杏仁核的发生。此外,一些证据表明,消退学习不仅仅是对原始恐惧记忆的抹去,而是一种独特的、平行的学习形式,它抑制了条件恐惧反应的表达。因此,似乎有两种形式的学习发生在基底外侧杏仁核中,它们通过杏仁核(中央核)的输出对条件性恐惧的表达产生相反的影响。我们假设这两种形式的学习将在构成杏仁核基底外侧复合体(BLA)联想学习回路的兴奋性和抑制性神经元亚群中产生不同的第二信使和转录因子激活模式。此外,我们假设,通过针对BLA神经元的一个特定亚群使用药理学和遗传学操作,我们可能能够选择性地改变这两种类型的学习之一,同时保持另一种类型的完整。
英文摘要
DESCRIPTION (provided by applicant): Both the learning of an aversive CS-US pairing in classical fear conditioning and the extinction of a fear response critically rely on the amygdala to occur. Additionally, several lines of evidence suggest that extinction learning is not simply an erasure of the original fear memory, but a distinct and parallel form of learning that suppresses the expression of the conditioned fear response. Thus there appear to be two forms of learning that occur in the basolateral amygdala which have opposing effects on the expression of conditioned fear through the output of the amygdala (the central nucleus). We hypothesize that these two forms of learning will produce differential patterns of second-messenger and transcription factor activation within the sub-populations of excitatory and inhibitory neurons that constitute the associative learning circuit in the basolateral complex of the amygdala (BLA). Furthermore, we hypothesize that by using pharmacologic and genetic manipulations targeting one particular sub-population of BLA neurons, we may be able to selectively alter one of these two types of learning while leaving the other intact.
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