Neuronal basis of social motivation and the failure to adapt to loss
社会动机的神经基础和无法适应损失
基本信息
- 批准号:9933419
- 负责人:
- 金额:$ 15.66万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2018
- 资助国家:美国
- 起止时间:2018-09-01 至 2023-05-31
- 项目状态:已结题
- 来源:
- 关键词:AddressAgeBehavioral ParadigmBereavementBiologicalBiological ProcessBrain regionCellsClinicalDistressEmotionalEmotionsExhibitsFailureFamily memberFriendsGrief reactionHealthHeart DiseasesHumanImageImpairmentIndividualInvestigationLearningLifeMental disordersMotivationNeuronsPainPair BondPartner in relationshipPathologicPopulationProcessPublic HealthRecoveryResearchRewardsSystemTestingTimeWorkbrain cellexperienceexperimental studyin vivoinsightloved onesmotivational processesneurogeneticsnovelprairie voleresponsesocialsocial attachmentsocial engagementtool
项目摘要
Project Summary
Social bonds between family members and friends can last a lifetime. As long as these attachments exist, the
selective motivation that drives us to seek out and interact with these individuals represents a healthy, reinforcing
mechanism that maintains these bonds. But what happens to these motivational systems when a bond is
permanently lost? Most people eventually learn to adapt to the loss of a loved one, but for some, the failure to
adapt leads to function-impairing grief that can last years. Clinically, this is known as complicated grief. Despite
the central importance of socio-motivational processes and their appropriate transformation following loss, their
neuronal basis remains unclear. To address this deficit, I propose to use monogamous prairie voles, which form
life-long bonds and exhibit distress following separation from their partner. Pair-bonded prairie voles will lever-
press to be reunited with their partner, enabling us to quantify bond-directed motivation. My lab is developing a
high-throughput operant system to quantify bond-directed motivation. I will combine this novel behavioral
paradigm with advanced neurogenetic tools to interrogate the neuronal substrates of bond-directed motivation.
I will test whether bond strength predicts levels of partner-directed motivation and how quickly this motivation
extinguishes following permanent partner separation. Then, using our operant paradigm in combination with in
vivo Ca2+ imaging and cell-specific manipulations of neuronal activity, I will test the hypothesis that distinct
neuronal populations within reward-related brain regions modulate partner-directed motivation. Finally, because
some people experience pathological forms of grief characterized by persistent dwelling on the lost bond, I will
ask whether artificially reactivating the neuronal ensemble that encodes a pair bond leads to prolonged
motivational responses following bond loss. Completion of these experiments will provide fundamental insights
into the engagement of social motivation systems at a neuronal level – both when a bond remains intact and
following its disruption. There is a pressing need for this research; there are no currently accepted paradigms for
studying selective social motivation or the emotional response to loss. As the U.S. population ages, there will be
a substantial public-health burden from increased rates of bereavement-induced mental illness, heart disease,
and complicated grief, and this work represents a means to elucidate important biological mechanisms that
contribute to these phenomena.
项目概要
家庭成员和朋友之间的社会纽带可以持续一生。只要这些执着存在,
驱使我们寻找这些人并与他们互动的选择性动机代表着一种健康的、强化的
维持这些债券的机制。但是,当纽带被破坏时,这些激励系统会发生什么?
永久丢失?大多数人最终都会学会适应失去亲人,但对某些人来说,无法适应
适应会导致功能受损的悲伤,这种悲伤可能会持续数年。临床上,这被称为复杂性悲伤。尽管
社会动机过程的核心重要性及其在失去后的适当转变,其
神经元基础仍不清楚。为了解决这一缺陷,我建议使用一夫一妻制的草原田鼠,它们形成
终生的纽带,并在与伴侣分离后表现出痛苦。成对的草原田鼠将撬开——
迫切希望与他们的伴侣团聚,使我们能够量化债券导向的动机。我的实验室正在开发一个
高通量操作系统来量化债券导向的动机。我将结合这种新颖的行为
使用先进的神经发生工具来探究债券导向动机的神经元基础的范例。
我将测试债券强度是否可以预测合作伙伴导向的动机水平以及这种动机的速度有多快
伴侣永久分离后消失。然后,结合使用我们的操作范式
体内 Ca2+ 成像和神经元活动的细胞特异性操作,我将检验以下假设:
与奖励相关的大脑区域内的神经元群调节伙伴导向的动机。最后,因为
有些人会经历病态的悲伤,其特征是持续沉迷于失去的联系,我会
询问人为地重新激活编码配对键的神经元集合是否会导致延长
失去联系后的动机反应。完成这些实验将提供基本的见解
在神经元水平上参与社会动机系统——无论是当纽带保持完整还是
其破坏之后。这项研究的迫切需要;目前还没有公认的范式
研究选择性的社会动机或对损失的情绪反应。随着美国人口老龄化,将会出现
丧亲之痛引发的精神疾病、心脏病、
和复杂的悲伤,这项工作代表了阐明重要生物机制的一种手段
促成了这些现象。
项目成果
期刊论文数量(2)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
How prior pair-bonding experience affects future bonding behavior in monogamous prairie voles.
- DOI:10.1016/j.yhbeh.2020.104847
- 发表时间:2020-11
- 期刊:
- 影响因子:3.5
- 作者:Harbert KJ;Pellegrini M;Gordon KM;Donaldson ZR
- 通讯作者:Donaldson ZR
PhAT: A flexible open-source GUI-driven toolkit for photometry analysis.
PhAT:一个灵活的开源 GUI 驱动工具包,用于光度分析。
- DOI:10.1101/2023.03.14.532489
- 发表时间:2023
- 期刊:
- 影响因子:0
- 作者:Murphy,KathleenZ;Haile,Eyobel;McTigue,Anna;Pierce,AnneF;Donaldson,ZoeR
- 通讯作者:Donaldson,ZoeR
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Zoe Rebecca Donaldson其他文献
Zoe Rebecca Donaldson的其他文献
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{{ truncateString('Zoe Rebecca Donaldson', 18)}}的其他基金
Dynamic entanglements: the functional role and mechanistic basis of inter-individual neural synchrony
动态纠缠:个体间神经同步的功能作用和机制基础
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10644475 - 财政年份:2023
- 资助金额:
$ 15.66万 - 项目类别:
The neuromolecular basis of adaptation to bond loss
适应键损失的神经分子基础
- 批准号:
10374344 - 财政年份:2022
- 资助金额:
$ 15.66万 - 项目类别:
The neuromolecular basis of adaptation to bond loss
适应键损失的神经分子基础
- 批准号:
10565940 - 财政年份:2022
- 资助金额:
$ 15.66万 - 项目类别:
Hippocampal neural dynamics driving affiliation and attachment
海马神经动力学驱动归属和依恋
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10225059 - 财政年份:2021
- 资助金额:
$ 15.66万 - 项目类别:
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血清素 1a 受体表达的变化是抑郁症风险的一个来源
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8618070 - 财政年份:2014
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$ 15.66万 - 项目类别:
Variation in serotonin 1a receptor expression as a source of depression risk
血清素 1a 受体表达的变化是抑郁症风险的一个来源
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8851682 - 财政年份:2014
- 资助金额:
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Variation in serotonin 1a receptor expression as a source of depression risk
血清素 1a 受体表达的变化是抑郁症风险的一个来源
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9352881 - 财政年份:2014
- 资助金额:
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