Decreased motivation during chronic pain requires long-term depression in the nucleus accumbens

被引:223
作者
Schwartz, Neil [1 ]
Temkin, Paul [1 ]
Jurado, Sandra [1 ,2 ]
Lim, Byung Kook [1 ,3 ]
Heifets, Boris D. [1 ]
Polepalli, Jai S. [1 ]
Malenka, Robert C. [1 ]
机构
[1] Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Nancy Pritzker Lab, Stanford, CA 94305 USA
[2] Univ Maryland, Sch Med, Dept Pharmacol, Baltimore, MD 21201 USA
[3] Univ Calif San Diego, Div Biol Sci, Neurobiol Sect, La Jolla, CA 92093 USA
关键词
MEDIUM SPINY NEURONS; NEUROPATHIC PAIN; INDIRECT PATHWAYS; ADENOSINE A(2A); ARCUATE NUCLEUS; MESSENGER-RNAS; BASAL GANGLIA; ANIMAL-MODELS; GALANIN; MECHANISMS;
D O I
10.1126/science.1253994
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Several symptoms associated with chronic pain, including fatigue and depression, are characterized by reduced motivation to initiate or complete goal-directed tasks. However, it is unknown whether maladaptive modifications in neural circuits that regulate motivation occur during chronic pain. Here, we demonstrate that the decreased motivation elicited in mice by two different models of chronic pain requires a galanin receptor 1-triggered depression of excitatory synaptic transmission in indirect pathway nucleus accumbens medium spiny neurons. These results demonstrate a previously unknown pathological adaption in a key node of motivational neural circuitry that is required for one of the major sequela of chronic pain states and syndromes.
引用
收藏
页码:535 / 542
页数:8
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