作者: Laura E. Been , Kelsey M. Moore , Bruce C. Kennedy , Robert L. Meisel
DOI: 10.1016/J.BIOPSYCH.2015.07.021
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摘要: Abstract Background Escalated aggression is a behavioral sign of numerous psychiatric disorders characterized by loss control. The neurobiology underlying escalated unknown and particularly understudied in females. Research our laboratory demonstrated that repeated aggressive experience female hamsters resulted an response to future encounters increase dendritic spine density on nucleus accumbens (NAc) neurons. We hypothesized the activation group I metabotropic glutamate receptor signaling though fragile X mental retardation protein (FMRP) pathway may underlie synaptic plasticity associated with escalation. Methods Female were given five daily tests or without prior treatment 5 (mGluR5) antagonist 2-methyl-6-(phenylethynyl)-pyridine. Following testing, messenger RNA expression levels measured for postsynaptic 95 (PSD-95) SAP90/PSD-95-associated 3, as well phosphorylated FMRP. Results Experience-dependent escalation depends mGluR5 receptors. Furthermore, decreases phosphorylation FMRP NAc, which coupled long-term scaffolding proteins PSD-95 3. Finally, experience-dependent prevented antagonism receptor. Conclusions Activation receptors involved regulating following experience. NAc novel target preclinical studies aggression, added benefit emerging therapeutic approaches are likely be effective treating pathologic both male subjects.