Graphene oxide prevents lateral amygdala dysfunctional synaptic plasticity and reverts long lasting anxiety behavior in rats

被引:18
作者
Biagioni, Audrey Franceschi [1 ]
Cellot, Giada [1 ]
Pati, Elisa [1 ]
Lozano, Neus [2 ,3 ]
Ballesteros, Belen [2 ,3 ]
Casani, Raffaele [1 ]
Coimbra, Norberto Cysne [4 ]
Kostarelos, Kostas [2 ,3 ,5 ,6 ]
Ballerini, Laura [1 ]
机构
[1] Int Sch Adv Studies SISSA, Neuron Physiol & Technol Lab, Neurosci, Via Bonomea 265, I-34136 Trieste, Italy
[2] CSIC, Catalan Inst Nanosci & Nanotechnol ICN2, Campus UAB, Barcelona 08193, Spain
[3] BIST, Campus UAB, Barcelona 08193, Spain
[4] Univ Sao Paulo FMRP USP, Dept Pharmacol, Lab Neuroanat & Neuropsychobiol, Ribeirao Preto Med Sch, Av Bandeirantes 3900, BR-14049900 Ribeirao Preto, SP, Brazil
[5] Univ Manchester, Natl Graphene Inst, Nanomed Lab, AV Hill Bldg,Oxford Rd, Manchester M13 9PL, Lancs, England
[6] Univ Manchester, Fac Biol Med & Hlth, AV Hill Bldg,Oxford Rd, Manchester M13 9PL, Lancs, England
基金
巴西圣保罗研究基金会;
关键词
Graphene-based nanovectors; Biotechnology of brain disorders; Synaptic plasticity; Patch-clamp; Amygdala;
D O I
10.1016/j.biomaterials.2021.120749
中图分类号
R318 [生物医学工程];
学科分类号
0831 ;
摘要
Engineered small graphene oxide (s-GO) sheets were previously shown to reversibly down-regulate glutamatergic synapses in the hippocampus of juvenile rats, disclosing an unexpected translational potential of these nanomaterials to target selective synapses in vivo. Synapses are anatomical specializations acting in the Central Nervous System (CNS) as functional interfaces among neurons. Dynamic changes in synaptic function, named synaptic plasticity, are crucial to learning and memory. More recently, pathological mechanisms involving dysfunctional synaptic plasticity were implicated in several brain diseases, from dementia to anxiety disorders. Hyper-excitability of glutamatergic neurons in the lateral nucleus of the amygdala complex (LA) is substantially involved in the storage of aversive memory induced by stressful events enabling post-traumatic stress disorder (PTSD). Here we translated in PTSD animal model the ability of s-GO, when stereotaxically administered to hamper LA glutamatergic transmission and to prevent the behavioral response featured in long-term aversive memory. We propose that s-GO, by interference with glutamatergic plasticity, impair LA-dependent memory retrieval related to PTSD.
引用
收藏
页数:10
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