Alcohol induces input-specific aberrant synaptic plasticity in the rat dorsomedial striatum

NEUROPHARMACOLOGY

卷:123

Article

Ma, Tengfei¹  Barbee, Britton¹  Wang, Xuehua¹  Wang, Jun¹ 

[1] Texas A&M Univ, Dept Neurosci & Expt Therapeut, Coll Med, Hlth Sci Ctr, 2106 Med Res & Educ Bldg,8447 Riverside Pkwy, Bryan, TX 77807 USA

关键词: Ethanol;    Medial prefrontal cortex;    Basolateral amygdala;    Dorsomedial striatum;    Glutamatergic receptor;    Optogenetics;   

DOI  :  10.1016/j.neuropharm.2017.05.014

来源: Elsevier

【 摘 要 】

Accumulated evidence suggests that the dorsomedial striatum (DMS) of the basal ganglia plays an essential role in pathological excessive alcohol consumption. The DMS receives multiple glutamatergic inputs. However, whether and how alcohol consumption distinctly affects these excitatory afferents to the DMS remains unknown. Here, we used optogenetics to selectively activate the rat medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) inputs in DMS slices, and measured the effects of alcohol consumption on glutamatergic transmission in these corticostriatal and amygdalostriatal circuits. We found that excessive alcohol consumption increased AMPA receptor- and NMDA receptor (NMDAR)mediated neurotransmission, as well as the GluN2B/NMDAR ratio, at the corticostriatal input to the DMS. The probability of glutamate release was increased selectively at the amygdalostriatal input. Interestingly, we discovered that paired activation of the mPFC and BLA inputs using dual-channel optogenetics induced robust long-term potentiation (LTP) of the corticostriatal input to the DMS. Taken together, these results indicate that excessive alcohol consumption potentiates glutamatergic transmission via a post synaptic mechanism for the corticostriatal input and via a presynaptic mechanism for the amygdalostriatal input. These changes may in turn contribute to pathological alcohol consumption. (c) 2017 Elsevier Ltd. All rights reserved.

【 授权许可】

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