Intermittent ethanol consumption depresses endocannabinoid-signaling in the dorsolateral striatum of rat

被引:50
作者
Adermark, Louise [1 ]
Jonsson, Susanne [1 ]
Ericson, Mia [1 ]
Soderpalm, Bo [1 ]
机构
[1] Univ Gothenburg, Inst Neurosci & Physiol, Dept Psychiat & Neurochem, Addict Biol Unit, S-40530 Gothenburg, Sweden
基金
英国医学研究理事会;
关键词
Alcohol; Basal ganglia; Cannabinoid; 1; receptor; GABA; Long-term; Synaptic plasticity; LONG-TERM DEPRESSION; DEPENDENT PLASTICITY; SYNAPTIC PLASTICITY; NUCLEUS-ACCUMBENS; DORSAL STRIATUM; WISTAR RATS; DOPAMINE; STRESS; REWARD; RECEPTORS;
D O I
10.1016/j.neuropharm.2011.01.014
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent research suggests that adaptations elicited by drugs of abuse share common features with traditional learning models, and that drugs of abuse cause long-term changes in behavior by altering synaptic function and plasticity. In this study, endocannabinoid (eCB) signaling in the dorsolateral striatum, a brain region vital for habit formation, was evaluated in acutely isolated brain slices from ethanol (EtOH)-consuming rats and control rats. EtOH-consuming rats had free access to a 20% EtOH solution for three 24 hour sessions a week during seven weeks and consumed an average of 3.4 g/kg per session. eCB-mediated long-lasting disinhibition (DLL) of population spike (PS) amplitude induced by moderate frequency stimulation was impaired in EtOH-consuming rats, and was not restored by the muscarinic receptor antagonist scopolamine (10 mu M). The lack of DLL could be linked to a reduced GABA(A) receptor tone, since bicuculline-mediated disinhibition of striatal output was significantly reduced in slices from EtOH-consuming rats. However, eCB signaling induced by high frequency stimulation (HFS) was also impaired in slices from EtOH-consuming rats and isolated control rats. Activation of presynaptic cannabinoid 1 receptors (CB1R) with WIN55,212-2 (250 nM, 1 mu M) significantly modulated PS amplitude in slices from age-matched control rats while slices from EtOH-consuming rats remained unaffected, indicating that eCB signaling is inhibited at a level that is downstream from CB1R activation. Intermittent alcohol intake for seven weeks might thus be sufficient to modulate a presynaptic mechanism that needs to be synergized with CB1R activation for induction of long-term depression (LTD). In conclusion, alcohol consumption inhibits striatal eCB signaling in a way that could be of importance for understanding the neurological underpinnings of addictive behavior. This article is part of a Special Issue entitled 'Synaptic Plasticity and Addiction'. (C) 2011 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1160 / 1165
页数:6
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