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首页> 外文期刊>Journal of Neurophysiology >Chronic ethanol and withdrawal differentially modulate pre- and postsynaptic function at glutamatergic synapses in rat basolateral amygdala.
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Chronic ethanol and withdrawal differentially modulate pre- and postsynaptic function at glutamatergic synapses in rat basolateral amygdala.

机译：慢性乙醇和戒断对大鼠基底外侧杏仁核的谷氨酸能突触有不同的调节突触前和突触后功能的作用。

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Withdrawal anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is long-lasting, can manifest well after the overt physical symptoms of withdrawal, and is frequently associated with relapse in recovering alcoholics. The neurobiological mechanisms governing these withdrawal-associated increases in anxiety are currently unknown. The basolateral amygdala (BLA) is a major emotional center in the brain and regulates the expression of both learned fear and anxiety. Neurotransmitter system alterations within this brain region may therefore contribute to withdrawal-associated anxiety. Because evidence suggests that glutamate-gated neurotransmitter receptors are sensitive to acute ethanol exposure, we examined the effect of chronic intermittent ethanol (CIE) and withdrawal (WD) on glutamatergic synaptic transmission in the BLA. We found that slices prepared from CIE and WD animals had significantly increased contributions by synaptic NMDA receptors. In addition, CIE increased the amplitude of AMPA-receptor-mediated spontaneous excitatory postsynaptic currents (sEPSCs), whereas only WD altered the amplitude and kinetics of tetrodotoxin-resistant spontaneous events (mEPSCs). Similarly, the frequency of sEPSCs was increased in both CIE and WD neurons, although only WD increased the frequency of mEPSCs. These data suggest that CIE and WD differentially alter both pre- and postsynaptic properties of BLA glutamatergic synapses. Finally, we show that microinjection of the AMPA-receptor antagonist, DNQX, can attenuate withdrawal-related anxiety-like behavior. Together, our results suggest that increased glutamatergic function may contribute to anxiety expressed during withdrawal from chronic ethanol.
机译：戒断焦虑是导致酗酒者持续酗酒的重要因素。这种焦虑症是持久的，可以在明显的戒断症状后很好地表现出来，并且经常与酒精中毒的复发有关。目前尚不清楚控制这些与戒断相关的焦虑增加的神经生物学机制。基底外侧杏仁核（BLA）是大脑中的主要情感中心，调节学习到的恐惧和焦虑的表达。因此，该大脑区域内的神经递质系统改变可能会导致与戒断相关的焦虑。因为有证据表明谷氨酸门控神经递质受体对急性乙醇暴露敏感，所以我们检查了慢性间歇性乙醇（CIE）和戒断（WD）对BLA中谷氨酸能突触传递的影响。我们发现，从CIE和WD动物制备的切片具有明显增加的突触NMDA受体贡献。此外，CIE增加了AMPA受体介导的自发性兴奋性突触后电流（sEPSCs）的幅度，而只有WD改变了抗河豚毒素的自发事件（mEPSCs）的幅度和动力学。同样，尽管只有WD增加了mEPSC的频率，但CIE和WD神经元中sEPSC的频率均增加了。这些数据表明，CIE和WD差异性地改变了BLA谷氨酸能突触的突触前和突触后特性。最后，我们表明，AMPA受体拮抗剂DNQX的显微注射可以减弱戒断相关的焦虑样行为。在一起，我们的研究结果表明增加的谷氨酸能功能可能有助于从慢性乙醇戒断期间表达的焦虑。

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