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海人酸受体激活增强伏隔核核心中的γ-氨基丁酸能突触传递。

Kainate receptor activation potentiates GABAergic synaptic transmission in the nucleus accumbens core.

作者信息

Crowder Tara L, Ariwodola Olusegun J, Weiner Jeff L

机构信息

Biosciences Division, SRI International, 333 Ravenswood Avenue, Menlo Park, CA 94025-34932, USA.

出版信息

Brain Res. 2006 May 9;1088(1):73-82. doi: 10.1016/j.brainres.2005.12.133. Epub 2006 Apr 19.

DOI:10.1016/j.brainres.2005.12.133
PMID:16626659
Abstract

Inhibitory synaptic transmission plays an important role in regulating the activity of medium spiny neurons (MSNs) in the nucleus accumbens (NAcc). The kainate (KA) subtype of ionotropic glutamate receptor has been shown to potently modulate GABAergic synaptic transmission in several brain regions. Although KA receptor subunits are expressed in the NAcc, KA receptor modulation of GABAergic synaptic transmission in this brain region has not been previously examined. In the current study, we sought to determine if KA receptor activation could alter inhibitory synaptic transmission in the NAcc as it has been shown to do in other brain regions. Using the whole cell patch-clamp technique, we demonstrate that KA receptor activation potentiates evoked GABAergic synaptic transmission and increases the frequency of spontaneous, but not miniature, GABA(A)-receptor-mediated IPSCs in the NAcc. In contrast, KA has no effect on currents evoked by exogenous application of GABA onto MSNs. Taken together, these data suggest that activation of KA receptors in the NAcc core potently facilitates action-potential-dependent GABAergic synaptic transmission, likely via an excitation of presynaptic GABAergic interneurons.

摘要

抑制性突触传递在调节伏隔核(NAcc)中中等棘状神经元(MSN)的活动方面发挥着重要作用。离子型谷氨酸受体的红藻氨酸(KA)亚型已被证明能有效调节多个脑区的GABA能突触传递。虽然KA受体亚单位在NAcc中表达,但此前尚未研究过KA受体对该脑区GABA能突触传递的调节作用。在本研究中,我们试图确定KA受体激活是否能像在其他脑区那样改变NAcc中的抑制性突触传递。使用全细胞膜片钳技术,我们证明KA受体激活增强了诱发的GABA能突触传递,并增加了NAcc中自发的(而非微小的)GABA(A)受体介导的抑制性突触后电流(IPSC)的频率。相反,KA对外源性应用GABA诱发的MSN电流没有影响。综上所述,这些数据表明,NAcc核心区KA受体的激活可能通过对突触前GABA能中间神经元的兴奋,有力地促进了动作电位依赖性GABA能突触传递。

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