Differential contribution of kainate receptors to excitatory postsynaptic currents in superficial layer neurons of the rat medial entorhinal cortex.
Differential contribution of kainate receptors to excitatory postsynaptic currents in superficial layer neurons of the rat medial entorhinal cortex.
复制标题
红藻氨酸受体对大鼠内侧内嗅皮层浅层神经元兴奋性突触后电流的差异贡献。
DOI：
10.1016/j.neuroscience.2007.02.035
复制
发表时间：
2007
期刊：
影响因子：
3.3
通讯作者：
Wilcox,KS
中科院分区：
文献类型：
--
作者：
West,PJ;Dalpé-Charron,A;Wilcox,KS
虽然原位杂交研究已经揭示了红藻氨酸受体（KAR）mRNA在大鼠内侧内嗅皮层（MEC）的神经元中的存在，这些受体的功能存在和作用才刚刚开始被检查。为了解决这一缺陷，局部诱发兴奋性突触后电流（EPSC）的全细胞电压钳记录从mEC层II和III神经元组合内嗅皮层海马脑切片。通过它们的电响应膜特性、位置和形态鉴定了三种类型的神经元：第II层中的星状“下垂”神经元（S）、第III层中的网状“无下垂”神经元（NS）和具有不同形态和位置的“中间下垂”神经元（IS）。这些神经元的非NMDA EPSC由两个成分组成，NS神经元的慢衰减成分比S和IS神经元的慢衰减成分具有更大的幅度，对组合EPSC的贡献更大。这种缓慢的成分是由KAR介导的，其特征是对1-（4-氨基苯基）-4-甲基-7，8-亚甲二氧基-5H-2，3-苯并二氮卓盐酸盐（GYKI 52466，100 μM）或1，2，3，4-四氢-6-硝基-2，3-二氧代-苯并[lsqb]f[rsqb]喹喔啉-7-磺酰胺（NBQX，1 μM），衰减动力学相对较慢，对6-氰基-7-硝基喹喔啉-2，3-二酮（CNQX，10-50 μM）敏感。KAR介导的EPSC在神经元样NS神经元的贡献显着高于合并的非NMDA EPSC从S和IS神经元。mEC的第III层神经元在人颞叶癫痫（TLE）和TLE的动物模型如红藻氨酸诱导的癫痫持续状态中选择性地易变性。表征损伤易感与损伤抵抗mEC神经元中表达的突触后受体的补体差异代表了理解TLE中所见的第III层神经元的脆弱性的重要一步。
Although in situ hybridization studies have revealed the presence of kainate receptor (KAR) mRNA in neurons of the rat medial entorhinal cortex (mEC), the functional presence and roles of these receptors are only beginning to be examined. To address this deficiency, whole cell voltage clamp recordings of locally evoked excitatory postsynaptic currents (EPSCs) were made from mEC layer II and III neurons in combined entorhinal cortex–hippocampal brain slices. Three types of neurons were identified by their electroresponsive membrane properties, locations, and morphologies: stellate-like “Sag” neurons in layer II (S), pyramidal-like “No Sag” neurons in layer III (NS), and “Intermediate Sag” neurons with varied morphologies and locations (IS). Non-NMDA EPSCs in these neurons were composed of two components, and the slow decay component in NS neurons had larger amplitudes and contributed more to the combined EPSC than did those observed in S and IS neurons. This slow component was mediated by KARs and was characterized by its resistance to either 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine hydrochloride (GYKI 52466, 100 μM) or 1,2,3,4-tetrahydro-6-nitro-2,3-dioxo-benzo[lsqb]f[rsqb]quinoxaline-7-sulfonamide (NBQX, 1 μM), relatively slow decay kinetics, and sensitivity to 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10–50 μM). KAR-mediated EPSCs in pyramidal-like NS neurons contributed significantly more to the combined non-NMDA EPSC than did those from S and IS neurons. Layer III neurons of the mEC are selectively susceptible to degeneration in human temporal lobe epilepsy (TLE) and animal models of TLE such as kainate-induced status epilepticus. Characterizing differences in the complement of postsynaptic receptors expressed in injury prone versus injury resistant mEC neurons represents an important step toward understanding the vulnerability of layer III neurons seen in TLE.