Convergence of nicotine-induced and auditory-evoked neural activity activates ERK in auditory cortex.
Convergence of nicotine-induced and auditory-evoked neural activity activates ERK in auditory cortex.
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DOI：
10.1002/syn.21647
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发表时间：
2013-08
期刊：
影响因子：
2.3
通讯作者：
Metherate, Raju
中科院分区：
文献类型：
--
作者：
Kawai, Hideki D.;La, Maggie;Kang, Ho-An;Hashimoto, Yusuke;Liang, Kevin;Lazar, Ronit;Metherate, Raju
已知给予全身性尼古丁后听觉皮层（ACx）声音诱发反应的增强依赖于细胞外信号调节激酶（ERK）的激活，但这种增强的性质尚不清楚。在这里，我们发现全身尼古丁增加了小鼠原代ACx（A1）中磷酸化（活化）ERK（P-ERK）免疫标记细胞的密度。皮质注射二氢-β-赤藓啶减少尼古丁诱导的P-ERK免疫标记，表明位于A1并含有α4和β2亚基的烟碱乙酰胆碱受体（nAChRs）的作用。P-ERK阳性细胞主要分布于第2/3层，较低层的细胞数量较少，且多数细胞在胞体和近端树突内表达P-ERK。约三分之一的P-ERK阳性细胞也表达钙结合蛋白。在丘脑，P-ERK免疫阳性细胞被发现在非丘系内侧膝状体（MG）和邻近的核团，但在丘系MG缺席。将广谱声刺激（白色噪声）与全身尼古丁配对增加了ACx中P-ERK免疫阳性细胞密度以及P-ERK蛋白总量，特别是ERK 2的磷酸化形式。然而，与尼古丁配对的窄谱（音调）刺激优先在A1内配对频率为特征频率（CF）的部位增加P-ERK免疫标记，相对于具有光谱远距CF（高于或低于配对频率两个倍频程）的第二个部位。总之，这些结果表明，ERK被激活的最佳烟碱信号和声音诱发的神经活动收敛。
Enhancement of sound-evoked responses in auditory cortex (ACx) following administration of systemic nicotine is known to depend on activation of extracellular-signaling regulated kinase (ERK), but the nature of this enhancement is not clear. Here, we show that systemic nicotine increases the density of cells immunolabeled for phosphorylated (activated) ERK (P-ERK) in mouse primary ACx (A1). Cortical injection of dihydro-β-erythroidine reduced nicotine-induced P-ERK immunolabel, suggesting a role for nicotinic acetylcholine receptors (nAChRs) located in A1 and containing α4 and β2 subunits. P-ERK expressing cells were distributed mainly in layers 2/3 and more sparsely in lower layers, with many cells exhibiting immunolabel within pyramidal-shaped somata and proximal apical dendrites. About one third of P-ERK positive cells also expressed calbindin. In the thalamus, P-ERK immunopositive cells were found in the nonlemniscal medial geniculate (MG) and adjacent nuclei, but were absent in the lemniscal MG. Pairing broad spectrum acoustic stimulation (white noise) with systemic nicotine increased P-ERK immunopositive cell density in ACx as well as the total amount of P-ERK protein, particularly the phosphorylated form of ERK2. However, narrow spectrum (tone) stimulation paired with nicotine increased P-ERK immunolabel preferentially at a site within A1 where the paired frequency was characteristic frequency (CF), relative to a second site with a spectrally-distant CF (two octaves above or below the paired frequency). Together, these results suggest that ERK is activated optimally where nicotinic signaling and sound-evoked neural activity converge.
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DOI：
10.1023/a:1024126110356
发表时间：
2002-03-01
期刊：
JOURNAL OF NEUROCYTOLOGY
影响因子：
--
作者：
Kawaguchi, Y;Kondo, S
通讯作者：
Kondo, S
影响因子：
16.2
作者：
Chang, KT;Berg, DK
通讯作者：
Berg, DK
影响因子：
25
作者：
Kawai, Hideki;Lazar, Ronit;Metherate, Raju
通讯作者：
Metherate, Raju
影响因子：
2.5
作者：
Kaur, S;Lazar, R;Metherate, R
通讯作者：
Metherate, R
影响因子：
2.5
作者：
FROST, DO;CAVINESS, VS
通讯作者：
CAVINESS, VS