Cholinergic Modulation of Neuronal Excitability in the Accessory Olfactory Bulb
Cholinergic Modulation of Neuronal Excitability in the Accessory Olfactory Bulb
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DOI：
10.1152/jn.00446.2010
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发表时间：
2010-12-01
影响因子：
2.5
通讯作者：
Araneda, Ricardo C.
中科院分区：
文献类型：
--
作者：
Smith, Richard S.;Araneda, Ricardo C.
Smith RS, Araneda RC。副嗅球神经元兴奋性的胆碱能调节。[J] .中国生物医学工程学报，2009,31(4):557 - 557。首次发表于2010年9月22日；doi: 10.1152 / jn.00446.2010。副嗅球（AOB）是vomeron鼻系统中化学感觉信息的第一个中继，接受来自基底前脑的广泛胆碱能神经支配。嗅球神经元活动的胆碱能调节已被假设在嗅觉加工中起重要作用；然而，对乙酰胆碱（ACh）在AOB中的细胞作用知之甚少。通过体外切片制备，我们发现毒毒碱乙酰胆碱受体（mAChR）的激活增加了AOB中颗粒细胞和二尖瓣细胞/簇状细胞（GCs和MCs）的神经元兴奋性。machr的激活通过三种不同的机制增加了GCs的兴奋性：诱导持久的去极化，激活缓慢的后去极化（sADP），以及由于MC去极化而增加兴奋性谷氨酸能输入。选择性激动剂4-[[[（3-氯苯基）氨基]羰基]氧]-N， N， N-三甲基-2-丁基-1-氯化铵（100 μ M）诱导去极化和sADP，并被低浓度的吡伦齐平（300 nM）阻断，表明它们是由m1样的machr激活引起的。相比之下，胆碱能刺激通过尼古丁achr （nachr）和m1样machr的募集增加了MCs的兴奋性。然而，这些受体的亚极大激活降低了MCs的兴奋性。令人惊讶的是，我们发现与主嗅球中的GCs不同，AOB中的GCs被出生后年轻神经元的mAChR激活激活，这表明这两个嗅球区域的胆碱能调节发育存在显著差异。
Smith RS, Araneda RC. Cholinergic modulation of neuronal excitability in the accessory olfactory bulb. J Neurophysiol 104: 2963-2974, 2010.. First published September 22, 2010; doi: 10.1152/jn.00446.2010. The accessory olfactory bulb (AOB), the first relay of chemosensory information in the Vomeronasal system, receives extensive cholinergic innervation from the basal forebrain. Cholinergic modulation of neuronal activity in the olfactory bulb has been hypothesized to play an important role in olfactory processing; however, little is known about the cellular actions of acetylcholine (ACh) within the AOB. Here using in vitro slice preparation, we show that muscarinic acetylcholine receptor (mAChR) activation increases neuronal excitability of granule and mitral/tufted cells (GCs and MCs) in the AOB. Activation of mAChRs increased excitability of GCs by three distinct mechanisms: induction of a long-lasting depolarization, activation of a slow afterdepolarization (sADP), and an increase in excitatory glutamatergic input due to MC depolarization. The depolarization and sADP were elicited by the selective agonist 4-[[[(3-chlorophenyl) amino] carbonyl] oxy]-N, N, N-trimethyl-2-butyn-1-aminium chloride (100 mu M) and blocked by low concentrations of pirenzepine (300 nM), indicating that they result from activation of M1-like mAChRs. In contrast, cholinergic stimulation increased the excitability of MCs via recruitment of nicotinic AChRs (nAChRs) and M1-like mAChRs. Submaximal activation of these receptors, however, decreased the excitability of MCs. Surprisingly, we found that unlike GCs in the main olfactory bulb, GCs in the AOB are excited by mAChR activation in young postnatal neurons, suggesting marked differences in cholinergic regulation of development between these two regions of the olfactory bulb.