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大鼠前额叶皮质失活可消除由感觉或感觉通路刺激诱发的皮质乙酰胆碱释放。

Inactivation of prefrontal cortex abolishes cortical acetylcholine release evoked by sensory or sensory pathway stimulation in the rat.

作者信息

Rasmusson D D, Smith S A, Semba K

机构信息

Department of Physiology and Biophysics, Dalhousie University, 5850 College Street, Halifax, NS, Canada B3H 1X5.

出版信息

Neuroscience. 2007 Oct 12;149(1):232-41. doi: 10.1016/j.neuroscience.2007.06.057. Epub 2007 Jul 28.

DOI:10.1016/j.neuroscience.2007.06.057
PMID:17850979
Abstract

Sensory stimulation and electrical stimulation of sensory pathways evoke an increase in acetylcholine release from the corresponding cortical areas. The pathways by which such sensory information reaches the cholinergic neurons of the basal forebrain that are responsible for this release are unclear, but have been hypothesized to pass through the prefrontal cortex (PFC). This hypothesis was tested in urethane-anesthetized rats using microdialysis to collect acetylcholine from somatosensory, visual, or auditory cortex, before and after the PFC was inactivated by local microdialysis delivery of the GABA-A receptor agonist muscimol (0.2% for 10 min at 2 microl/min). Before PFC inactivation, peripheral sensory stimulation and ventral posterolateral thalamic stimulation evoked 60 and 105% increases, respectively, in acetylcholine release from somatosensory cortex. Stimulation of the lateral geniculate nucleus evoked a 57% increase in acetylcholine release from visual cortex and stimulation of the medial geniculate nucleus evoked a 72% increase from auditory cortex. Muscimol delivery to the PFC completely abolished each of these evoked increases (overall mean change from baseline = -7%). In addition, the spontaneous level of acetylcholine release in somatosensory, visual, and auditory cortices was reduced by 15-59% following PFC inactivation, suggesting that PFC activity has a tonic facilitatory influence on the basal forebrain cholinergic neurons. These experiments demonstrate that the PFC is necessary for sensory pathway evoked cortical ACh release and strongly support the proposed sensory cortex-to-PFC-to-basal forebrain circuit for each of these modalities.

摘要

感觉刺激和感觉通路的电刺激会引起相应皮质区域乙酰胆碱释放增加。此类感觉信息到达负责这种释放的基底前脑胆碱能神经元的通路尚不清楚,但据推测是通过前额叶皮质(PFC)。在使用微透析从躯体感觉、视觉或听觉皮质收集乙酰胆碱的乌拉坦麻醉大鼠中,通过局部微透析给予GABA - A受体激动剂蝇蕈醇(0.2%,以2微升/分钟的速度持续10分钟)使PFC失活前后,对这一假设进行了测试。在PFC失活前,外周感觉刺激和腹后外侧丘脑刺激分别使躯体感觉皮质的乙酰胆碱释放增加60%和105%。外侧膝状体核的刺激使视觉皮质的乙酰胆碱释放增加57%,内侧膝状体核的刺激使听觉皮质的乙酰胆碱释放增加72%。向PFC给予蝇蕈醇完全消除了这些诱发的增加(相对于基线的总体平均变化 = -7%)。此外,PFC失活后,躯体感觉、视觉和听觉皮质中乙酰胆碱的自发释放水平降低了15 - 59%,这表明PFC活动对基底前脑胆碱能神经元具有紧张性促进作用。这些实验表明,PFC对于感觉通路诱发的皮质乙酰胆碱释放是必需的,并有力地支持了针对每种感觉模式所提出的从感觉皮质到PFC再到基底前脑的回路。

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