Disney Anita A, Alasady Hussein A, Reynolds John H
Systems Neurobiology Laboratories, The Salk Institute for Biological Studies La Jolla, California.
Brain Behav. 2014 May;4(3):431-45. doi: 10.1002/brb3.225. Epub 2014 Mar 21.
In the mammalian neocortex, cells that express parvalbumin (PV neurons) comprise a dominant class of inhibitory neuron that substantially overlaps with the fast/narrow-spiking physiological phenotype. Attention has pronounced effects on narrow-spiking neurons in the extrastriate cortex of macaques, and more consistently so than on their broad-spiking neighbors. Cortical neuromodulation by acetylcholine (ACh) is a candidate mechanism for aspects of attention and in the primary visual cortex (V1) of the macaque, receptors for ACh (AChRs) are strongly expressed by inhibitory neurons. In particular, most PV neurons in macaque V1 express m1 muscarinic AChRs and exogenously applied ACh can cause the release of γ-aminobutyric acid. In contrast, few PV neurons in rat V1 express m1 AChRs. While this could be a species difference, it has also been argued that macaque V1 is anatomically unique when compared with other cortical areas in macaques.
The aim of this study was to better understand the extent to which V1 offers a suitable model circuit for cholinergic anatomy in the macaque occipital lobe, and to explore cholinergic modulation as a biological basis for the changes in circuit behavior seen with attention.
We compared expression of m1 AChRs by PV neurons between area V1 and the middle temporal visual area (MT) in macaque monkeys using dual-immunofluorescence confocal microscopy.
We find that, as in V1, most PV neurons in MT express m1 AChRs but, unlike in V1, it appears that so do most excitatory neurons. This provides support for V1 as a model of cholinergic modulation of inhibition in macaque visual cortex, but not of cholinergic modulation of visual cortical circuits in general. We also propose that ACh acting via m1 AChRs is a candidate underlying mechanism for the strong effects of attention on narrow-spiking neurons observed in behaving animals.
在哺乳动物新皮层中，表达小白蛋白的细胞（小白蛋白神经元）构成了一类主要的抑制性神经元，与快速/窄峰生理表型基本重叠。注意力对猕猴纹外皮层中的窄峰神经元有显著影响，比对其宽峰相邻神经元的影响更为一致。乙酰胆碱（ACh）介导的皮质神经调节是注意力相关方面的一种潜在机制，在猕猴的初级视觉皮层（V1）中，抑制性神经元强烈表达ACh受体（AChRs）。特别是，猕猴V1中的大多数小白蛋白神经元表达M1型毒蕈碱AChRs，外源性应用ACh可导致γ-氨基丁酸的释放。相比之下，大鼠V1中很少有小白蛋白神经元表达M1型AChRs。虽然这可能是种属差异，但也有人认为，与猕猴的其他皮质区域相比，猕猴V1在解剖学上具有独特性。
本研究的目的是更好地了解V1在多大程度上为猕猴枕叶胆碱能解剖学提供了合适的模型回路，并探索胆碱能调节作为注意力引起的回路行为变化的生物学基础。
我们使用双免疫荧光共聚焦显微镜比较了猕猴V1区和颞中视觉区（MT）中，小白蛋白神经元对M1型AChRs的表达情况。
我们发现，与V1区一样，MT区的大多数小白蛋白神经元表达M1型AChRs，但与V1区不同的是，大多数兴奋性神经元似乎也表达。这为V1作为猕猴视觉皮层中胆碱能抑制调节模型提供了支持，但不能作为整个视觉皮层回路胆碱能调节的模型。我们还提出，通过M1型AChRs起作用的ACh是行为动物中观察到的注意力对窄峰神经元产生强烈影响的潜在机制。
