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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Optogenetic stimulation of GABA neurons can decrease local neuronal activity while increasing cortical blood flow
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Optogenetic stimulation of GABA neurons can decrease local neuronal activity while increasing cortical blood flow

机译：GABA神经元的光遗传刺激可以减少局部神经元活动，同时增加皮层血流量

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摘要

We investigated the link between direct activation of inhibitory neurons, local neuronal activity, and hemodynamics. Direct optogenetic cortical stimulation in the sensorimotor cortex of transgenic mice expressing Channelrhodopsin-2 in GABAergic neurons (VGAT-ChR2) greatly attenuated spontaneous cortical spikes, but was sufficient to increase blood flow as measured with laser speckle contrast imaging. To determine whether the observed optogenetically evoked gamma aminobutyric acid (GABA)neuron hemodynamic responses were dependent on ionotropic glutamatergic or GABAergic synaptic mechanisms, we paired optogenetic stimulation with application of antagonists to the cortex. Incubation of glutamatergic antagonists directly on the cortex (NBQX and MK-801) blocked cortical sensory evoked responses (as measured with electroencephalography and intrinsic optical signal imaging), but did not significantly attenuate optogenetically evoked hemodynamic responses. Significant light-evoked hemodynamic responses were still present after the addition of picrotoxin (GABA-A receptor antagonist) in the presence of the glutamatergic synaptic blockade. This activation of cortical inhibitory interneurons can mediate large changes in blood flow in a manner that is by and large not dependent on ionotropic glutamatergic or GABAergic synaptic transmission. This supports the hypothesis that activation of inhibitory neurons can increase local cerebral blood flow in a manner that is not entirely dependent on levels of net ongoing neuronal activity.
机译：我们调查了抑制神经元的直接激活，局部神经元活动和血液动力学之间的联系。在GABA能神经元（VGAT-ChR2）中表达Channelrhodopsin-2的转基因小鼠的感觉运动皮层中的直接光遗传学皮层刺激极大地减弱了自发皮层棘突，但是通过激光散斑对比成像测量，足以增加血流量。为了确定观察到的光遗传诱发的γ-氨基丁酸（GABA）神经元的血流动力学响应是否依赖于离子型谷氨酸能或GABA能突触机制，我们将光遗传刺激与对皮质的拮抗剂结合使用。将谷氨酸能拮抗剂直接在皮质上孵育（NBQX和MK-801）可阻断皮质感觉诱发反应（如通过脑电图和内在光学信号成像测量），但不会显着减弱光遗传诱发的血液动力学反应。在存在谷氨酸能突触阻滞剂的情况下，添加微毒素（GABA-A受体拮抗剂）后，仍然存在明显的光诱发的血液动力学反应。皮质抑制性中间神经元的这种激活可以以基本上不依赖于离子型谷氨酸能或GABA能突触传递的方式介导血流的大变化。这支持了以下假设：抑制性神经元的激活可以以不完全取决于净进行中神经元活动水平的方式增加局部脑血流量。

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