Optogenetic astrocyte activation modulates response selectivity of visual cortex neurons in vivo

Perea, Gertrudis; Yang, Aimei; Boyden, Edward S.; Sur, Mriganka

doi:10.1038/ncomms4262

Cited by 215 publications

(247 citation statements)

References 49 publications

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“…This conclusion is warranted because the global cues governing development of Ϫastrocyte neurons and ϩastrocyte neurons are identical in our preparation, as the two classes are interspersed on the same coverslip. Furthermore, we found no significant effects on overall quantal content, frequency, or quantal size of EPSCs, all of which may be affected by astrocyte activity (Kucukdereli et al, 2011;Perea et al, 2014). Nevertheless, a fair question is, how local are these local astrocytic cues?…”

Section: Discussionmentioning

confidence: 63%

Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro

Sobieski¹,

Jiang²,

Crawford³

et al. 2015

Journal of Neuroscience

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Neuron-astrocyte interactions are critical for proper CNS development and function. Astrocytes secrete factors that are pivotal for synaptic development and function, neuronal metabolism, and neuronal survival. Our understanding of this relationship, however, remains incomplete due to technical hurdles that have prevented the removal of astrocytes from neuronal circuits without changing other important conditions. Here we overcame this obstacle by growing solitary rat hippocampal neurons on microcultures that were comprised of either an astrocyte bed (ϩastrocyte) or a collagen bed (Ϫastrocyte) within the same culture dish. ϪAstrocyte autaptic evoked EPSCs, but not IPSCs, displayed an altered temporal profile, which included increased synaptic delay, increased time to peak, and severe glutamate release asynchrony, distinct from previously described quantal asynchrony. Although we observed minimal alteration of the somatically recorded action potential waveform, action potential propagation was altered. We observed a longer latency between somatic initiation and arrival at distal locations, which likely explains asynchronous EPSC peaks, and we observed broadening of the axonal spike, which likely underlies changes to evoked EPSC onset. No apparent changes in axon structure were observed, suggesting altered axonal excitability. In conclusion, we propose that local astrocyte support has an unappreciated role in maintaining glutamate release synchrony by disturbing axonal signal propagation.

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Section: Discussionmentioning

confidence: 63%

Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro

Sobieski¹,

Jiang²,

Crawford³

et al. 2015

Journal of Neuroscience

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“…The functional significance of this is unclear, but to the extent that glial sheaths control transmitter availability [e.g., (3,118)], such a process would be absent in glomeruli. A final point is that synapses from interneuronal axons are also often found in glomeruli, but these make conventional, simple synapses, unlike their dendritic counterparts.…”

Section: Thalamic Circuit Propertiesmentioning

confidence: 99%

Functioning of Circuits Connecting Thalamus and Cortex

Sherman¹

2017

Comprehensive Physiology

131

108

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Glutamatergic pathways in thalamus and cortex are divided into two distinct classes: driver, which carries the main information between cells, and modulator, which modifies how driver inputs function. Identifying driver inputs helps to reveal functional computational circuits, and one set of such circuits identified by this approach are cortico-thalamo-cortical (or transthalamic corticocortical) circuits. This, in turn, leads to the conclusion that there are two types of thalamic relay: first order nuclei (such as the lateral geniculate nucleus) that relay driver input from a subcortical source (i.e., retina), and higher order nuclei (such as the pulvinar) which are involved in these transthalamic pathways by relaying driver input from layer 5 of one cortical area to another. This thalamic division is also seen in other sensory pathways and beyond these so that most of thalamus by volume consists of higher-order relays. Many, and perhaps all, direct driver connections between cortical areas are paralleled by an indirect cortico-thalamo-cortical (transthalamic) driver route involving higher order thalamic relays. Such thalamic relays represent a heretofore unappreciated role in cortical functioning, and this assessment challenges and extends conventional views regarding both the role of thalamus and mechanisms of corticocortical communication. Finally, many and perhaps the vast majority of driver inputs relayed through thalamus arrive via branching axons, with extrathalamic targets often being subcortical motor centers. This raises the possibility that inputs relayed by thalamus to cortex also serve as efference copies, and this may represent an important feature of information relayed up the cortical hierarchy via transthalamic circuits. © 2017 American Physiological Society. Compr Physiol 7:713-739, 2017.

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“…Glial cells in culture or in visual cortex slices, expressing channelrhodopsin-2, release calcium from intracellular stores upon illumination (Figueiredo et al 2014;Perea et al 2014), as evidenced by the blockade of opsin-mediated calcium signals when such stores are depleted with the drug thapsigargin. Deliberately targeting proton pumps to mitochondria of yeast or mammalian cells has been reported to result in cell survival with less reliance on oxidative phosphorylation (Hoffmann et al 1994;Hara et al 2013).…”

Section: Channel and Pump Activitymentioning

confidence: 99%

Principles of designing interpretable optogenetic behavior experiments

2015

Self Cite

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Over the last decade, there has been much excitement about the use of optogenetic tools to test whether specific cells, regions, and projection pathways are necessary or sufficient for initiating, sustaining, or altering behavior. However, the use of such tools can result in side effects that can complicate experimental design or interpretation. The presence of optogenetic proteins in cells, the effects of heat and light, and the activity of specific ions conducted by optogenetic proteins can result in cellular side effects. At the network level, activation or silencing of defined neural populations can alter the physiology of local or distant circuits, sometimes in undesired ways. We discuss how, in order to design interpretable behavioral experiments using optogenetics, one can understand, and control for, these potential confounds.

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Optogenetic astrocyte activation modulates response selectivity of visual cortex neurons in vivo

Cited by 215 publications

References 49 publications

Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro

Loss of Local Astrocyte Support Disrupts Action Potential Propagation and Glutamate Release Synchrony from Unmyelinated Hippocampal Axon Terminals In Vitro

Functioning of Circuits Connecting Thalamus and Cortex

Principles of designing interpretable optogenetic behavior experiments

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