Optogenetic experimentation on astrocytes

Figueiredo, MF; Lane, SL; Tang, Feige; Liu, BH; Hewinson, James; Marina, Nephtalı́; Kasymov, Vitaliy; Souslova, EA; Chudakov, Dmitriy M.; Gourine, AV; Teschemacher, AG; Kasparov, Sergey

doi:10.1113/expphysiol.2010.052597

Cited by 74 publications

(55 citation statements)

References 66 publications

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“…All these effects could change the activities of astrocytes and regulate the release of gliotransmitters. Indeed, it has been reported that the activation of ChR2 triggers ATP release from ChR2-expressing astrocytes resulting from the elevation of [Ca 2+ ] i (Gourine et al, 2010;Figueiredo et al, 2011;Chen et al, 2013). Astrocytes can release glutamate through Ca 2+ -dependent and -independent mechanisms (Haydon and Carmignoto, 2006;Malarkey and Parpura, 2007).…”

Section: Depolarizing Actuators Control Astroglial Release Of Atp Andmentioning

confidence: 98%

Optogenetic control of astrocytes: Is it possible to treat astrocyte-related epilepsy?

Wang

2015

Brain Research Bulletin

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Section: Depolarizing Actuators Control Astroglial Release Of Atp Andmentioning

confidence: 98%

Optogenetic control of astrocytes: Is it possible to treat astrocyte-related epilepsy?

Wang

2015

Brain Research Bulletin

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“…Given the lack of success for novel therapies targeting neuronal entities, it is perhaps surprising that to date few astrocyte targets have been identified. Advances in technology have increased our understanding of astrocytes and their interactions (255), which is still limited by poor astrocyte-specific markers which lack the robust nature of neuronal markers (5). The publication of the astrocytic transcriptome (24) revealed potential new cellular biomarkers that provide tools for generating specific therapeutic approaches to target astrocytes for the purpose of reducing neurodegeneration in AD.…”

Section: Future Perspectivesmentioning

confidence: 99%

Astrocytic transporters in Alzheimer's disease

Ugbode

Whalley

et al. 2017

Biochemical Journal

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Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic support, neurotransmission and synaptic architecture. Therefore, specific targeting of individual transporter families has the potential to suppress neurodegeneration, a characteristic hallmark of AD. A small number of the 400 transporter superfamilies are expressed in astrocytes, with evidence highlighting a fraction of these are implicated in AD. Here, we review the current evidence for six astrocytic transporter subfamilies involved in AD, as reported in both animal and human studies. This review confirms that astrocytes are indeed a viable target, highlights the complexities of studying astrocytes and provides future directives to exploit the potential of astrocytes in tackling AD.

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“…ChR2 expression in primary cardiac fibroblasts was stable, persisting for at least 6 weeks, without detrimental effects to cell viability and proliferation (Yu et al, 2013). This is in contrast to severe negative effects and cell death reported in astrocytes when high viral titers > 10 11 transducing units/ml of AAV–sGFAP–ChR2 were used (Figueiredo et al, 2011). …”

Section: Cell-specific Optogenetic Targeting In the Heart And Its mentioning

confidence: 91%

Cardiac applications of optogenetics

Ambrosi

Klimas

Jia

et al. 2014

Progress in Biophysics and Molecular Biology

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In complex multicellular systems, such as the brain or the heart, the ability to selectively perturb and observe the response of individual components at the cellular level and with millisecond resolution in time, is essential for mechanistic understanding of function. Optogenetics uses genetic encoding of light sensitivity (by the expression of microbial opsins) to provide such capabilities for manipulation, recording, and control by light with cell specificity and high spatiotemporal resolution. As an optical approach, it is inherently scalable for remote and parallel interrogation of biological function at the tissue level; with implantable miniaturized devices, the technique is uniquely suitable for in vivo tracking of function, as illustrated by numerous applications in the brain. Its expansion into the cardiac area has been slow. Here, using examples from published research and original data, we focus on optogenetics applications to cardiac electrophysiology, specifically dealing with the ability to manipulate membrane voltage by light with implications for cardiac pacing, cardioversion, cell communication, and arrhythmia research, in general. We discuss gene and cell delivery methods of inscribing light sensitivity in cardiac tissue, functionality of the light-sensitive ion channels within different types of cardiac cells, utility in probing electrical coupling between different cell types, approaches and design solutions to all-optical electrophysiology by the combination of optogenetic sensors and actuators, and specific challenges in moving towards in vivo cardiac optogenetics.

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Optogenetic experimentation on astrocytes

Cited by 74 publications

References 66 publications

Optogenetic control of astrocytes: Is it possible to treat astrocyte-related epilepsy?

Optogenetic control of astrocytes: Is it possible to treat astrocyte-related epilepsy?

Astrocytic transporters in Alzheimer's disease

Cardiac applications of optogenetics

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