In Vivo Wireless Optogenetic Control of Skilled Motor Behavior

10.3791/63082 ◽  
2021 ◽  
Author(s):  
Diana L. Rodriguez-Munoz ◽  
Omar Jaidar ◽  
Marcela Palomero-Rivero ◽  
Mario A. Arias-Garcia ◽  
Gordon W. Arbuthnott ◽  
...  
Keyword(s):  
Motor Behavior ◽  
Optogenetic Control

Interaction of ibogaine and d-amphetamine: in vivo microdialysis and motor behavior in rats

1992 ◽  
Vol 579 (1) ◽  
pp. 87-92 ◽  
Author(s):  
I.M. Maisonneuve ◽  
R.W. Keller ◽  
S.D. Glick
Keyword(s):  
Motor Behavior ◽  
In Vivo Microdialysis

Exogenous L-lactate promotes astrocyte plasticity but is not sufficient for enhancing striatal synaptogenesis or motor behavior in mice

2020 ◽  
Author(s):  
Adam J. Lundquist ◽  
Tyler J. Gallagher ◽  
Giselle M. Petzinger ◽  
Michael W. Jakowec
Keyword(s):  
Motor Behavior ◽  
Early Gene ◽  
Specific Gene ◽  
Motor Circuits ◽  
Specific Manner ◽  
Primary Astrocytes ◽  
Exercise Induced ◽  
The Brain

AbstractL-lactate is an energetic and signaling molecule that is key to the metabolic and neuroplastic connection between astrocytes and neurons and may be involved in exercise-induced neuroplasticity. This study sought to explore the role of L-lactate in astrocyte reactivity and neuroplasticity. Using in vitro cultures of primary astrocytes, we show L-lactate increased expression of plasticity-related genes, including neurotrophic factors, Bdnf, Gdnf, Cntf and the immediate early gene cFos. L-lactate’s promotion of neurotrophic factor expression may be mediated in part by the lactate receptor HCAR1 since application of the HCAR1 agonist 3,5-DHBA also increased expression of Bdnf in primary astrocytes. In vivo L-lactate administration to healthy mice caused a similar increase in the expression of plasticity-related genes as well as increased astrocyte morphological complexity in a region-specific manner, with increased astrocytic response found in the striatum but not the ectorhinal cortex, regions of the brain where increases in regional cerebral blood flow are increased or unaltered, respectively, with motor behavior. Additionally, L-lactate administration did not cause synaptogenesis or improve motor behavior based on the latency to fall on the accelerating rotarod, suggesting that L-lactate administration can initiate astrocyte-specific gene expression, but the activation of motor circuits is necessary to initiate striatal neuroplasticity. These results suggest that peripheral L-lactate is likely an important molecular component of exercise-induced neuroplasticity by acting in an astrocyte-specific manner to prime the brain for neuroplasticity.

scholarly journals Smcr8 deficiency disrupts axonal transport-dependent lysosomal function and promotes axonal swellings and gain of toxicity in C9ALS/FTD mouse models

2019 ◽  
Vol 28 (23) ◽  
pp. 3940-3953 ◽  
Author(s):  
Chen Liang ◽  
Qiang Shao ◽  
Wei Zhang ◽  
Mei Yang ◽  
Qing Chang ◽  
...  
Keyword(s):  
Axonal Transport ◽  
Mouse Models ◽  
Motor Neurons ◽  
Neuromuscular Junctions ◽  
Motor Behavior ◽  
In Vivo Studies ◽  
Lysosomal Function ◽  
Repeat Expansions ◽  
Axonal Swellings

Abstract G4C2 repeat expansions in an intron of C9ORF72 cause the most common familial amyotrophic lateral sclerosis and frontotemporal dementia (collectively, C9ALS/FTD). Mechanisms and mediators of C9ALS/FTD pathogenesis remain poorly understood. C9orf72 and Smcr8 form a protein complex. Here, we show that expression of Smcr8, like C9orf72, is reduced in C9ALS/FTD mouse models and patient tissues. Since Smcr8 is highly conserved between human and mouse, we evaluated the effects of Smcr8 downregulation in mice. Smcr8 knockout (KO) mice exhibited motor behavior deficits, which resemble those of C9ALS/FTD mouse models, and displayed axonal swellings in their spinal cords and neuromuscular junctions. These deficits are caused by impaired autophagy-lysosomal functions due to disrupted axonal transport in mutant motor neurons. Consistent with its interaction with C9orf72 and their downregulation in patient tissues, Smcr8 deficiency exacerbated autophagy-lysosomal impairment in C9orf72 KO mice. The disease relevance of Smcr8 downregulation was reflected by exacerbated axonal swellings and gain of toxicity pathology arising from Smcr8 haploinsufficiency in a mouse model of C9ALS/FTD. Thus, our in vivo studies suggested that Smcr8 deficiency impairs axonal transport dependent autophagy-lysosomal function and exacerbates axonal degeneration and gain of toxicity in C9ALS/FTD mouse models.

scholarly journals Depth-specific optogenetic control in vivo with a scalable, high-density μLED neural probe

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Robert Scharf ◽  
Tomomi Tsunematsu ◽  
Niall McAlinden ◽  
Martin D. Dawson ◽  
Shuzo Sakata ◽  
...  
Keyword(s):  
High Density ◽  
Neural Probe ◽  
Optogenetic Control

scholarly journals Modal demultiplexing properties of tapered and nanostructured optical fibers for in vivo optogenetic control of neural activity

2015 ◽  
Vol 6 (10) ◽  
pp. 4014 ◽  
Author(s):  
Marco Pisanello ◽  
Andrea Della Patria ◽  
Leonardo Sileo ◽  
Bernardo L. Sabatini ◽  
Massimo De Vittorio ◽  
...  
Keyword(s):  
Optical Fibers ◽  
Neural Activity ◽  
Optogenetic Control

scholarly journals Insulin-like growth factor-2 does not improve behavioral deficits in mouse and rat models of Angelman Syndrome

2021 ◽  
Author(s):  
Elizabeth Berg ◽  
Stela Petkova ◽  
Heather A Born ◽  
Anna Adhikari ◽  
Anne E Anderson ◽  
...  
Keyword(s):  
Growth Factor ◽  
Angelman Syndrome ◽  
Motor Behavior ◽  
Neurodevelopmental Disorder ◽  
Model Systems ◽  
Seizure Threshold ◽  
Insulin Like Growth Factor ◽  
Behavioral Deficits ◽  
Rat Models

Background: Angelman Syndrome (AS) is a rare neurodevelopmental disorder for which there is currently no cure or effective therapeutic. Since the genetic cause of AS is known to be dysfunctional expression of the maternal allele of ubiquitin protein ligase E3A (UBE3A), several genetic animal models of AS have been developed. Both the Ube3a maternal deletion mouse and rat models of AS reliably demonstrate behavioral phenotypes of relevance to AS and therefore offer suitable in vivo systems in which to test potential therapeutics. One promising candidate treatment is insulin-like growth factor-2 (IGF-2), which has recently been shown to ameliorate behavioral deficits in the mouse model of AS and improve cognitive abilities across model systems. Methods: We used both the Ube3a maternal deletion mouse and rat models of AS to evaluate the ability of IGF-2 to improve electrophysiological and behavioral outcomes. Results: Acute systemic administration of IGF-2 had an effect on electrophysiological activity in the brain and on a metric of motor ability, however the effects were not enduring or extensive. Additional metrics of motor behavior, learning, ambulation, and coordination were unaffected and IGF-2 did not improve social communication, seizure threshold, or cognition. Limitations: The generalizability of these results to humans is difficult to predict and it remains possible that dosing schemes (i.e., chronic or subchronic dosing), routes, and/or post-treatment intervals other than that used herein may show more efficacy. Conclusions: Despite a few observed effects of IGF-2, our results taken together indicate that IGF-2 treatment does not profoundly improve behavioral deficits in mice or rat models of AS. These findings shed cautionary light on the potential utility of acute systemic IGF-2 administration in the treatment of AS.

scholarly journals Optogenetic control of Neisseria meningitidis Cas9 genome editing using an engineered, light-switchable anti-CRISPR protein

2020 ◽  
Author(s):  
Mareike D Hoffmann ◽  
Jan Mathony ◽  
Julius Upmeier zu Belzen ◽  
Zander Harteveld ◽  
Sabine Aschenbrenner ◽  
...  
Keyword(s):  
Neisseria Meningitidis ◽  
Genome Editing ◽  
Blue Light ◽  
Mammalian Cells ◽  
Type Ii ◽  
Binding Surface ◽  
Engineering Work ◽  
Endogenous Loci ◽  
Optogenetic Control

Abstract Optogenetic control of CRISPR–Cas9 systems has significantly improved our ability to perform genome perturbations in living cells with high precision in time and space. As new Cas orthologues with advantageous properties are rapidly being discovered and engineered, the need for straightforward strategies to control their activity via exogenous stimuli persists. The Cas9 from Neisseria meningitidis (Nme) is a particularly small and target-specific Cas9 orthologue, and thus of high interest for in vivo genome editing applications. Here, we report the first optogenetic tool to control NmeCas9 activity in mammalian cells via an engineered, light-dependent anti-CRISPR (Acr) protein. Building on our previous Acr engineering work, we created hybrids between the NmeCas9 inhibitor AcrIIC3 and the LOV2 blue light sensory domain from Avena sativa. Two AcrIIC3-LOV2 hybrids from our collection potently blocked NmeCas9 activity in the dark, while permitting robust genome editing at various endogenous loci upon blue light irradiation. Structural analysis revealed that, within these hybrids, the LOV2 domain is located in striking proximity to the Cas9 binding surface. Together, our work demonstrates optogenetic regulation of a type II-C CRISPR effector and might suggest a new route for the design of optogenetic Acrs.

scholarly journals Optogenetic Control of Airway Cholinergic Neurons In Vivo

2020 ◽  
Vol 62 (4) ◽  
pp. 423-429 ◽  
Author(s):  
Alexandra B. Pincus ◽  
Sweta Adhikary ◽  
Katherine M. Lebold ◽  
Allison D. Fryer ◽  
David B. Jacoby
Keyword(s):  
Cholinergic Neurons ◽  
Optogenetic Control

scholarly journals In Vivo Optogenetic Control of Striatal and Thalamic Neurons in Non-Human Primates

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e50808 ◽  
Author(s):  
Adriana Galvan ◽  
Xing Hu ◽  
Yoland Smith ◽  
Thomas Wichmann
Keyword(s):  
Thalamic Neurons ◽  
Optogenetic Control
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