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Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey
Viral vectors are promising tools for the dissection of neural circuits. In principle, they can manipulate neurons at a level of specificity not otherwise achievable. While many studies have used viral vector-based approaches in the rodent brain, only a few have employed this technique in the non-hu...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2012
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378014/ https://www.ncbi.nlm.nih.gov/pubmed/22723770 http://dx.doi.org/10.3389/fnsys.2012.00048 |
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author | Nielsen, Kristina J. Callaway, Edward M. Krauzlis, Richard J. |
author_facet | Nielsen, Kristina J. Callaway, Edward M. Krauzlis, Richard J. |
author_sort | Nielsen, Kristina J. |
collection | PubMed |
description | Viral vectors are promising tools for the dissection of neural circuits. In principle, they can manipulate neurons at a level of specificity not otherwise achievable. While many studies have used viral vector-based approaches in the rodent brain, only a few have employed this technique in the non-human primate, despite the importance of this animal model for neuroscience research. Here, we report evidence that a viral vector-based approach can be used to manipulate a monkey's behavior in a task. For this purpose, we used the allatostatin receptor/allatostatin (AlstR/AL) system, which has previously been shown to allow inactivation of neurons in vivo. The AlstR was expressed in neurons in monkey V1 by injection of an adeno-associated virus 1 (AAV1) vector. Two monkeys were trained in a detection task, in which they had to make a saccade to a faint peripheral target. Injection of AL caused a retinotopic deficit in the detection task in one monkey. Specifically, the monkey showed marked impairment for detection targets placed at the visual field location represented at the virus injection site, but not for targets shown elsewhere. We confirmed that these deficits indeed were due to the interaction of AlstR and AL by injecting saline, or AL at a V1 location without AlstR expression. Post-mortem histology confirmed AlstR expression in this monkey. We failed to replicate the behavioral results in a second monkey, as AL injection did not impair the second monkey's performance in the detection task. However, post-mortem histology revealed a very low level of AlstR expression in this monkey. Our results demonstrate that viral vector-based approaches can produce effects strong enough to influence a monkey's performance in a behavioral task, supporting the further development of this approach for studying how neuronal circuits control complex behaviors in non-human primates. |
format | Online Article Text |
id | pubmed-3378014 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-33780142012-06-21 Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey Nielsen, Kristina J. Callaway, Edward M. Krauzlis, Richard J. Front Syst Neurosci Neuroscience Viral vectors are promising tools for the dissection of neural circuits. In principle, they can manipulate neurons at a level of specificity not otherwise achievable. While many studies have used viral vector-based approaches in the rodent brain, only a few have employed this technique in the non-human primate, despite the importance of this animal model for neuroscience research. Here, we report evidence that a viral vector-based approach can be used to manipulate a monkey's behavior in a task. For this purpose, we used the allatostatin receptor/allatostatin (AlstR/AL) system, which has previously been shown to allow inactivation of neurons in vivo. The AlstR was expressed in neurons in monkey V1 by injection of an adeno-associated virus 1 (AAV1) vector. Two monkeys were trained in a detection task, in which they had to make a saccade to a faint peripheral target. Injection of AL caused a retinotopic deficit in the detection task in one monkey. Specifically, the monkey showed marked impairment for detection targets placed at the visual field location represented at the virus injection site, but not for targets shown elsewhere. We confirmed that these deficits indeed were due to the interaction of AlstR and AL by injecting saline, or AL at a V1 location without AlstR expression. Post-mortem histology confirmed AlstR expression in this monkey. We failed to replicate the behavioral results in a second monkey, as AL injection did not impair the second monkey's performance in the detection task. However, post-mortem histology revealed a very low level of AlstR expression in this monkey. Our results demonstrate that viral vector-based approaches can produce effects strong enough to influence a monkey's performance in a behavioral task, supporting the further development of this approach for studying how neuronal circuits control complex behaviors in non-human primates. Frontiers Media S.A. 2012-06-19 /pmc/articles/PMC3378014/ /pubmed/22723770 http://dx.doi.org/10.3389/fnsys.2012.00048 Text en Copyright © 2012 Nielsen, Callaway and Krauzlis. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited. |
spellingShingle | Neuroscience Nielsen, Kristina J. Callaway, Edward M. Krauzlis, Richard J. Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title | Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title_full | Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title_fullStr | Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title_full_unstemmed | Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title_short | Viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
title_sort | viral vector-based reversible neuronal inactivation and behavioral manipulation in the macaque monkey |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3378014/ https://www.ncbi.nlm.nih.gov/pubmed/22723770 http://dx.doi.org/10.3389/fnsys.2012.00048 |
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