Journal
NEURON
Volume 98, Issue 5, Pages 905-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2018.05.028
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Funding
- National Science Foundation (NSF) Early Concept Grants for Exploratory Research (EAGER) [1547967]
- National Institute of Health [U01 NS094288]
- NARSAD Young Investigator Award [26726]
- Direct For Biological Sciences
- Division Of Integrative Organismal Systems [1547967] Funding Source: National Science Foundation
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Retrogradely transported neurotropic viruses enable genetic access to neurons based on their long-range projections and have become indispensable tools for linking neural connectivity with function. A major limitation of viral techniques is that they rely on cell-type-specific molecules for uptake and transport. Consequently, viruses fail to infect variable subsets of neurons depending on the complement of surface receptors expressed (viral tropism). We report a receptor complementation strategy to overcome this by potentiating neurons for the infection of the virus of interest-in this case, canine adenovirus type-2 (CAV-2). We designed AAV vectors for expressing the coxsackievirus and adenovirus receptor (CAR) throughout candidate projection neurons. CAR expression greatly increased retrograde-labeling rates, which we demonstrate for several long-range projections, including some resistant to other retrograde-labeling techniques. Our results demonstrate a receptor complementation strategy to abrogate endogenous viral tropism and thereby facilitate efficient retrograde targeting for functional analysis of neural circuits.
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