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. 2020 Aug 18;21(16):5937. doi: 10.3390/ijms21165937

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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The limitations of current H129-derived tracers. (A–C). Limitations of labeling intensity. (A) Some tracers label the neurons with relatively low intensity. (B) Current monosynaptic tracers do not replicate after monosynaptically transmitting to postsynaptic neurons. Labeling intensity in second-order neurons is very low, making the neurites invisible even after immunostaining. (C) The labeling intensity of the entire neuron is not evenly distributed. The soma is labeled much more brightly than the neurites, resulting in axon and axonal terminals that are difficult to observe or even invisible. (D–G). Limitations of the tracer transmission. (D) H129-derived tracers mainly invade the neuron from the soma and transmit further (solid arrow). However, they can also be potentially picked up by the axonal terminal of the upstream neurons (dashed arrows), and label them with the fluorescent protein. (E) Besides the predominant anterograde transmission (solid arrows), H129-derived tracers were reported to potentially transmit retrogradely and label upstream neurons (dashed arrows). (F) H129 may potentially transmit to adjacent neurons from varicosity (indicated as the enlarged region of the axon) (dashed arrows). (G) H129 may potentially infect astrocytes. In astrocytes, H129-dTK may replicate in the absence of helper virus, and the progeny virions may transmit to adjacent neurons (dashed arrows). (H,I). Limitations of cytotoxicity. (H) The polysynaptic tracers (indicated by the enveloped virion with green genome) are replication-competent. Their anterograde transmission requires tracer replication and progeny production. The viral replication causes severe damage or even neuron death (indicated by the cracks). (I) Monosynaptic tracers (indicated by the enveloped virion with red genome) are replication-deficient in the absence of a helper virus. Due to replication deficiency, only a few viral proteins are synthesized, leading to less damage to the cells. Therefore, they show attenuated toxicity to the postsynaptic neurons after monosynaptic transmission (the red neuron). However, under the assistance of the helper virus (indicated by the unenveloped virion with green genome), H129-derived monosynaptic tracers replicate in the starter neurons (the yellow neuron) and cause severe damage to the starter neurons (indicated by the cracks).