Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jun 17;13:261. doi: 10.1186/s13287-022-02933-w

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 4 — SKN neuronal engraftment and synaptic rescue in rodent model of age-related memory dysfunction. A Experimental paradigm. B Canine SKN cell transplantation rescues hippocampally-dependent Place Recognition Memory (PRM) back to young animal level (Time X Group F1,14 = 6.934, p = 0.02; left; see Additional file 1: Figure S24 for individual animal data) and has no effect on intact ORM (right). Untreated young and old animal data from our prior report [37]. C Exemplar trace of rodent exploration of familiar object in a novel position during PRM before and after treatment. D Canine-specific lamin marker of donor cells (see Additional file 1: Figures S15–17 for controls) shows extensive survival and engraftment of canine SKN cells in CA1 in main experiment (N = 16; see Additional file 1: Figure S18 for engraftment in other hippocampal areas). E Extension study (N = 2) with GFP-genetically labelled donor cells shows engraftment in CA1 with anatomically-correct cell bodies and penetrating dendrites; see Additional file 1: Figure S19 for co-expression with mature neuronal NeuN and neurofilament. F Stereological counts of donor cells throughout hippocampus marked by canine lamin, and Lamin + βIII tubulin co-expression indicative of in vivo neuronal differentiation (N = 16; see Additional file 1: Figure S19 for confocal fluorescent images). G Synaptophysin was restored to young animal levels throughout hippocampus compared to media vehicle (N = 16). H Donor cells genetically labelled with pZs-Green1 (green), allowing cell identification in a fresh hippocampal slice preparation, here filled with biocytin (red) to reveal pyramidal morphology including dendritic spines on primary dendrites (z-stack image, see Additional file 1: Figures S21–23 for orthogonal confocal images and high magnification of secondary dendrite with intense decoration by synaptic spines). I In a hippocampal slice preparation, SKN donor cells (k = 3) displayed elicited action potentials in CA1 under current clamp and J voltage clamp conditions. K Spontaneous action potentials in SKN donor cell in the dentate gyrus. L Excitatory post-synaptic currents in CA1 (same cell as in H) following stimulation of distal Schaffer collateral fibres, abolishable by AMPA-receptor blockade, indicating that canine SKN cells can integrate into physiological neuronal circuits. D, E and H are from independent animals