Reviving through human hippocampal newborn neurons

Mendez‐David, Indira; Schofield, Ryan M.; Tritschler, Laurent; Colle, Romain; Guilloux, Jean‐Philippe; Gardier, Alain M.; Hen, René; David, Denis J.

doi:10.1016/j.encep.2021.09.001

Cited by 1 publication

(1 citation statement)

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“…Most reports indicate that adult‐born granule cells are generated until old age (Boldrini et al, 2018; Boldrini et al, 2019b; Flor‐Garcia et al, 2020; Tartt et al, 2018; Zhou et al, 2022), but a few reports suggest that the production of young neurons becomes negligible in humans after adolescence (Franjic et al, 2022; Sorrells et al, 2018). This controversy may be partially due to experimental conditions (such as post‐mortem intervals as well as tissue conservation and fixation; Flor‐Garcia et al, 2020) but also to the fact that there are few markers of young neurons that have been studied in the human brain (Mendez‐David et al, 2022); most studies have used doublecortin (DCX) and as we show in the current study the number of DCX‐expressing cells is not always a good estimate of the number of adult‐born neurons.…”

Section: Introductionmentioning

confidence: 99%

A complex relation between levels of adult hippocampal neurogenesis and expression of the immature neuron marker doublecortin

et al. 2023

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We investigated the mechanisms underlying the effects of the antidepressant fluoxetine on behavior and adult hippocampal neurogenesis (AHN). After confirming our earlier report that the signaling molecule β‐arrestin‐2 (β‐Arr2) is required for the antidepressant‐like effects of fluoxetine, we found that the effects of fluoxetine on proliferation of neural progenitors and survival of adult‐born granule cells are absent in the β‐Arr2 knockout (KO) mice. To our surprise, fluoxetine induced a dramatic upregulation of the number of doublecortin (DCX)‐expressing cells in the β‐Arr2 KO mice, indicating that this marker can be increased even though AHN is not. We discovered two other conditions where a complex relationship occurs between the number of DCX‐expressing cells compared to levels of AHN: a chronic antidepressant model where DCX is upregulated and an inflammation model where DCX is downregulated. We concluded that assessing the number of DCX‐expressing cells alone to quantify levels of AHN can be complex and that caution should be applied when label retention techniques are unavailable.

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