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Genetic loss of norepinephrine does not alter adult hippocampal neurogenesis in dopamine beta-hydroxylase deficient mice. | LitMetric

AI Article Synopsis

  • * The study examined dopamine β hydroxylase knockout mice, which lack NE from birth, and found that their adult hippocampal progenitor proliferation and survival were unaffected.
  • * In contrast, using the neurotoxin DSP-4 to target noradrenergic afferents in adult mice led to a decrease in hippocampal progenitor proliferation, suggesting that adult neurogenesis is sensitive to changes in NE levels.

Article Abstract

Norepinephrine (NE), and specific adrenoceptors, have been reported to influence distinct aspects of adult hippocampal neurogenesis, including latent stem cell activation, progenitor proliferation, and differentiation. These findings are predominantly based on the use of pharmacological approaches in both and systems. Here, we sought to assess the consequences of genetic ablation of NE on adult hippocampal neurogenesis, by examining dopamine β hydroxylase knockout () mice, which lack NE from birth. We find that mice exhibit no difference in adult hippocampal progenitor proliferation and survival. Further, the number of immature newborn neurons, labeled using stage-specific developmental markers within the hippocampal neurogenic niche, was also unaltered in mice. In contrast, the noradrenergic neurotoxin DSP-4, which had previously been shown to reduce adult hippocampal neurogenesis in rats, also resulted in a decline in hippocampal progenitor proliferation in C57/Bl6N mice. These findings indicate that pharmacological lesioning of noradrenergic afferents in adulthood, but not the complete genetic loss of NE from birth, impairs adult hippocampal neurogenesis in mice.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9643407PMC
http://dx.doi.org/10.1016/j.ibneur.2022.10.010DOI Listing

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