Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

Kahn, Laëtitia; Alonso, Gérard; Normand, Elisabeth; Manzoni, Olivier J.

doi:10.1111/j.1460-9568.2005.03883.x

Cited by 84 publications

(67 citation statements)

References 50 publications

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“…Our study provides evidence that morphine exerts its toxic effects through the induction of autophagy in the rat brain. The results are consistent with a previous study which shows that chronic exposure to morphine dramatically alters neuronal phenotypes in the dentate gyrus-CA3 region of the adult rat hippocampus, 50 although autophagy was not documented in this study. Why Morphine treatments.…”

Section: Methodssupporting

confidence: 83%

Morphine induces Beclin 1- and ATG5-dependent autophagy in human neuroblastoma SH-SY5Y cells and in the rat hippocampus

Zhao¹,

Zhu²,

Wang³

et al. 2010

Autophagy

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Section: Methodssupporting

confidence: 83%

Morphine induces Beclin 1- and ATG5-dependent autophagy in human neuroblastoma SH-SY5Y cells and in the rat hippocampus

Zhao¹,

Zhu²,

Wang³

et al. 2010

Autophagy

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“…A few reports have appreciated the difference and relationship between cells and clusters in the rat (Cameron and McKay, 2001, Kahn et al, 2005, Kim et al, 2005 and mouse , Donovan et al, 2006, and one found differential regulation of cells versus clusters (Kahn et al, 2005). Given that the vasculature niche appears critical to the stability and regulation of the clusters of dividing cells (Palmer et al, 2000, Ernst andChristie, 2006), it is surprising that clusters have received relatively little attention.…”

Section: Time Course Of Cluster and Cells Per Cluster Counts In The Sgzmentioning

confidence: 99%

“…Proliferating cells in the adult SGZ divide in clusters (Cameron and McKay, 2001, Kahn et al, 2005. To determine the rate at which cells multiply in the adult mouse SGZ, and to determine key aspects of cell and cluster division, we injected adult mice with an S phase-saturating dose of BrdU (150 mg/kg).…”

Section: Brdu-ir Cells and Clusters In Adult Mouse Sgzmentioning

confidence: 99%

Determination of key aspects of precursor cell proliferation, cell cycle length and kinetics in the adult mouse subgranular zone

Mandyam¹,

Harburg²,

Eisch³

2007

Neuroscience

189

205

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Neurogenesis studies on the adult mouse hippocampal subgranular zone (SGZ) typically report increases or decreases in proliferation. However, key information is lacking about these proliferating SGZ precursors, from the fundamental -what dose of bromodeoxyuridine (BrdU) is appropriate for labeling all S phase cells? -to the detailed -what are the kinetics of BrdU-labeled cells and their progeny? To address these questions, adult C57BL/6J mice were injected with BrdU and BrdUimmunoreactive (IR) cells were quantified. Initial experiments with a range of BrdU doses (25-500 mg/kg) suggested that 150 mg/kg labels all actively dividing precursors in the mouse SGZ. Experiments using a saturating dose of BrdU suggested BrdU bioavailability is less than 15 minutes, notably shorter than in the developing mouse brain. We next explored precursor division and maturation by tracking the number of BrdU-IR cells and colabeling of BrdU with other cell cycle proteins from 15 min to 30 days after BrdU. We found that BrdU and the G 2 /M phase protein pHisH3 maximally colocalized 8 hr after BrdU, indicating that the mouse SGZ precursor cell cycle length is 14 hr. In addition, triple labeling with BrdU and PCNA and Ki-67 showed that BrdU-IR precursors and/or their progeny express these endogenous cell cycle proteins up to 4 days after BrdU injection. However, the proportion of BrdU/Ki-67-IR cells declined at a greater rate than the proportion of BrdU/PCNA-IR cells. This suggests that PCNA protein is detectable long after cell cycle exit, and that reliance on PCNA may overestimate the length of time a cell remains in the cell cycle. These findings will be critical for future studies examining the regulation of SGZ precursor kinetics in adult mice, and hopefully will encourage the field to move beyond counting BrdU-IR cells to a more mechanistic analysis of adult neurogenesis.

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“…All stages of hippocampal progenitor development -proliferation, differentiation, and survival -can be influenced by environmental and physiological stimuli (Cameron et al, 1998, Eisch, 2002, Abrous et al, 2005. For example, adult in vivo exposure to MOR agonists decreases the proliferation and survival of new neurons in the hippocampus (Eisch et al, 2000, Mandyam et al, 2004, Kahn et al, 2005, Eisch and Harburg, 2006. In order to examine the impact of loss of MOR on adult hippocampal neurogenesis, we examine the proliferation, differentiation, and survival of new neurons in the hippocampus of adult transgenic mice lacking exon 1 of MOR (Sora et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Knockout of the mu opioid receptor enhances the survival of adult-generated hippocampal granule cell neurons

Harburg¹,

Hall²,

Harrist³

et al. 2007

Neuroscience

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Recent evidence suggests that mu opioid receptors (MOR) are key regulators of hippocampal structure and function. For example, exogenous MOR agonists morphine and heroin negatively impact hippocampal function and decrease adult hippocampal neurogenesis. Here we explored the role of MOR in the birth and survival of hippocampal progenitor cells by examining adult neurogenesis in mice that lack MOR. Adult male mice lacking exon 1 of MOR were injected with the S phase marker bromodeoxyuridine (BrdU) and sacrificed either two hours or four weeks later to evaluate proliferating and surviving BrdU-immunoreactive (IR) cells, respectively, in the adult hippocampal granule cell layer. WT, heterozygote, and homozygote mice did not differ in the number of BrdU-IR cells at a proliferation time point. However, four weeks after BrdU injection, heterozygote and homozygote mice had 57% and 54% more surviving BrdU-IR cells in the hippocampal granule cell layer as compared to WT mice. A decrease in apoptosis in the heterozygote and homozygote mice did not account for the difference in number of surviving BrdU-IR cells since there were no alterations in number of pyknotic, TUNEL-positive, or activated caspase 3-IR cells compared to WT. In concordance with the increased numbers of granule cells maturing into neurons, heterozygote and homozygote mice had larger hippocampal granule cell layers and increased numbers of granule cells. These findings indicate that MOR may play a role in regulating progenitor cell survival and more generally encourage further exploration of how MOR activation can influence hippocampal structure and function.

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Repeated morphine treatment alters polysialylated neural cell adhesion molecule, glutamate decarboxylase‐67 expression and cell proliferation in the adult rat hippocampus

Cited by 84 publications

References 50 publications

Morphine induces Beclin 1- and ATG5-dependent autophagy in human neuroblastoma SH-SY5Y cells and in the rat hippocampus

Morphine induces Beclin 1- and ATG5-dependent autophagy in human neuroblastoma SH-SY5Y cells and in the rat hippocampus

Determination of key aspects of precursor cell proliferation, cell cycle length and kinetics in the adult mouse subgranular zone

Knockout of the mu opioid receptor enhances the survival of adult-generated hippocampal granule cell neurons

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