Experience-dependent regulation of adult hippocampal neurogenesis: Effects of long-term stimulation and stimulus withdrawal

Kempermann, Gerd; Gage, Fred H.

doi:10.1002/(sici)1098-1063(1999)9:3<321::aid-hipo11>3.0.co;2-c

Cited by 214 publications

(136 citation statements)

References 38 publications

(63 reference statements)

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“…In earlier experiments studying the effects of environmental enrichment on adult neurogenesis, we had found that, besides an acute effect on the progeny of dividing neural precursor cells, living in a challenging environment might also have a trophic effect on the population of precursor cells itself (19,27). It is thus possible that the early postnatal manipulation might have more long-lasting effects on neurogenesis than became obvious in this study.…”

Section: Discussionmentioning

confidence: 66%

Running in pregnancy transiently increases postnatal hippocampal neurogenesis in the offspring

Bick-Sander

Steiner

Wolf

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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Voluntary wheel running of mice in pregnancy and lactation led to a twofold increase in hippocampal precursor-cell proliferation and in the number of Prox1-expressing lineage-determined cells at postnatal day 8 (P8). At P36, the number of newly generated granule cells approximately doubled, resulting in a 40% higher total number of granule cells in pups from running dams as compared with controls. Cell proliferation at embryonic day 15 (E15), in contrast, was decreased in the progeny of exercising mice, and the birth weight was reduced. At P49, body weight had normalized, and hippocampal neurogenesis was not different between the two groups. mRNA for FGF2 was expressed at higher levels at E15 and P8 in runner pups, whereas VEGF was increased only at E15. Insulin-like growth factor did not show differences at any time point. At P36, no differences for any of the factors were found. Our data indicate that maternal behavior and physical activity affects infantile growth-factor expression and can transiently stimulate postnatal hippocampal development in the offspring.

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Section: Discussionmentioning

confidence: 66%

Running in pregnancy transiently increases postnatal hippocampal neurogenesis in the offspring

Bick-Sander

Steiner

Wolf

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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“…A broader functional perspective might, for example, help to explain, why different groups obtained conflicting results when the direct effect of water maze performance on the regulation of adult hippocampal neurogenesis was investigated (Gould et al, 1999a;Van Praag et al, 1999a). "Experience," which is learning in a very broad sense, can stimulate adult hippocampal neurogenesis (Kempermann et al, 1997(Kempermann et al, , 1998aKempermann and Gage, 1999), but spatial learning might benefit from increased neurogenesis (as seen in our experiment with 129/SvJ; Kempermann et al, 1998b) without being the most relevant factor to stimulate neurogenesis. This idea is supported by the otherwise surprising finding that physical activity causes a dramatic increase in adult neurogenesis and leads to improved performance in the water maze task (Van Praag et al, 1999a,b).…”

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confidence: 81%

“…However, it did not lead to increased adult hippocampal neurogenesis later in life (Kohl et al, 2002). In contrast, withdrawal from a post-weaning enrichment paradigm had lasting effects at least on the level of cell proliferation (Kempermann and Gage, 1999). One possible interpretation is that the lack of an effect in preweaning enrichment is based on the fact that preweaning enrichment does not involve physical activity or active exploratory pursuit.…”

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confidence: 92%

Why New Neurons? Possible Functions for Adult Hippocampal Neurogenesis

2002

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“…A large number of the newborn daughter cells are known to die rapidly, likely via apoptosis. 142 In view of bcl-2's major neuroprotective and neurotrophic role, a study was undertaken to determine if lithium, administrated at therapeutically relevant concentrations, affects neurogenesis in the adult rodent brain. After treatment with lithium for 14 days, mice were administered single doses of BrdU (bromodeoxyuridine, a thymidine analog which is incorporated into the DNA of dividing cells) for 12 consecutive days.…”

Section: Lithium Increases Hippocampal Neurogenesismentioning

confidence: 99%

Neuroplasticity and cellular resilience in mood disorders

et al. 2000

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Although mood disorders have traditionally been regarded as good prognosis diseases, a growing body of data suggests that the long-term outcome for many patients is often much less favorable than previously thought. Recent morphometric studies have been investigating potential structural brain changes in mood disorders, and there is now evidence from a variety of sources demonstrating significant reductions in regional CNS volume, as well as regional reductions in the numbers and/or sizes of glia and neurons. Furthermore, results from recent clinical and preclinical studies investigating the molecular and cellular targets of mood stabilizers and antidepressants suggest that a reconceptualization about the pathophysiology and optimal long-term treatment of recurrent mood disorders may be warranted. It is proposed that impairments of neuroplasticity and cellular resilience may underlie the pathophysiology of mood disorders, and further that optimal long-term treatment for these severe illnesses may only be achieved by the early and aggressive use of agents with neurotrophic/ neuroprotective effects. It is noteworthy that lithium, valproate and antidepressants indirectly regulate a number of factors involved in cell survival pathways including CREB, BDNF, bcl-2 and MAP kinases, and may thus bring about some of their delayed long-term beneficial effects via underappreciated neurotrophic effects. The development of novel treatments which more directly target molecules involved in critical CNS cell survival and cell death pathways have the potential to enhance neuroplasticity and cellular resilience, and thereby modulate the long-term course and trajectory of these devastating illnesses. Molecular Psychiatry (2000) 5, 578-593.Keywords: atrophy; cell death; neuroprotection; lithium; bcl-2; MAP kinase; neurite; neurotrophic; neurogenesis; N-acetylaspartate; gray matter There is mounting evidence that recurrent mood disorders-once considered 'good prognosis diseases'-are, in fact, often very severe and life-threatening illnesses. Recurrent mood disorders can have devastating long-term effects, and the cost of these illnesses in terms of human suffering, productivity and health care is enormous. Suicide is the cause of death in 10-20% of individuals, and in addition to suicide, mood disorders are associated with many other deleterious health-related effects. 1-5 Indeed, a recent study which controlled for physical illness, smoking and alcohol consumption found that the magnitude of the increased mortality risk conferred by the presence of high depressive symptoms was similar to that of stroke and congestive heart failure. 5 Not surprisingly, the costs associated with disability and premature death represent an economic burden of tens of billions of dollars annually in the United States alone. 1,6,7 It is now recognized that, for many patients, the long-term outCorrespondence: HK Manji, MD,

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Experience-dependent regulation of adult hippocampal neurogenesis: Effects of long-term stimulation and stimulus withdrawal

Cited by 214 publications

References 38 publications

Running in pregnancy transiently increases postnatal hippocampal neurogenesis in the offspring

Running in pregnancy transiently increases postnatal hippocampal neurogenesis in the offspring

Why New Neurons? Possible Functions for Adult Hippocampal Neurogenesis

Neuroplasticity and cellular resilience in mood disorders

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