Enhanced proliferation of progenitor cells following long-term potentiation induction in the rat dentate gyrus

Chun, Sungkun; Sun, Woong; Park, Joong Jean; Jung, Min Whan

doi:10.1016/j.nlm.2006.05.005

Cited by 75 publications

(70 citation statements)

References 38 publications

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“…Not surprisingly, LTP significantly increased the number of NSPCs entering the cell cycle, which was confirmed by the expression of the proliferation marker, proliferating cell nuclear antigen (PCNA). These results confirmed that LTP does indeed increase the proliferation of NSPCs [53]. When the competitive NMDA antagonist, 4-(3-phosphonopropyl)-2-piperazine-carboxylic acid (CPP), was administered before each HFS, LTP and the LTP-mediated increase in proliferation was blocked, which indicated the enhancement of proliferation by LTP is dependent on NMDAR activation.…”

Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Hisupporting

confidence: 58%

“…In a similar study, LTP was induced in the DG of chronically-implanted rats, each day for three consecutive days, while BrdU was administered 1 h after each HFS, as well as the day before the LTP induction protocol commenced [53]. The cumulative induction of LTP significantly enhanced the number of proliferating NSPCs in the DG, as measured by BrdU incorporation.…”

Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Himentioning

confidence: 98%

“…When the competitive NMDA antagonist, 4-(3-phosphonopropyl)-2-piperazine-carboxylic acid (CPP), was administered before each HFS, LTP and the LTP-mediated increase in proliferation was blocked, which indicated the enhancement of proliferation by LTP is dependent on NMDAR activation. Interestingly, in the low-frequency stimulated hemisphere, CPP induced a significant increase in the number of BrdU-labelled cells compared with control-injected rats [53]. The ability of NMDAR antagonists to promote proliferation in the adult SGZ is addressed below.…”

Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Himentioning

confidence: 99%

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The role of the N-methyl-d-aspartate receptor in the proliferation of adult hippocampal neural stem and precursor cells

Taylor

Bartlett

2014

Sci. China Life Sci.

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New neurons are continuously generated from resident pools of neural stem and precursor cells (NSPCs) in the adult brain. There are multiple pathways through which adult neurogenesis is regulated, and here we review the role of the N-methyl-D-aspartate receptor (NMDAR) in regulating the proliferation of NSPCs in the adult hippocampus. Hippocampal-dependent learning tasks, enriched environments, running, and activity-dependent synaptic plasticity, all potently up-regulate hippocampal NSPC proliferation. We first consider the requirement of the NMDAR in activity-dependent synaptic plasticity, and the role the induction of synaptic plasticity has in regulating NSPCs and newborn neurons. We address how specific NMDAR agonists and antagonists modulate proliferation, both in vivo and in vitro, and then review the evidence supporting the hypothesis that NMDARs are present on NSPCs. We believe it is important to understand the mechanisms underlying the activation of adult neurogenesis, given the potential that endogenous stem cell populations have for repopulating the hippocampus with functional new neurons. In conditions such as age-related memory decline, neurodegeneration and psychiatric disease, mature neurons are lost or become defective; as such, stimulating adult neurogenesis may provide a therapeutic strategy to overcome these conditions. The adult brain continuously generates new neurons throughout life. These adult-born neurons arise from endogenous neural stem and precursor cells (NSPCs), which primarily reside within two neurogenic niches: the subgranular zone (SGZ) in the dentate gyrus (DG) of the hippocampus, and the subventricular zone (SVZ) of the lateral ventricles. In the 20 years since adult mammalian neurogenesis started receiving substantial attention [1,2], scientists have made great progress in understanding the mechanisms that regulate stem cell maintenance, proliferation, differentiation, maturation and integration [3,4]. Early on, extrinsic cues from the environment, such as learning [5], physical activity [6], and enriched environments [7,8], were found to potently enhance hippocampal neurogenesis. It was not long before a link was made to synaptic plasticity [9], which is also enhanced by physical exercise [10], and is widely accepted as the synaptic mechanism underlying hippocampal learning and memory [11]. Synaptic plasticity and adult hippocampal neurogenesis are intimately linked, as long-term potentiation (LTP), an activity-dependent change in synaptic efficacy, can influence the activation and proliferation of NSPCs in the DG (e.g., [12]), as well as the survival of newborn neurons (e.g., [13]). These newborn neurons have biophysical characteris-

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Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Hisupporting

confidence: 58%

Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Himentioning

confidence: 98%

Section: Hippocampal Ltp Activates Nspc Proliferation In the Adult Himentioning

confidence: 99%

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The role of the N-methyl-d-aspartate receptor in the proliferation of adult hippocampal neural stem and precursor cells

Taylor

Bartlett

2014

Sci. China Life Sci.

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“…The rapid (15-min post-SE) increase in ERK activation in the dentate gyrus GCL raised the possibility that progenitor cells proliferation was directly regulated by the release of glutamate. Supporting a role for NMDA receptors, Deisseroth et al (2004) reported that NMDA receptor activation increased progenitor cell proliferation and Chun et al (2006) found that tetanic stimulation of the perforant pathway increased neurogenesis in an NMDA receptor-dependent manner. On the other hand, NMDA receptor antagonist injection has been shown to increase progenitor cell proliferation (Cameron et al, 1995).…”

Section: Discussionmentioning

confidence: 98%

“…First, pathophysiological stimuli, including SE and ischemia activate the MAPK pathway within the hippocampus Hu et al, 2000). Second, an array of signaling molecules, including glutamate and neurotrophins stimulate both the MAPK cascade and progenitor cell proliferation and postmitotic cell differentiation (Chun et al, 2006;Deisseroth et al, 2004;Lee et al, 2002). Third, the MAPK cascade has been implicated in progenitor cell proliferation or differentiation in a number of model systems.…”

Section: Introductionmentioning

confidence: 99%

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

Choi

Cho

Hoyt

et al. 2008

Glia

132

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Adult progenitor cell proliferation in the subgranular zone (SGZ) of the dentate gyrus is a dynamic process that is modulated by an array of physiological process, including locomotor activity and novel environmental stimuli. In addition, pathophysiological events, such as ischemia and status epilepticus (SE), have been shown to stimulate neurogenesis. Currently, limited information is available regarding the extracellular stimuli, receptors, and downstream intracellular effectors that couple excitotoxic stimulation to progenitor cell proliferation. Here we show that pilocarpineinduced SE triggers a set of signaling events that impinge upon the p42/44 mitogen-activated protein kinase (MAPK) pathway to drive progenitor cell proliferation in the SGZ at 2-days post-SE. Increased proliferation was dependent on insulin-like growth factor-1 (IGF-1), which was localized to activated microglia near the SGZ. Using a combination of techniques, we show that IGF-1 is a CREB-regulated gene and that SE triggered CRE-dependent transcription in microglia at 2-days post-SE. Together, these data identify a potential signaling program that couples SE to progenitor cell proliferation. SE triggers CREB-dependent transcription in reactive microglia. As a CREB-target gene, IGF-1 expression is upregulated, and by 2-days post-SE, IGF-1 triggers MAPK pathway activation in progenitor cells and, in turn, an increase in progenitor cell proliferation.

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Modification of hippocampal circuitry by adult neurogenesis

Song

Christian

Guo

et al. 2012

Developmental Neurobiology

117

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The adult hippocampus is one of the primary neural structures involved in memory formation. In addition to synapse-specific modifications thought to encode information at the sub-cellular level, changes in the intrahippocampal neuro-populational activity and dynamics at the circuit-level may contribute substantively to the functional capacity of this region. Within the hippocampus, the dentate gyrus has the potential to make a preferential contribution to neural circuit modification owing to the continuous addition of new granule cell population. The integration of newborn neurons into pre-existing circuitry is hypothesized to deliver a unique processing capacity, as opposed to merely replacing dying granule cells. Recent studies have begun to assess the impact of hippocampal neurogenesis by examining the extent to which adult-born neurons participate in hippocampal networks, including when newborn neurons become engaged in ongoing network activity and how they modulate circuit dynamics via their unique intrinsic physiological properties. Understanding the contributions of adult neurogenesis to hippocampal function will provide new insight into the fundamental aspects of brain plasticity, which can be used to guide therapeutic interventions to replace neural populations damaged by disease or injury.

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Enhanced proliferation of progenitor cells following long-term potentiation induction in the rat dentate gyrus

Cited by 75 publications

References 38 publications

The role of the N-methyl-d-aspartate receptor in the proliferation of adult hippocampal neural stem and precursor cells

The role of the N-methyl-d-aspartate receptor in the proliferation of adult hippocampal neural stem and precursor cells

IGF‐1 receptor‐mediated ERK/MAPK signaling couples status epilepticus to progenitor cell proliferation in the subgranular layer of the dentate gyrus

Modification of hippocampal circuitry by adult neurogenesis

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