A Role for N-Methyl-&lt;i&gt;D&lt;/i&gt;-Aspartate Receptors in the Regulation of Synaptogenesis and Expression of the Polysialylated Form of the Neural Cell Adhesion Molecule in the Developing Striatum

Butler, Amy K.; Uryu, Kunihiro; Chesselet, Marie‐Françoise

doi:10.1159/000017319

Cited by 45 publications

(43 citation statements)

References 108 publications

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“…Accordingly, LTP is preferentially expressed in dorsomedial striatum in younger rats under normal physiological conditions. This is consistent with the fact that synapses within the striatum develop along a lateralmedial gradient, with the synapses in lateral striatum maturing earlier than those in medial striatum [25] . Nevertheless, it is not surprising that LTD was invariably recorded in our experiment, given the use of older rats (2-3 months) and the recording subregion of striatum (DLS).…”

Section: Discussionsupporting

confidence: 85%

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Cui

Wang

et al. 2011

Acta Pharmacol Sin

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Aim:The dorsal striatum has been proposed to contribute to the formation of drug-seeking behaviors, leading to excessive and compulsive drug usage, such as addiction. The current study aimed to investigate the involvement of extracellular signal-regulated kinase (ERK) pathway in the modification of striatal synaptic plasticity. Methods: Ethanol was administered to rats in drinking water at concentration of 6% (v/v) for 30 days. Rats were sacrificed on day 10, 20, or 30 during ethanol intake or on withdrawal day 1, 3, or 7 following 30-d ethanol intake. The striata were removed either for electrophysiological recording or for protein immuno-blot analysis. Extracellular recording technique was used to record population spikes (PS) induced by high-frequency stimulation (HFS) in the dorsolateral striatum (DLS). Results: Corticostriatal long-term depression (LTD) was determined to be dependent upon ERK signaling. Chronic ethanol intake (CEI) attenuated ERK phosphorylation and LTD induction, whereas withdrawal for one day (W1D) potentiated ERK phosphorylation and LTD induction. These results showed that the impact of chronic ethanol intake and withdrawal on corticostriatal synaptic plasticity was associated with ethanol's effect on ERK phosphorylation. In particular, pharmacological inhibition of ERK hyper-phosphorylation by U0126 prevented LTD induction in the DLS and attenuated ethanol withdrawal syndrome as well. Conclusion: In rat DLS, chronic ethanol intake and withdrawal altered LTD induction via ERK signaling pathway. Ethanol withdrawal syndrome is mediated, at least partly, by ERK hyper-phosphorylation in the DLS.

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Section: Discussionsupporting

confidence: 85%

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Cui

Wang

et al. 2011

Acta Pharmacol Sin

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“…7 Analysis of DCX-immunoreactive cells in the DG of vehicleand MK-801-treated exercised rats (n = 5 per group; * P \ 0.05, significantly different from the vehicle-treated group). The bars indicate the means ± SEM treatment reduced polysialylated neuronal cell adhesion molecule in the neuroblast of developing mouse striatum (Butler et al 1998). Conversely, activation of NR on proliferating progenitors induced neuronal differentiation of adult-derived neural progenitor cells in vitro, and NR increased the fraction of microtubule associated protein-2-positive cells, suggesting that the maturation of postmitotic neurons was altered by NR activation (Joo et al 2007).…”

Section: Discussionmentioning

confidence: 99%

Effects of Treadmill Exercise Combined with MK 801 Treatment on Neuroblast Differentiation in the Dentate Gyrus in Rats

et al. 2010

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N-methyl-D-aspartate receptor (NR) is involved in activity-dependent synaptic plasticity, such as associative long-term potentiation, and in related central functions, such as learning and memory. In this study, we observed effects of treadmill exercise on NR1 and doublecortin (DCX, a marker for neuroblast differentiation) in the subgranular zone of the dentate gyrus (DG). At 6 weeks of age, rats were put on a treadmill with or without running for 1 h/day for 5 consecutive days at 22 m/min for 5 weeks. Exercise increased NR1 immunoreactivity and protein level in the hippocampus. To identify the correlations between NR and neuroblasts, we intraperitoneally administered a NR antagonist, MK-801, to the exercised rats. MK-801 treatment reduced NR1 protein level in the hippocampus of the exercised rats. In addition, in the MK-801-treated group, the number of DCX cells was significantly decreased in the subgranular zone of the DG. These results suggest that NR may be one of the important factors that modulate neuroblast differentiation during exercise in rats.

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“…For example, activity-dependent upregulation of NCAM on cultured striatal neurons depends on NF-κB activation (Simpson and Morris, 2000). NCAM is widely expressed on the dendrites and axons of a variety of neurons in the developing brain, and becomes progressively localized to synapses with age (Butler et al, 1998;Chung et al, 1991;Fox et al, 1995;Persohn and Schachner, 1990). NCAM stimulates neurite growth from many kinds of neurons in vitro (Skaper et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

NF-κB signalling regulates the growth of neural processes in the developing PNS and CNS

et al. 2005

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The proper growth and elaboration of neural processes is essential for the establishment of a functional nervous system during development and is an integral feature of neural plasticity throughout life. Nuclear factor-kappa B(NF-κB) is classically known for its ubiquitous roles in inflammation,immune and stress-related responses and regulation of cell survival in all tissues, including the nervous system. NF-κB participation in other cellular processes remains poorly understood. Here we report a mechanism for controlling the growth of neural processes in developing peripheral and central neurons involving the transcription factor NF-κB. Inhibiting NF-κB activation with super-repressor IκB-α, BAY 11 7082(IκB-α phosphorylation inhibitor) or N-acetyl-Leu-Leu-norleucinal(proteosomal degradation inhibitor), or inhibiting NF-κB transcriptional activity with κB decoy DNA substantially reduced the size and complexity of the neurite arbors of sensory neurons cultured with brain-derived neurotrophic factor while having no effect on their survival. NF-κB exerted this effect during a restricted period of development following the phase of naturally occurring neuronal death when the processes and connections of the remaining neurons are extensively modified and refined. Inhibiting NF-κB activation or NF-κB transcriptional activity in layer 2 pyramidal neurons in postnatal somatosensory cortical slices reduced dendritic arbor size and complexity. This function of NF-κB has important implications for neural development and may provide an explanation for reported involvement of NF-κB in learning and memory.

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A Role for N-Methyl-<i>D</i>-Aspartate Receptors in the Regulation of Synaptogenesis and Expression of the Polysialylated Form of the Neural Cell Adhesion Molecule in the Developing Striatum

Cited by 45 publications

References 108 publications

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Alteration of synaptic plasticity in rat dorsal striatum induced by chronic ethanol intake and withdrawal via ERK pathway

Effects of Treadmill Exercise Combined with MK 801 Treatment on Neuroblast Differentiation in the Dentate Gyrus in Rats

NF-κB signalling regulates the growth of neural processes in the developing PNS and CNS

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