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The effects of various neurotransmitter agonists and antagonists on the synthesis and release of methionine enkephalin (mENK) in neuronal cultures of mouse spinal cord and dorsal root ganglia have been measured. Blockade of electrical activity with tetrodotoxin between days 9 and 13 in culture caused a > 95% decrease in the number of mENK-immunoreactive neurons. This effect was also seen upon the blockade of glycine and beta-adrenergic receptors with strychnine and propranolol, respectively, and stimulation of GABA receptors with muscimol. Stimulation of beta-adrenergic receptors with isoproterenol, or blockade of glutamate and GABA receptors with 2-aminophosphonovalerate and strychnine, respectively, had a qualitatively opposite action on both the number of mENK-immunoreactive neurons and enkephalin peptide levels measured by radioimmunoassay. Application of substance P also enhanced the mENK cell number. These data suggest that, at least in the spinal cord, characteristics other than the average level of impulse activity in the afferent input may be critical to the regulation of expression of mENK.  相似文献
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The ten‐eleven translocation (TET) family of methylcytosine dioxygenases catalyze oxidation of 5‐methylcytosine (5mC) to 5‐hydroxymethylcytosine (5hmC) and promote DNA demethylation. Despite the abundance of 5hmC and TET proteins in the brain, little is known about their role in oligodendrocytes (OLs). Here, we analyzed TET expression during OL development in vivo and in vitro, and found that three TET family members possess unique subcellular and temporal expression patterns. Furthermore, the level of 5hmC exhibits dynamic changes during OL maturation, which implies that 5hmC modification may play a role in the expression of critical genes necessary for OL maturation. siRNA‐mediated silencing of the TET family proteins in OLs demonstrated that each of the TET proteins is required for OL differentiation. However, based on their unique domain structures, we speculate that the three TET members may function by different mechanisms. In summary, we have established the temporal expression of TET proteins and the dynamic level of 5hmC during OL development and demonstrate that all three TET members are necessary for OL differentiation. GLIA 2014;62:914–926  相似文献
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Nitric oxide (NO) plays a key role in neurogenesis as a regulator of cell proliferation and differentiation. NO is synthesized from the amino acid L‐arginine by nitric oxide synthases (NOS1, NOS2, and NOS3), which are encoded by separate genes and display different tissue distributions. We used an in vitro model of RA‐induced neural differentiation of NT2 cells to examine which of the three NO‐synthesizing enzymes is involved in this process. The results revealed a transient induction of NOS3 (known as the constitutively expressed endothelial nitric oxide synthase; eNOS) during the time course of the RA treatment. The peak of gene expression and the nuclear presence of NOS3 protein coincided with cell cycle exit of NT2‐derived neuronal precursors. The subsequent analysis of cytosine methylation and histone H3 acetylation of the human NOS3 5′ regulatory sequences indicated that epigenetic modifications, especially upstream of the proximal promoter (?734 to ?989, relative to exon 2 TSS at +1), were also taking place. NOS1 was expressed only in the differentiated neurons (NT2‐N), whereas NOS2 was not expressed at all in this cellular model. Thus, a burst of NO production, possibly required to inhibit neural cell proliferation, was generated by the transient expression of NOS3. This pattern of gene expression, in turn, required epigenetic remodeling of its regulatory region. Published 2012 Wiley Periodicals, Inc.  相似文献
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We determined total Purkinje cell (PC) numbers in cerebella of wild-type (+/+) and heterozygous (rl/+) reeler mice of either sex during early postnatal development; in parallel, we quantified levels of neuroactive steroids in the cerebellum with mass spectrometry. We also quantified reelin mRNA and protein expression with RT-PCR and Western blotting. PC numbers are selectively reduced at postnatal day 15 (P15) in rl/+ males in comparison to +/+ males, +/+ females, and rl/+ females. Administration of 17β-estradiol (17β-E) into the cisterna magna at P5 increases PC numbers in rl/+ males, but not in the other groups; conversely, estrogen antagonists 4-OH-tamoxifen or ICI 182,780 reduce PC numbers in +/+ and rl/+ females, but have no effect in males. Testosterone (T) levels at P5 are much higher in males than in females, reflecting the perinatal testosterone surge in males. In addition, rl/+ male cerebella at P5 show a peculiar hormonal profile in comparison with the other groups, consisting of increased levels of T and 17β-E, and decreased levels of dihydrotestosterone. RT-PCR analysis indicated that heterozygosity leads to a 50% reduction of reelin mRNA in the cerebellum in both sexes, as expected, and that 17β-E upregulates reelin mRNA, particularly in rl/+ males; reelin mRNA upregulation is associated with an increase of all major reelin isoforms. These effects may represent a novel model of how reelin deficiency interacts with variable perinatal levels of neuroactive steroids, leading to gender-dependent differences in genetic vulnerability.  相似文献
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Recognition of an object's location in space is supported by hippocampus‐dependent recollection. Converging evidence strongly suggests that the interplay between the prefrontal cortex and hippocampus is critical for spatial memory. Lesion, pharmacological, and genetic studies have been successful in dissecting the role of plasticity in the hippocampal circuit in a variety of neural processes relevant to spatial memory, including memory for the location of objects. However, prefrontal mechanisms underlying spatial memory are less well understood. Here, we show that an acute hypofunction of the cyclic‐AMP regulatory element binding protein (CREB) Binding Protein (CBP) histone acetyltransferase (HAT) in the medial prefrontal cortex (mPFC) results in delay‐dependent disruption of object‐location memory. These data suggest that mechanisms involving CBP HAT‐mediated lysine acetylation of nuclear proteins support selectively long‐term encoding in the mPFC circuits. Evidence from the object‐location task suggests that long‐term memory encoding within the mPFC complements hippocampus‐dependent spatial memory mechanisms and may be critical for broader network integration of information necessary for an assessment of subtle spatial differences to guide appropriate behavioral response during retrieval of spatial memories. © 2015 Wiley Periodicals, Inc.  相似文献
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