PSA-NCAM expression in the rat medial prefrontal cortex

Varea, Emilio; Nácher, Juan; Blasco-Ibáñez, José Miguel; Gómez-Climent, María Ángeles; Castillo-Gómez, Esther; Crespo, Carlos; Martı́nez-Guijarro, Francisco José

doi:10.1016/j.neuroscience.2005.08.009

Cited by 70 publications

(75 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous reports have also identified 5-HTR3 expression in cortical interneurons expressing CCK, calbindin, and calretinin, although it is not present in parvalbumin expressing interneurons (Morales and Bloom, 1997). These results are in accordance with our previous report describing calbindin immunoreactivity in most mPFC PSA-NCAM expressing neurons and the absence of parvalbumin immunostaining in these cells (Varea et al, 2005).…”

Section: Involvement Of 5-ht In the Modulation Of Psa-ncam Expressionsupporting

confidence: 93%

“…The immunoreactivity was located in neurons, mainly characterized as interneurons, and in the neuropil with a clear lamination in the staining (Varea et al, 2005). PSA-NCAM immunoreactive neurons were located in all the layers of the mPFC but they were most abundant in deep layers.…”

Section: Relationship Between Psa-ncam Immunoreactive Neurons and 5-hmentioning

confidence: 92%

“…These receptors were chosen because they are expressed by mPFC interneurons (Puig et al, 2004) and previous results from our laboratory have demonstrated that most PSA-NCAM immunoreactive cells in the rat mPFC are interneurons (Varea et al, 2005). 5-HT1A and 5-HT2A receptors are also expressed by pyramidal neurons, while 5-HT3 receptor is only expressed by interneurons (Puig et al, 2004).…”

Section: -Ht Receptor Expression In Psa-ncam Immunoreactive Neuronsmentioning

confidence: 99%

“…A previous report has described that PSA-NCAM expressing neurons in the rat mPFC are mainly interneurons and that pyramidal neurons do not appear to express this molecule (Varea et al, 2005). Interneurons in the mPFC can be targets of 5-HT action because they are known to express 5-HT1A, 5-HT2A, and 5-HT3 receptors (Morales et al, 1996;Puig et al, 2004;Santana et al, 2004).…”

Section: Involvement Of 5-ht In the Modulation Of Psa-ncam Expressionmentioning

confidence: 99%

“…Consequently, the expression of PSA-NCAM allows neurons to participate in plastic events such as neurite outgrowth (Zhang et al, 1992) or synaptic reorganization (Seki and Rutishauser, 1998). Recently, our laboratory has shown the presence of PSA-NCAM in certain neurons and the neuropil of the adult rat mPFC (Varea et al, 2005), suggesting that PSA-NCAM may also mediate the structural changes occurring in this region.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Varea

Blasco-Ibáñez

Gómez-Climent

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

Recent hypotheses suggest that changes in neuronal structure and connectivity may underlie the etiology of depression. The medial prefrontal cortex (mPFC) is affected by depression and shows neuronal remodeling during adulthood. This plasticity may be mediated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM), which is intensely expressed in the adult mPFC. As the expression of PSA-NCAM is increased by serotonin in other cerebral regions, antidepressants acting on serotonin reuptake may influence PSA-NCAM expression and thus counteract the effects of depression by modulating neuronal structural plasticity. Using immunohistochemistry, we have studied the relationship between serotoninergic fibers and PSA-NCAM expressing neurons in the adult rat mPFC and the expression of serotonin receptors in these cells. The effects of fluoxetine treatment for 14 days on mPFC PSA-NCAM expression have also been analyzed. Although serotoninergic fibers usually do not contact PSA-NCAM immunoreactive neurons, most of these cells express 5-HT3 receptors. In general, chronic fluoxetine treatment induces significant increases in the number of PSA-NCAM immunoreactive neurons and in neuropil immunostaining and coadministration of the 5-HT3 antagonist ondansetron blocks the effects of fluoxetine on PSA-NCAM expression. These results indicate that fluoxetine, acting through 5-HT3 receptors, can modulate PSA-NCAM expression in the mPFC. This modulation may mediate the structural plasticity of this cortical region and opens new perspectives on the study of the molecular bases of depression.

show abstract

Section: Involvement Of 5-ht In the Modulation Of Psa-ncam Expressionsupporting

confidence: 93%

Section: Relationship Between Psa-ncam Immunoreactive Neurons and 5-hmentioning

confidence: 92%

Section: -Ht Receptor Expression In Psa-ncam Immunoreactive Neuronsmentioning

confidence: 99%

Section: Involvement Of 5-ht In the Modulation Of Psa-ncam Expressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Varea

Blasco-Ibáñez

Gómez-Climent

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

Malignant phyllodes tumor of the female breast

Macdonald

Lee

Tward

et al. 2006

Cancer

197

View full text Add to dashboard Cite

BACKGROUND.Malignant phyllodes tumor is a rare and potentially aggressive breast neoplasm. Little information is available regarding the optimal management of these lesions and rarer still are data regarding survival. The current study used a large population database to determine prognostic factors that predict cause‐specific survival (CSS).METHODS.Data were obtained from the Surveillance, Epidemiology, and End Results Program (SEER) for the years 1983–2002. Women receiving resection for primary nonmetastatic malignant phyllodes tumor of the breast were included (n = 821). Analyses of patient, pathologic, and treatment characteristics were performed using univariate and multivariate Cox regression analyses for the CSS endpoint.RESULTS.With a median follow‐up of 5.7 years, CSS was 91%, 89%, and 89%, at 5, 10, and 15 years, respectively. Mastectomy was performed in 428 women (52%) and wide excision or lumpectomy in 393 (48%). Women undergoing mastectomy were significantly older (P = .004) and had larger tumors (P = .009). Wide excision was associated with equivalent or improved CSS relative to mastectomy on univariate and multivariate analyses. Older age predicted for cause‐specific mortality on multivariate analysis. Adjuvant radiotherapy (RT) predicted for worse CSS when implemented compared with surgery alone.CONCLUSIONS.Mastectomy was not found to provide a benefit in CSS compared with wide excision in malignant phyllodes tumor of the breast. Women undergoing wide excision had at the minimum similar cancer‐specific mortality compared with those who received mastectomy. The role of adjuvant RT is uncertain and requires further investigation. Cancer 2006. © 2006 American Cancer Society.

show abstract

Collagen XIX is expressed by interneurons and contributes to the formation of hippocampal synapses

Gorse

Ramirez

et al. 2009

J of Comparative Neurology

145

View full text Add to dashboard Cite

Extracellular matrix (ECM) molecules contribute to the formation and maintenance of synapses in the mammalian nervous system. We previously discovered a family of nonfibrillar collagens that organize synaptic differentiation at the neuromuscular junction (NMJ). Although many NMJorganizing cues contribute to central nervous system (CNS) synaptogenesis, whether similar roles for collagens exist at central synapses remained unclear. In the present study we discovered that col19a1, the gene encoding nonfibrillar collagen XIX, is expressed by subsets of hippocampal neurons. Colocalization with the interneuron-specific enzyme glutamate decarboxylase 67 (Gad67), but not other cell-type-specific markers, suggests that hippocampal expression of col19a1 is restricted to interneurons. However, not all hippocampal interneurons express col19a1 mRNA; subsets of neuropeptide Y (NPY)-, somatostatin (Som)-, and calbindin (Calb)-immunoreactive interneurons express col19a1, but those containing parvalbumin (Parv) or calretinin (Calr) do not. To assess whether collagen XIX is required for the normal formation of hippocampal synapses, we examined synaptic morphology and composition in targeted mouse mutants lacking collagen XIX. We show here that subsets of synaptotagmin 2 (Syt2)-containing hippocampal nerve terminals appear malformed in the absence of collagen XIX. The presence of Syt2 in inhibitory hippocampal synapses, the altered distribution of Gad67 in collagen XIXdeficient subiculum, and abnormal levels of gephyrin in collagen XIX-deficient hippocampal extracts all suggest inhibitory synapses are affected by the loss of collagen XIX. Together, these data not only reveal that collagen XIX is expressed by central neurons, but show for the first time that a nonfibrillar collagen is necessary for the formation of hippocampal synapses. INDEXING TERMSextracellular matrix; collagen; synaptogenesis; hippocampus; interneuron Synapse formation is a multistep process orchestrated by developmentally regulated signals that are either passed between putative synaptic partners or present in the extracellular environment. Initial advances in identifying synaptic organizing signals came from studies of the accessible neuromuscular junction (NMJ), where extracellular factors embedded in the basal lamina separating motor nerve terminals from postsynaptic muscle membrane were sufficient to induce synaptogenesis (Sanes et al., 1978;Burden et al., 1979; for review, see NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript Sanes and Lichtman, 1999;Fox and Umemori, 2006). Biochemical, molecular, and genetic studies have since identified roles for agrin, laminin α chains, and Wnts in the organization of the postsynaptic apparatus (Nitkin et al., 1987;Gautam et al., 1996;Sanes and Lichtman, 1999;Burgess et al., 1999;Lin et al., 2001 Lin et al., , 2005Misgeld et al., 2005;Kummer et al., 2006;Nishimune et al., 2008;Henriquez et al., 2008) and collagen IV, laminin β2, and fibroblast growth factors (FGFs) in the formation of...

show abstract

PSA-NCAM expression in the rat medial prefrontal cortex

Cited by 70 publications

References 65 publications

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Chronic Fluoxetine Treatment Increases the Expression of PSA-NCAM in the Medial Prefrontal Cortex

Malignant phyllodes tumor of the female breast

Collagen XIX is expressed by interneurons and contributes to the formation of hippocampal synapses

Contact Info

Product

Resources

About