<?xml version="1.0" encoding="UTF-8"?>
<feed xmlns="http://www.w3.org/2005/Atom" xmlns:dc="http://purl.org/dc/elements/1.1/">
<title>Departamento Anatomía e Histología Humanas</title>
<link href="http://hdl.handle.net/10366/3948" rel="alternate"/>
<subtitle/>
<id>http://hdl.handle.net/10366/3948</id>
<updated>2026-05-09T17:37:09Z</updated>
<dc:date>2026-05-09T17:37:09Z</dc:date>
<entry>
<title>Mejora del aprendizaje de las competencias prácticas en el área de histología de los alumnos del Grado en Medicina utilizando imágenes interactivas</title>
<link href="http://hdl.handle.net/10366/170817" rel="alternate"/>
<author>
<name>García Sánchez, Omar</name>
</author>
<author>
<name>Benito Garzón, Lorena</name>
</author>
<id>http://hdl.handle.net/10366/170817</id>
<updated>2026-04-07T13:39:35Z</updated>
<published>2025-11-01T00:00:00Z</published>
<summary type="text">[ES]En la parte práctica de la asignatura Histología Humana del Grado en Medicina de la Universidad&#13;
de Salamanca se observaron diferentes preparaciones histológicas. Los resultados académicos&#13;
en esta parte práctica fueron sistemáticamente peores que los de la parte teórica, por lo que implementar&#13;
una nueva herramienta docente de apoyo a los estudiantes parece imprescindible. Para facilitar la&#13;
adquisición de habilidades prácticas por parte de los alumnos, se ha desarrollado un nuevo proyecto de&#13;
innovación docente basado en imágenes interactivas que contienen varios botones con diferentes funcionalidades&#13;
(textos explicativos y audios, fotografías de diferentes aumentos de cada preparación, señalización&#13;
de elementos, preguntas de repaso, etc.). Comparando los resultados académicos de los alumnos&#13;
de los cursos en los que se utilizaron las imágenes interactivas con aquellos en los que no, se observó&#13;
una mejora del rendimiento académico. Además, las encuestas de satisfacción realizadas a los alumnos&#13;
mostraron que éstos tenían una muy buena opinión de las imágenes interactivas y afirmaron que les ha&#13;
sido muy útil para ayudarles en la asimilación de los conceptos prácticos de la asignatura. Por lo tanto,&#13;
se puede concluir que las imágenes interactivas podrían considerarse una herramienta eficaz para ayudar&#13;
a los estudiantes a adquirir habilidades prácticas en el área de Histología.
</summary>
<dc:date>2025-11-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>An animal ex vivo model comparing two different methods of sinus floor elevation with great elevation heights: Macroscopic, microscopic and radiological analysis</title>
<link href="http://hdl.handle.net/10366/170799" rel="alternate"/>
<author>
<name>Fernández Castellano, Erick Rafael</name>
</author>
<author>
<name>Benito Garzón, Lorena</name>
</author>
<author>
<name>Márquez Sánchez, Magaly Teresa</name>
</author>
<author>
<name>Flores Fraile, Javier</name>
</author>
<id>http://hdl.handle.net/10366/170799</id>
<updated>2026-03-26T01:01:10Z</updated>
<published>2024-10-22T00:00:00Z</published>
<summary type="text">[EN]Introduction: Maxillary sinus pneumatization increases with age and tooth loss, leading&#13;
to a reduction in the maxillary alveolar ridge, which often results in insufficient bone height for the&#13;
proper placement of dental implants. This study focused on performing maxillary sinus elevations&#13;
in ex vivo bisected pig heads using novel access and elevation devices, comparing these with the&#13;
osteotome sinus floor elevation (OSFE) technique. Materials and Methods:An experimental study&#13;
was conducted using 20 ex vivo adult pig heads. The sinus elevations were divided into two groups:&#13;
10 heads were treated using the osteotome technique, and 10 heads were treated using a new device,&#13;
which consists of a syringe with latex and saline solution, as well as a burr system for membrane&#13;
access and control. Results: In the osteotome technique, perforations of the Schneiderian membrane&#13;
were observed, whereas the inflatable balloon device did not cause any lacerations. Conclusions:&#13;
OSFE resulted in sinus membrane perforations at greater elevation heights, while the new balloon&#13;
device successfully elevated the membrane without tearing it. Within the limitations of this study,&#13;
maxillary sinus lifts using the new balloon technique proved to be minimally invasive procedures.
</summary>
<dc:date>2024-10-22T00:00:00Z</dc:date>
</entry>
<entry>
<title>Osteogenic potential of a biomaterial enriched with osteostatin and mesenchymal stem cells in osteoporotic rabbits</title>
<link href="http://hdl.handle.net/10366/170791" rel="alternate"/>
<author>
<name>Luengo Alonso, Gonzalo</name>
</author>
<author>
<name>Bravo Jiménez, Beatriz</name>
</author>
<author>
<name>Lozano, Daniel</name>
</author>
<author>
<name>Heras, Clara</name>
</author>
<author>
<name>Sánchez Salcedo, Sandra</name>
</author>
<author>
<name>Benito Garzón, Lorena</name>
</author>
<author>
<name>Abella, Monica</name>
</author>
<author>
<name>Vallet-Regí, María</name>
</author>
<author>
<name>Cecilia-López, David</name>
</author>
<author>
<name>Salinas, Antonio J.</name>
</author>
<id>http://hdl.handle.net/10366/170791</id>
<updated>2026-03-26T01:00:22Z</updated>
<published>2024-01-23T00:00:00Z</published>
<summary type="text">[EN]Mesoporous bioactive glasses (MBGs) of the SiO2–CaO–P2O5 system are biocompatible&#13;
materials with a quick and effective in vitro and in vivo bioactive response. MBGs can be enhanced&#13;
by including therapeutically active ions in their composition, by hosting osteogenic molecules&#13;
within their mesopores, or by decorating their surfaces with mesenchymal stem cells (MSCs). In&#13;
previous studies, our group showed that MBGs, ZnO-enriched and loaded with the osteogenic peptide&#13;
osteostatin (OST), and MSCs exhibited osteogenic features under in vitro conditions. The aim&#13;
of the present study was to evaluate bone repair capability after large bone defect treatment in distal&#13;
femur osteoporotic rabbits using MBGs (76%SiO2–15%CaO–5%P2O5–4%ZnO (mol-%)) before and&#13;
after loading with OST and MSCs from a donor rabbit. MSCs presence and/or OST in scaffolds significantly&#13;
improved bone repair capacity at 6 and 12 weeks, as confirmed by variations observed in&#13;
trabecular and cortical bone parameters obtained by micro-CT as well as histological analysis results.&#13;
A greater effect was observed when OST and MSCs were combined. These findings may indicate&#13;
the great potential for treating critical bone defects by combining MBGs with MSCs and osteogenic&#13;
peptides such as OST, with good prospects for translation to clinical practice.
</summary>
<dc:date>2024-01-23T00:00:00Z</dc:date>
</entry>
<entry>
<title>Differential role of the RasGEFs Sos1 and Sos2 in mouse skin homeostasis and carcinogenesis</title>
<link href="http://hdl.handle.net/10366/169724" rel="alternate"/>
<author>
<name>Liceras Boillos, Pilar</name>
</author>
<author>
<name>Jimeno García, David</name>
</author>
<author>
<name>García Navas, Rósula Mercedes</name>
</author>
<author>
<name>Lorenzo Martín, Luis Francisco</name>
</author>
<author>
<name>Menacho Márquez, Mauricio Ariel</name>
</author>
<author>
<name>Segrelles, Carmen</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Calzada, Nuria</name>
</author>
<author>
<name>Fuentes Mateos, Rocío</name>
</author>
<author>
<name>Paramio, Jesús M</name>
</author>
<author>
<name>Bustelo, Xosé R.</name>
</author>
<author>
<name>Baltanás, Fernando C.</name>
</author>
<author>
<name>Santos de Dios, Eugenio Miguel</name>
</author>
<id>http://hdl.handle.net/10366/169724</id>
<updated>2026-02-12T01:00:57Z</updated>
<published>2018-01-01T00:00:00Z</published>
<summary type="text">[EN]ABSTRACT Using Sos1 knockout (Sos1-KO), Sos2-KO, and Sos1/2 double-knockout&#13;
(Sos1/2-DKO) mice, we assessed the functional role of Sos1 and Sos2 in skin homeostasis under physiological and/or pathological conditions. Sos1 depletion resulted in&#13;
significant alterations of skin homeostasis, including reduced keratinocyte proliferation, altered hair follicle and blood vessel integrity in dermis, and reduced adipose&#13;
tissue in hypodermis. These defects worsened significantly when both Sos1 and Sos2&#13;
were absent. Simultaneous Sos1/2 disruption led to severe impairment of the ability&#13;
to repair skin wounds, as well as to almost complete ablation of the neutrophilmediated inflammatory response in the injury site. Furthermore, Sos1 disruption delayed the onset of tumor initiation, decreased tumor growth, and prevented malignant progression of papillomas in a DMBA (7,12-dimethylbenz[]anthracene)/TPA&#13;
(12-O-tetradecanoylphorbol-13-acetate)-induced skin carcinogenesis model. Finally,&#13;
Sos1 depletion in preexisting chemically induced papillomas resulted also in decreased tumor growth, probably linked to significantly reduced underlying keratinocyte proliferation. Our data unveil novel, distinctive mechanistic roles of Sos 1 and&#13;
Sos2 in physiological control of skin homeostasis and wound repair, as well as in&#13;
pathological development of chemically induced skin tumors. These observations&#13;
underscore the essential role of Sos proteins in cellular proliferation and migration&#13;
and support the consideration of these RasGEFs as potential biomarkers/therapy targets in Ras-driven epidermal tumors.
</summary>
<dc:date>2018-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Phosphorylation of SOS1 on tyrosine 1196 promotes its RAC GEF activity and contributes to BCR-ABL leukemogenesis</title>
<link href="http://hdl.handle.net/10366/169720" rel="alternate"/>
<author>
<name>Gerboth, S.</name>
</author>
<author>
<name>Frittoli, E.</name>
</author>
<author>
<name>Palamiessi, A.</name>
</author>
<author>
<name>Baltanas, F. C.</name>
</author>
<author>
<name>Salek, M.</name>
</author>
<author>
<name>Rappsilber, J.</name>
</author>
<author>
<name>Giuliani, C.</name>
</author>
<author>
<name>Troglio, F.</name>
</author>
<author>
<name>Rolland, Y.</name>
</author>
<author>
<name>Pruneri, G.</name>
</author>
<author>
<name>Kreutmair, S.</name>
</author>
<author>
<name>Pallavicini, I.</name>
</author>
<author>
<name>Zobel, M.</name>
</author>
<author>
<name>Cinquanta, M.</name>
</author>
<author>
<name>Minucci, S.</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Santos de Dios, Eugenio Miguel</name>
</author>
<author>
<name>Illert, A. L.</name>
</author>
<author>
<name>Scita, G.</name>
</author>
<id>http://hdl.handle.net/10366/169720</id>
<updated>2026-02-12T01:00:54Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">[EN]Son of Sevenless 1 (SOS1) is a dual guanine nucleotide exchange factor (GEF) that activates the small GTPases RAC and RAS. Although the molecular mechanisms of RAS GEF catalysis have been unveiled, how SOS1 acquires RAC GEF activity and what is the physio-pathological relevance of this activity is much less understood. Here we show that SOS1 is tyrosine phosphorylated on Y1196 by ABL. Phosphorylation of Y1196 controls SOS1 inter-molecular interaction, is required to promote the exchange of nucleotides on RAC in vitro and for platelet-derived growth factor (PDGF) activation of RAC- and RAC-dependent actin remodeling and cell migration. SOS1 is also phosphorylated on Y1196 by BCR-ABL in chronic myelogenous leukemic cells. Importantly, in these cells, SOS1 is required for BCR-ABL-mediated activation of RAC, cell proliferation and transformation in vitro and in a xenograft mouse model. Finally, genetic removal of Sos1 in the bone marrow-derived cells (BMDCs) from Sos1fl/fl mice and infected with BCR-ABL causes a significant delay in the onset of leukemogenesis once BMDCs are injected into recipient, lethally irradiated mice. Thus, SOS1 is required for full transformation and critically contribute to the leukemogenic potential of BCR-ABL.
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Pax6 Is essential for the maintenance and multi-lineage differentiation of neural stem cells, and for neuronal incorporation into the adult olfactory bulb</title>
<link href="http://hdl.handle.net/10366/169693" rel="alternate"/>
<author>
<name>Curto, Gloria G.</name>
</author>
<author>
<name>Nieto Estévez, Vanesa</name>
</author>
<author>
<name>Hurtado Chong, Anahí</name>
</author>
<author>
<name>Valero, Jorge</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<author>
<name>Vicario-Abejón, Carlos</name>
</author>
<id>http://hdl.handle.net/10366/169693</id>
<updated>2026-02-11T01:00:51Z</updated>
<published>2014-01-01T00:00:00Z</published>
<summary type="text">[EN]The paired type homeobox 6 (Pax6) transcription factor (TF) regulates multiple aspects of neural stem cell&#13;
(NSC) and neuron development in the embryonic central nervous system. However, less is known about the role&#13;
of Pax6 in the maintenance and differentiation of adult NSCs and in adult neurogenesis. Using the + /SeyDey&#13;
mouse, we have analyzed how Pax6 heterozygosis influences the self-renewal and proliferation of adult ol factory bulb stem cells (aOBSCs). In addition, we assessed its influence on neural differentiation, neuronal&#13;
incorporation, and cell death in the adult OB, both in vivo and in vitro. Our results indicate that the Pax6&#13;
mutation alters Nestin + -cell proliferation in vivo, as well as self-renewal, proliferation, and survival of aOBSCs&#13;
in vitro although a subpopulation of + /SeyDey progenitors is able to expand partially similar to wild-type&#13;
progenitors. This mutation also impairs aOBSC differentiation into neurons and oligodendrocytes, whereas it&#13;
increases cell death while preserving astrocyte survival and differentiation. Furthermore, Pax6 heterozygosis&#13;
causes a reduction in the variety of neurochemical interneuron subtypes generated from aOBSCs in vitro and in&#13;
the incorporation of newly generated neurons into the OB in vivo. Our findings support an important role of&#13;
Pax6 in the maintenance of aOBSCs by regulating cell death, self-renewal, and cell fate, as well as in neuronal&#13;
incorporation into the adult OB. They also suggest that deregulation of the cell cycle machinery and TF&#13;
expression in aOBSCs which are deficient in Pax6 may be at the origin of the phenotypes observed in this adult&#13;
NSC population.
</summary>
<dc:date>2014-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Ras-GRF2 regulates nestin-positive stem cell density and onset of differentiation during adult neurogenesis in the mouse dentate gyrus</title>
<link href="http://hdl.handle.net/10366/169690" rel="alternate"/>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Jimeno García, David</name>
</author>
<author>
<name>Fernández Medarde, Alberto</name>
</author>
<author>
<name>García Navas, Rósula Mercedes</name>
</author>
<author>
<name>Calzada, Nuria</name>
</author>
<author>
<name>Santos de Dios, Eugenio Miguel</name>
</author>
<id>http://hdl.handle.net/10366/169690</id>
<updated>2026-02-11T01:00:55Z</updated>
<published>2017-01-01T00:00:00Z</published>
<summary type="text">[EN]Various parameters of neurogenesis were analyzed in parallel in the two neurogenic areas (the Dentate Gyrus[DG] and the Subventricular Zone[SVZ]/Rostral Migratory Stream[RMS]/Main Olfactory Bulb[MOB] neurogenic system) of adult WT and KO mouse strains for the Ras-GRF1/2 genes (Ras-GRF1-KO, Ras-GRF2-KO, Ras-GRF1/2-DKO). Significantly reduced numbers of doublecortin[DCX]-positive cells were specifically observed in the DG, but not the SVZ/RMS/MOB neurogenic region, of Ras-GRF2-KO and Ras-GRF1/2-DKO mice indicating that this novel Ras-GRF2-dependent phenotype is spatially restricted to a specific neurogenic area. Consistent with a role of CREB as mediator of Ras-GRF2 function in neurogenesis, the density of p-CREB-positive cells was also specifically reduced in all neurogenic regions of Ras-GRF2-KO and DKO mice. Similar levels of early neurogenic proliferation markers (Ki67, BrdU) were observed in all different Ras-GRF genotypes analyzed but significantly elevated levels of nestin-immunolabel, particularly of undifferentiated, highly ramified, A-type nestin-positive neurons were specifically detected in the DG but not the SVZ/RMS/MOB of Ras-GRF2-KO and DKO mice. Together with assays of other neurogenic markers (GFAP, Sox2, Tuj1, NeuN), these observations suggest that the deficit of DCX/p-CREB-positive cells in the DG of Ras-GRF2-depleted mice does not involve impaired neuronal proliferation but rather delayed transition from the stem cell stage to the differentiation stages of the neurogenic process. This model is also supported by functional analyses of DG-derived neurosphere cultures and transcriptional characterization of the neurogenic areas of mice of all relevant Ras-GRF genotypes suggesting that the neurogenic role of Ras-GRF2 is exerted in a cell-autonomous manner through a specific transcriptional program.
</summary>
<dc:date>2017-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>RasGRF2 controls nuclear migration in postnatal retinal cone photoreceptors</title>
<link href="http://hdl.handle.net/10366/169689" rel="alternate"/>
<author>
<name>Jimeno García, David</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Calzada, Nuria</name>
</author>
<author>
<name>Villa, Pedro de la</name>
</author>
<author>
<name>Lillo Delgado, María Concepción</name>
</author>
<author>
<name>Santos de Dios, Eugenio Miguel</name>
</author>
<id>http://hdl.handle.net/10366/169689</id>
<updated>2026-02-11T01:00:54Z</updated>
<published>2016-01-01T00:00:00Z</published>
<summary type="text">[EN]Detailed immunocytochemical analyses comparing wild-type (WT), GRF1-knockout (KO), GRF2-KO and GRF1/2 double-knockout (DKO) mouse retinas uncovered the specific accumulation of misplaced, ‘ectopic’ cone photoreceptor nuclei in the photoreceptor segment (PS) area of retinas from GRF2-KO and GRF1/2-DKO, but not of WT or GRF1-KO mice. Localization of ectopic nuclei in the PS area of GRF2-depleted retinas occurred postnatally and peaked between postnatal day (P)11 and P15. Mechanistically, the generation of this phenotype involved disruption of the outer limiting membrane and intrusion into the PS layer by cone nuclei displaying significant perinuclear accumulation of signaling molecules known to participate in nuclear migration and cytoskeletal reorganization, such as PAR3, PAR6 and activated, phosphorylated forms of PAK, MLC2 and VASP. Electroretinographic recordings showed specific impairment of cone-mediated retinal function in GRF2-KO and GRF1/2-DKO retinas compared with WT controls. These data identify defective cone nuclear migration as a novel phenotype in mouse retinas lacking GRF2 and support a crucial role of GRF2 in control of the nuclear migration processes required for proper postnatal development and function of retinal cone photoreceptors.
</summary>
<dc:date>2016-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Chemical characterization of Pax6-immunoreactive periglomerular neurons in the mouse olfactory bulb</title>
<link href="http://hdl.handle.net/10366/169685" rel="alternate"/>
<author>
<name>Baltanás, Fernando C.</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<author>
<name>Murias, Azucena R.</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Curto, Gloria G.</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169685</id>
<updated>2026-02-11T01:00:49Z</updated>
<published>2009-01-01T00:00:00Z</published>
<summary type="text">[EN]The Pax6 transcription factor is a key element along brain development in both the visual and olfactory systems. The involvement of Pax6 in neural fate is well documented in the visual system, whereas in the olfactory system, and in particular in the olfactory bulb (OB), its expression during adulthood has only begun to be elucidated. In the OB, the modulation of primary sensory information is first performed by periglomerular cells (PG). A considerable body of information has unveiled the neurochemical heterogeneity of these neurons. Thus it is well known that Pax6 coexists with dopaminergic/GABAergic mouse PG. However, the presence of this transcription factor in other mouse PG subpopulations has not been studied. Here, we analyzed whether Pax6 is expressed in PG containing the calcium-binding proteins neurocalcin and parvalbumin, and the neuropeptide cholecystokinin. Our results show that Pax6 is not expressed by these PG subpopulations, suggesting that it is mainly restricted to GABAergic PG populations. These findings provide new data in the chemical characterization of mouse Pax6-positive PG.
</summary>
<dc:date>2009-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Changes in the connections of the main olfactory bulb after mitral cell selective neurodegeneration</title>
<link href="http://hdl.handle.net/10366/169654" rel="alternate"/>
<author>
<name>Recio, Javier S.</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Valero, Jorge</name>
</author>
<author>
<name>Briñón, Jesús G.</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169654</id>
<updated>2026-02-10T01:03:35Z</updated>
<published>2007-01-01T00:00:00Z</published>
<summary type="text">[EN]The connections of the main olfactory bulb (OB) of themouse were studied with iontophoretic injections of bi-otinylated dextran amine. To sort efferences from mitralcells and tufted cells, the Purkinje cell degeneration(PCD) mouse was used. This mutant animal undergoesa speciﬁc neurodegeneration of mitral cells, whereastufted cells do not degenerate. The unilateral tracerinjections used were small and conﬁned largely to theOB of both PCD and control mice at P120. Seven daysafter tracer injection, the efferences from the OB andthe centrifugal afferences from secondary olfactorystructures to it were studied. Although there is a largeoverlap of their target ﬁelds, mitral cell axons inner-vated more caudal regions of the olfactory cortex thantufted cell axons, thus providing deﬁnitive evidence ofthe differential projections of olfactory output neurons.Additionally, an important increase in retrogradely-labeled neurons was detected in the ipsilateral anteriorolfactory nucleus of the mutant animals. This was notobserved in any other secondary olfactory structure,suggesting a strengthening of the centrifugal input tothe OB from that central area after mitral cell loss.Moreover, we recorded a complete loss of bilaterality inthe olfactory connections of the PCD mice due todegeneration of the anterior commissure. These resultspoint to an important reorganization of this essentialolfactory circuit between the anterior olfactory nucleusand the OB, and hint at a transsynaptic level of plastic-ity not considered previously in literature
</summary>
<dc:date>2007-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Changes in cell migration and survival in the olfactory bulb of the pcd/pcd mouse</title>
<link href="http://hdl.handle.net/10366/169645" rel="alternate"/>
<author>
<name>Valero , Jorge</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<author>
<name>Murias, A.R.</name>
</author>
<author>
<name>Recio, J.S.</name>
</author>
<author>
<name>Curto, G. G.</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169645</id>
<updated>2026-02-10T01:01:54Z</updated>
<published>2007-01-01T00:00:00Z</published>
<summary type="text">[EN]Postnatally, the Purkinje cell degen-eration mutant mice lose the main projecting neurons ofthe main olfactory bulb (OB): mitral cells (MC). Inadult animals, progenitor cells from the rostral migra-tory stream (RMS) differentiate into bulbar interneur-ons that modulate MC activity. In the present work, westudied changes in proliferation, tangential migration,radial migration patterns, and the survival of thesenewly generated neurons in this neurodegeneration ani-mal model. The animals were injected with bromodeoxy-uridine 2 weeks or 2 months before killing in order tolabel neuroblast incorporation into the OB and to ana-lyze the survival of these cells after differentiation,respectively. Both the organization and cellular compo-sition of the RMS and the differentiation of the newly generated neurons in the OB were studied using speciﬁcmarkers of glial cells, neuroblasts, and mature neurons.No changes were observed in the cell proliferation ratenor in their tangential migration through the RMS, indi-cating that migrating neuroblasts are only weakly re-sponsive to the alteration in their target region, the OB.However, the absence of MC does elicit differences inthe ﬁnal destination of the newly generated interneur-ons. Moreover, the loss of MC also produces changes inthe survival of the newly generated interneurons, in ac-cordance with the dramatic decrease in the number ofsynaptic targets available
</summary>
<dc:date>2007-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Chemical organization of the macaque monkey olfactory bulb: III. Distribution of cholinergic markers</title>
<link href="http://hdl.handle.net/10366/169644" rel="alternate"/>
<author>
<name>Porteros Herrero, Ángel Fernando</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Valero, Jorge</name>
</author>
<author>
<name>Calvo Baltanás, Fernando</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169644</id>
<updated>2026-02-10T01:01:44Z</updated>
<published>2007-01-01T00:00:00Z</published>
<summary type="text">[EN]The distribution patterns of choline acetyltransferase (ChAT) and acetylcholinesterase(AChE) were studied in the olfactory bulb (OB) of three species of macaque. AChE wasdetected by a histochemical method and ChAT immunoreactivity by immunocytochemistry.Similar results were observed in all species analyzed. With the exception of the olfactorynerve layer, all layers of the macaque monkey OB demonstrated a dense innervation ofAChE- and ChAT-positive ﬁbers. The distribution patterns of AChE- and ChAT-labeled ﬁberswere similar for both cholinergic markers, although the number of AChE-labeled ﬁbers wasclearly higher than the number of ChAT-immunoreactive ﬁbers. The highest density of AChEand ChAT-stained ﬁbers was observed in the interface between the glomerular layer and theexternal plexiform layer and in the internal plexiform layer. Dense bundles of labeled ﬁberswere observed in the caudal OB, coursing from the olfactory peduncle. All ChAT-immunopositive elements were identiﬁed as centrifugal ﬁbers, derived from neurons caudalto the OB. Neither olfactory ﬁbers nor intrinsic neurons were observed after ChAT immu-nocytochemistry. However, a few AChE-positive cells were observed in the glomerular layerand in both external and internal plexiform layers. These neurons were presumably identi-ﬁed as periglomerular cells, superﬁcial short-axon cells, and/or external tufted cells and deepshort-axon cells. Contrary to other neurotransmitters and neuroactive substances, the dis-tribution patterns of ChAT and AChE activities in the macaque monkey OB closely resem-bled the patterns described in macrosmatic mammals and showed laminar differences withthe distribution pattern observed in humans.
</summary>
<dc:date>2007-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Sex differences in catechol contents in the olfactory bulb of control and unilaterally deprived rats</title>
<link href="http://hdl.handle.net/10366/169640" rel="alternate"/>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Briñón, J.G.</name>
</author>
<author>
<name>Valero , Jorge</name>
</author>
<author>
<name>Recio, J.S.</name>
</author>
<author>
<name>Murias, A. R.</name>
</author>
<author>
<name>Curto, G. G.</name>
</author>
<author>
<name>Orio, L.</name>
</author>
<author>
<name>Colado, M. I.</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169640</id>
<updated>2026-02-10T01:01:46Z</updated>
<published>2007-01-01T00:00:00Z</published>
<summary type="text">[EN]The dopaminergic system plays important roles in the modulation of olfactory transmission. The present study examines the&#13;
distribution of dopaminergic cells and the content of dopamine (DA) and its metabolites in control and deprived olfactory bulbs (OB),&#13;
focusing on the differences between sexes. The content of DA and of its metabolites, dihydroxyphenylacetic acid (DOPAC) and&#13;
homovanillic acid (HVA), were measured by HPLC. The morphology and distribution of dopaminergic neurons were studied using&#13;
tyrosine hydroxylase (TH) immunohistochemistry. Cells were typified with TH–parvalbumin, TH–cholecystokinin or TH–neurocalcin&#13;
double-immunofluorescence assays. Biochemical analyses revealed sex differences in the content of DA and of its metabolites. In&#13;
normal conditions, the OBs of male rats had higher concentrations of DA, DOPAC and HVA than the OBs of females. The&#13;
immunohistochemical data pointed to sex differences in the number of TH-immunopositive cells (higher in male than in female rats).&#13;
Colocalization analyses revealed that dopaminergic cells constitute a different cell subpopulation from those labelled after&#13;
parvalbumin, cholecystokinin or neurocalcin immunostaining. Unilateral olfactory deprivation caused dramatic alterations in the&#13;
dopaminergic system. The DA content and the density of dopaminergic cells decreased, the contents of DA and DOPAC as well as&#13;
TH immunoreactivity were similar in deprived males and females and, finally, the metabolite ⁄ neurotransmitter ratio increased. Our&#13;
results show that the dopaminergic modulation of olfactory transmission seems to differ between males and females and that it is&#13;
regulated by peripheral olfactory activity. A possible role of the dopaminergic system in the sexually different olfactory sensitivity,&#13;
discrimination and memory is discussed
</summary>
<dc:date>2007-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Differential glial activation during the degeneration of Purkinje cells and mitral cells in the PCD mutant mice</title>
<link href="http://hdl.handle.net/10366/169624" rel="alternate"/>
<author>
<name>Baltanás, Fernando C.</name>
</author>
<author>
<name>Berciano, María T.</name>
</author>
<author>
<name>Valero Gómez Lobo, Jorge</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Díaz López, David</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<author>
<name>Lafarga, Miguel</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<id>http://hdl.handle.net/10366/169624</id>
<updated>2026-02-10T01:01:56Z</updated>
<published>2012-01-01T00:00:00Z</published>
<summary type="text">[EN]Purkinje Cell Degeneration (PCD) mice harbor a nna1 genemutation which leads to an early and rapid degeneration ofPurkinje cells (PC) between the third and fourth week ofage. This mutation also underlies the death of mitral cells(MC) in the olfactory bulb (OB), but this process is slowerand longer than in PC. No clear interpretations supportingthe marked differences in these neurodegenerative proc-esses exist. Growing evidence suggests that either beneﬁ-cial or detrimental effects of gliosis in damaged regionswould underlie these divergences. Here, we examined thegliosis occurring during PC and MC death in the PCDmouse. Our results demonstrated different glial reactionsin both affected regions. PC disappearance stimulated asevere gliosis characterized by strong morphologicalchanges, enhanced glial proliferation, as well as the releaseof pro-inﬂammatory mediators. By contrast, MC degenera-tion seems to promote a more attenuated glial response inthe PCD OB compared with that of the cerebellum. Strik-ingly, cerebellar oligodendrocytes died by apoptosis in thePCD, whereas bulbar ones were not affected. Interestingly,the level of nna1 mRNA under normal conditions washigher in the cerebellum than in the OB, probably relatedto a faster neurodegeneration and stronger glial reaction inits absence. The glial responses may thus inﬂuence theneurodegenerative course in the cerebellum and OB of themutant mouse brain, providing harmful and beneﬁcialmicroenvironments, respectively
</summary>
<dc:date>2012-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Zincergic innervation from the anterior olfactory nucleus to the olfactory bulb displays plastic responses after mitral cell loss</title>
<link href="http://hdl.handle.net/10366/169621" rel="alternate"/>
<author>
<name>Airado, Carmen</name>
</author>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Sánchez Recio, Javier</name>
</author>
<author>
<name>Baltanás, Fernando C.</name>
</author>
<author>
<name>Weruaga Prieto, Eduardo</name>
</author>
<author>
<name>Alonso Peña, José Ramón</name>
</author>
<id>http://hdl.handle.net/10366/169621</id>
<updated>2026-02-10T01:01:55Z</updated>
<published>2008-01-01T00:00:00Z</published>
<summary type="text">[EN]Zinc ions are selectively accumulated in certain neurons (zinc-enriched neurons). The mouse olfactory bulb is richly innervated by zinc-enriched terminals. Here, the plasticity of the zincergic system was studied in the olfactory bulb of the Purkinje Cell Degeneration mutant mouse, an animal with specific postnatal neurodegeneration of the main projection neurons of the olfactory bulb. The analysis focused particularly on the anterior olfactory nucleus since most centrifugal afferents coming to the olfactory bulb arise from this structure. Zinc-enriched terminals in the olfactory bulb and zinc-enriched somata in the anterior olfactory nucleus were visualized after selenite injections. Immunohistochemistry against the vesicular zinc transporter was also carried out to confirm the distribution pattern of zinc-enriched terminals in the olfactory bulb. The mutant mice showed a clear reorganization of zincergic centrifugal projections from the anterior olfactory nucleus to the olfactory bulb. First, all zincergic contralateral neurons projecting to the olfactory bulb were absent in the mutant mice. Second, a significant increase in the number of stained somata was detected in the ipsilateral anterior olfactory nucleus. Since no noticeable changes were observed in the zinc-enriched terminals in the olfactory bulb, it is conceivable that mitral cell loss could induce a reorganization of zinc-enriched projections coming from the anterior olfactory nucleus, probably directed at balancing the global zincergic centrifugal modulation. These results show that zincergic anterior olfactory nucleus cells projecting to the olfactory bulb undergo plastic changes to adapt to the loss of mitral cells in the olfactory bulb of Purkinje Cell Degeneration mutant mice.
</summary>
<dc:date>2008-01-01T00:00:00Z</dc:date>
</entry>
<entry>
<title>Differential effects of unilateral olfactory deprivation on noradrenergic and cholinergic systems in the main olfactory bulb of the rat</title>
<link href="http://hdl.handle.net/10366/169616" rel="alternate"/>
<author>
<name>Gómez Rodríguez, Carmela</name>
</author>
<author>
<name>Briñón, J.G.</name>
</author>
<author>
<name>Colado, M. I.</name>
</author>
<author>
<name>Orio, L.</name>
</author>
<author>
<name>Vidal, M.</name>
</author>
<author>
<name>Barbado, M.V.</name>
</author>
<author>
<name>Alonso, J.R.</name>
</author>
<id>http://hdl.handle.net/10366/169616</id>
<updated>2026-02-10T01:01:40Z</updated>
<published>2006-01-01T00:00:00Z</published>
<summary type="text">[EN]The lack of environmental olfactory stimulation produced by sensory deprivation causes significant changes in the deprived olfactory bulb. Olfactory transmission in the main olfactory bulb (MOB) is strongly modulated by centrifugal systems. The present report examines the effects of unilateral deprivation on the noradrenergic and cholinergic centrifugal systems innervating the MOB. The morphology, distribution, and density of positive axons were studied in the MOBs of control and deprived rats, using dopamine-beta-hydroxylase (DBH)-immunohistochemistry and acetylcholinesterase (AChE) histochemistry in serial sections. Catecholamine content was compared among the different groups of MOBs (control, contralateral, and ipsilateral to the deprivation) using high-performance liquid chromatography analysis. Sensory deprivation revealed that the noradrenergic system developed adaptive plastic changes after olfactory deprivation, including important modifications in its fiber density and distribution, while no differences in cholinergic innervation were observed under the same conditions. The noradrenergic system underwent an important alteration in the glomerular layer, in which some glomeruli showed a dense noradrenergic innervation that was not detected in control animals. The DBH-positive glomeruli with the highest noradrenergic fiber density were compared with AChE-stained sections and it was observed that the strongly noradrenergic-innervated glomeruli were always atypical glomeruli (characterized by their strong degree of cholinergic innervation). In addition to the morphological findings, our biochemical data revealed that olfactory deprivation caused a decrease in the content of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid in the ipsilateral MOB in comparison to the contralateral and control MOBs, together with an increase in noradrenaline levels in both the ipsilateral and contralateral MOBs. Our results show that regulation of the noradrenergic centrifugal system in the MOB depends on environmental olfactory stimulation and that it is highly reactive to sensory deprivation. By contrast, the cholinergic system is fairly stable and does not exhibit clear changes after the loss of sensory inputs.
</summary>
<dc:date>2006-01-01T00:00:00Z</dc:date>
</entry>
</feed>
