<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-04-14T21:05:26Z</responseDate><request verb="GetRecord" identifier="oai:uvadoc.uva.es:10324/6341" metadataPrefix="dim">https://uvadoc.uva.es/oai/request</request><GetRecord><record><header><identifier>oai:uvadoc.uva.es:10324/6341</identifier><datestamp>2021-06-23T09:51:53Z</datestamp><setSpec>com_10324_1134</setSpec><setSpec>com_10324_931</setSpec><setSpec>com_10324_894</setSpec><setSpec>col_10324_1213</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
<dim:field mdschema="dc" element="contributor" qualifier="author" authority="6c6cfe3c63dd2c44" confidence="500" orcid_id="0000-0003-4573-7930">García-Sancho Martín, Francisco Javier</dim:field>
<dim:field mdschema="dc" element="contributor" qualifier="author" authority="5dea812b-5817-496a-85bf-cf25229b8d04" confidence="500" orcid_id="">Diego, Antonio M. G. de</dim:field>
<dim:field mdschema="dc" element="contributor" qualifier="author" authority="57f33cbe-6809-402a-b718-c5b537f4a80f" confidence="500" orcid_id="">García, Antonio G.</dim:field>
<dim:field mdschema="dc" element="date" qualifier="accessioned">2014-09-30T16:12:08Z</dim:field>
<dim:field mdschema="dc" element="date" qualifier="available">2014-09-30T16:12:08Z</dim:field>
<dim:field mdschema="dc" element="date" qualifier="issued">2012</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="citation" lang="es">Pflügers Archiv European Journal of Physiology, 2012, vol. 464, p. 33-41</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="issn" lang="es">0031-6768</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="uri">http://uvadoc.uva.es/handle/10324/6341</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="doi" lang="es">10.1007/s00424-012-1074-2</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="publicationfirstpage" lang="es">33</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="publicationlastpage" lang="es">41</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="publicationtitle" lang="es">Pflügers Archiv European Journal of Physiology</dim:field>
<dim:field mdschema="dc" element="identifier" qualifier="publicationvolume" lang="es">464</dim:field>
<dim:field mdschema="dc" element="description" lang="es">Producción Científica</dim:field>
<dim:field mdschema="dc" element="description" qualifier="abstract" lang="es">Chromaffin cells are an excellent model for stimulus–&#xd;
secretion coupling. Ca2+ entry through plasma membrane&#xd;
voltage-operated Ca2+ channels (VOCC) is the trigger&#xd;
for secretion, but the intracellular organelles contribute subtle&#xd;
nuances to the Ca2+ signal. The endoplasmic reticulum&#xd;
amplifies the cytosolic Ca2+ ([Ca2+]C) signal by Ca2+-&#xd;
induced Ca2+ release (CICR) and helps generation of microdomains&#xd;
with high [Ca2+]C (HCMD) at the subplasmalemmal&#xd;
region. These HCMD induce exocytosis of the docked&#xd;
secretory vesicles. Mitochondria close to VOCC take up&#xd;
large amounts of Ca2+ from HCMD and stop progression&#xd;
of the Ca2+ wave towards the cell core. On the other hand,&#xd;
the increase of [Ca2+] at the mitochondrial matrix stimulates&#xd;
respiration and tunes energy production to the increased&#xd;
needs of the exocytic activity. At the end of stimulation,&#xd;
[Ca2+]C decreases rapidly and mitochondria release the Ca2+&#xd;
accumulated in the matrix through the Na+/Ca2+ exchanger.&#xd;
VOCC, CICR sites and nearby mitochondria form functional&#xd;
triads that co-localize at the subplasmalemmal area, where&#xd;
secretory vesicles wait ready for exocytosis. These triads&#xd;
optimize stimulus–secretion coupling while avoiding&#xd;
propagation of the Ca2+ signal to the cell core. Perturbation&#xd;
of their functioning in neurons may contribute to the genesis&#xd;
of excitotoxicity, ageing mental retardation and/or neurodegenerative&#xd;
disorders.</dim:field>
<dim:field mdschema="dc" element="format" qualifier="mimetype" lang="es">application/pdf</dim:field>
<dim:field mdschema="dc" element="language" qualifier="iso" lang="es">eng</dim:field>
<dim:field mdschema="dc" element="publisher" lang="es">Springer-Verlag</dim:field>
<dim:field mdschema="dc" element="rights" qualifier="accessRights" lang="es">info:eu-repo/semantics/openAccess</dim:field>
<dim:field mdschema="dc" element="rights" qualifier="uri">http://creativecommons.org/licenses/by-nc-nd/4.0/</dim:field>
<dim:field mdschema="dc" element="rights">Attribution-NonCommercial-NoDerivatives 4.0 International</dim:field>
<dim:field mdschema="dc" element="subject" lang="es">Nervioso, Sistema - Enfermedades</dim:field>
<dim:field mdschema="dc" element="subject">Fisiología</dim:field>
<dim:field mdschema="dc" element="title" lang="es">Mitochondria and chromaffin cell function</dim:field>
<dim:field mdschema="dc" element="type" lang="es">info:eu-repo/semantics/article</dim:field>
<dim:field mdschema="dc" element="peerreviewed" lang="es">SI</dim:field>
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