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 PMID:15820695  

CAPS1 regulates catecholamine loading of large dense-core vesicles.

Dina Speidel | Cathrin E Bruederle | Carsten Enk | Thomas Voets | Frederique Varoqueaux | Kerstin Reim | Ute Becherer | Francesco Fornai | Stefano Ruggieri | Yvonne Holighaus | Eberhard Weihe | Dieter Bruns | Nils Brose | Jens Rettig
Neuron | 2005

CAPS1 is thought to play an essential role in mediating exocytosis from large dense-core vesicles (LDCVs). We generated CAPS1-deficient (KO) mice and studied exocytosis in a model system for Ca2+-dependent LDCV secretion, the adrenal chromaffin cell. Adult heterozygous CAPS1 KO cells display a gene dosage-dependent decrease of CAPS1 expression and a concomitant reduction in the number of docked vesicles and secretion. Embryonic homozygous CAPS1 KO cells show a strong reduction in the frequency of amperometrically detectable release events of transmitter-filled vesicles, while the total number of fusing vesicles, as judged by capacitance recordings or total internal reflection microscopy, remains unchanged. We conclude that CAPS1 is required for an essential step in the uptake or storage of catecholamines in LDCVs.

Pubmed ID: 15820695

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