Journal of NeurochemistryVolume 147, Issue 4 Issue CoverFree Access Issue Cover (November 2018) First published: 26 November 2018 https://doi.org/10.1111/jnc.14201 Read the full article: ‘Altered excitability and exocytosis in chromaffin cells from the R6/1 mouse model of Huntington's disease is linked to over-expression of mutated huntingtin’ by C. Martínez-Ramírez, A. M. Baraibar, C. Nanclares, I. Méndez-López, A. Gómez, Ma. P. Muñoz, A. M. G. de Diego, L. Gandía, M. J. Casarejos, A. G. García (J. Neurochem. 2018, vol. 147 (4), pp. 454–476) on doi: 10.1111/jnc.14585 AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Graphical Abstract Front cover: Background: Neurodegenerative diseases are primarily linked to alterations of neurotransmitter release and synaptic plasticity in the brain. However, the peripheral sympatho-adrenal axis has been found to be also altered in some of those diseases. Here we present a study on morphological and functional alterations in adrenal chromaffin cells (CCs) of the R6/1 mouse model of Huntington's disease (HD). Main finding: We have found (i) huntingtin overexpression as nuclear aggregates in CCs; (ii) smaller CC size with decreased dopamine β-hydroxylase expression, indicating lesser number of chromaffin secretory vesicles; (iii) reduced adrenal tissue catecholamine content; (iv) reduced Na+ currents with (v) membrane hyperpolarisation and reduced ACh-evoked action potentials; (v) reduced [Ca2+]c transients with faster Ca2+ clearance; (vi) diminished quantal secretion with smaller vesicle quantal size; (vii) faster kinetics of the exocytotic fusion pore, pore expansion, and closure. Implications: As the sympatho-adrenal axis plays an essential role in adaptation to stress through the fight-or-flight response, this study suggests that such response could be sharply deteriorated in HD patients. Image Content: The image shows an immunohistochemical staining for mutated huntingtin (Htt) in adrenal medulla chromaffin cells of the R6/1 mice at predisease stages (2 months age, 2m) before phenotypic motor alterations appear. Read the full article ‘Altered excitability and exocytosis in chromaffin cells from the R6/1 mouse model of Huntington's disease is linked to over-expression of mutated huntingtin’ by C. Martínez-Ramírez, A. M. Baraibar, C. Nanclares, I. Méndez-López, A. Gómez, Ma. P. Muñoz, A. M. G. de Diego, L. Gandía, M. J. Casarejos, A. G. García (J. Neurochem. 2018, vol. 147 (4), pp. 454–476) on doi: 10.1111/jnc.14585 Volume147, Issue4November 2018 RelatedInformation