Issue Cover (November 2018)

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+ cleara nce; (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 ...
Source: Journal of Neurochemistry - Category: Neurology Tags: Issue Cover Source Type: research