112 research outputs found
Neurokinin 1 receptor antagonism promotes active stress coping via enhanced septal 5-HT transmission
Septal urocortin 3 modulates stress-coping behaviour but not hypothalamic-pituitary-adrenal axis activity during forced swimming
Modulation of magnesium deficiency-induced anxiety and HPA axis dysregulation by therapeutic drug treatment
Chronic treatment with a selective neurokinin-1 receptor antagonist in a mouse model of trait anxiety and depression: focus on behaviour and neuropeptidergic mechanisms
129S1/SvImJ mice display impaired contextual fear extinction, enhanced fear incubation and deficit extinction consolidation phenotypes: rescue via pharmacological and non-pharmacological treatments
Influence of estrous cycle on explorative behaviour of wild-type and prodynorphin knockout mice
Oligodendroglial alpha-synucleinopathy and MSA-like cardiovascular autonomic failure: Experimental evidence
AbstractMultiple system atrophy (MSA) is a fatal, rapidly progressive neurodegenerative disease with limited symptomatic treatment options. Discrimination of MSA from other degenerative disorders crucially depends on the presence of early and severe cardiovascular autonomic failure (CAF). We have previously shown that neuropathologic lesions in the central autonomic nuclei similar to the human disease are present in transgenic MSA mice generated by targeted oligodendroglial overexpression of α-syn using the PLP promoter. We here explore whether such lesions result in abnormalities of heart rate variability (HRV) and circadian rhythmicity which are typically impaired in MSA patients.HRV analysis was performed in five month old transgenic PLP-α-syn (tg) MSA mice and age-matched wild type controls. Decreased HRV and alterations in the circadian rhythmicity were detected in the tg MSA group. The number of choline-acetyltransferase-immunoreactive neurons in the nucleus ambiguus was significantly decreased in the tg group, whereas the levels of arginine-vasopressin neurons in the suprachiasmatic and paraventricular nucleus were not affected. Our finding of impaired HRV and circadian rhythmicity in tg MSA mice associated with degeneration of the nucleus ambiguus suggests that a cardinal non-motor feature of human MSA can be reproduced in the mouse model strengthening its role as a valuable testbed for studying selective vulnerability and assessing translational therapies
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