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Boyanova, S.

Publications and source records attributed to Boyanova, S..

2 recordsLinked to original sources

Using machine learning to automate the analysis of an olfactory habituation-dishabituation task in mice

IntroductionImproving the efficiency and accuracy of annotation and extraction of performance data from mouse behavioural tasks will improve both the throughput and scientific value of preclinical research. MethodsHere, we present and validate an automated pipeline for the annotation and quantification of performance in a mouse olfactory habituation-dishabituation task, using a single side-view camera, resulting in occluded body parts. We created a pipeline for task analysis, combining DeepLabCut, for pose-estimation, and SimBA, for behavioural classification to automatically quantify odour interaction (sniffing time) in a three-odour (water, familiar mouse social odour, novel mouse social odour) variant of the task. We used a subset of previously published, fully manually annotated datasets to train the models and unseen videos from the same study to validate the utility of our machine learning pipeline. Results and conclusionOur analysis pipeline estimated behavioural performance in the task with high accuracy, and the data produces similar technical and biological results to manual methods when analysed by linear mixed modelling. Thus, we validated the utility of our new pipeline for the automated scoring of this mouse sensory task.

animal behavior and cognition↗

Enhanced mGluR1 function causes motor deficits and region-specific Purkinje cell dysfunction

Spinocerebellar ataxias (SCAs) are autosomal dominantly inherited neurodegenerative disorders with no effective treatment. Aberrant signalling through the metabotropic glutamate receptor (mGluR1) has been implicated in several SCAs. However, whether disease is caused through decreased or increased mGluR1 signalling remains controversial. Here, we generate the first mouse model of enhanced mGluR1 function by introducing a gain-of-function mutation (p.Y792C) that causes SCA44 in the metabotropic glutamate receptor 1 (Grm1) gene. Grm1 mutant mice recapitulate key pathophysiological aspects of SCA, including progressive motor deficits, altered climbing fibre innervation and perturbed Purkinje cell spontaneous activity. We report that changes in synaptic innervation and intrinsic Purkinje cell activity upon overactive mGluR1 signalling manifest in a lobule- and disease-stage-specific manner. Our findings demonstrate that enhanced mGluR1 function is a direct and specific driver of Purkinje cell dysfunction and pathology and provide a mechanism for understanding the selective vulnerability of different Purkinje cell populations in SCA.

neuroscience↗