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Impaired pre-synaptic plasticity and visual responses in auxilin-knockout mice
Xi Cheng1, Yu Tang1, D J Vidyadhara2,3
1Department of Biological Sciences, Purdue Institute for Integrative Neuroscience, Purdue Autism Research Center, Purdue University, West Lafayette, IN 47907, USA.
Iscience
|September 28, 2023
Summary
Loss of auxilin (DNAJC6/PARK19) impairs synaptic vesicle recycling, leading to visual cortex dysfunction and motor deficits seen in Parkinson's disease.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Auxilin (DNAJC6/PARK19) is a crucial co-chaperone for synaptic vesicle endocytosis.
- Loss-of-function mutations in auxilin are linked to familial Parkinson's disease (PD).
Purpose of the Study:
- To investigate the role of auxilin in synaptic plasticity and visual cortical function.
- To understand the pre-synaptic endocytosis deficits in auxilin-knockout (Aux-KO) mice.
Main Methods:
- Utilized auxilin-knockout (Aux-KO) mouse models.
- Performed electrophysiological recordings in the primary visual cortex (V1).
- Employed computational modeling and pupillometry.
Main Results:
- Aux-KO mice showed impaired pre-synaptic plasticity (short-term facilitation and depression) in V1.
- Disrupted visual cortical circuit responses, including reduced orientation selectivity and altered theta oscillations.
- Deficits in visual mismatch negativity and optokinetic response were observed.
Conclusions:
- Auxilin is essential for maintaining pre-synaptic plasticity and normal visual cortical function.
- Auxilin-dependent endocytosis dysfunction contributes to early-stage Parkinson's disease-like symptoms.
