Changes in intrinsic excitability of hippocampal pyramidal cells in Parkinsons disease model

Abstract

Parkinsons disease (PD) is the second most common fatal neurodegenerative disease in the world, and it reduces patients quality of life by causing movement disorders (e.g., tremors, muscle stiffness, and impaired balance) and non-motor disorders (e.g., depression, anxiety, and dementia). Previous research has mostly concentrated on dopamine-producing neurons in the substantia nigra compacta (SNc) that are dying off, which restricts therapeutic options and renders the search for disease-modifying therapies fruitless. In order to make a breakthrough, pathological changes in other brain areas deserve more attention. Previous PD studies reported atrophy in the hippocampus, an indispensable part of spatial and temporal memory formation. To answer the question of the cellular mechanism of hippocampus atrophy, this paper intends to research previously uncharted hippocampal intrinsic plasticity alterations. After analysing intercellular recordings of pyramidal neurons gathered from normal mice and genetically engineered PD mice, this paper demonstrates disparities in the intrinsic factors not noted in the previous research, such as peaks and afterhyperpolarization. These findings represent a progressive advancement in our comprehension of hippocampal pyramidal neurons, indicating potential therapeutic targets for Parkinsons disease treatment via SK channels, BK channels, and sodium channels.