期刊
NEUROBIOLOGY OF AGING
卷 80, 期 -, 页码 29-37出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2019.03.014
关键词
Parkinson's disease; Alpha-synuclein; Serotonin; Prefrontal cortex; Serotonin transporter
资金
- University Hospital Erlangen, Germany [ELAN MN-12-08-06-1]
- Deutsche Forschungsgemeinschaft (DFG) [INST 410/45-1 FUGG]
- Bavarian Research Network for Induced Pluripotent Stem Cells (ForIPS)
- Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [270949263/GRK2162]
Axonal pathology precedes dopaminergic cell loss in Parkinson's disease (PD), indicating a dying back axonopathy of nigrostriatal projections. Although most attention focused on the dopaminergic system, increasing evidence implies a compromised serotonergic system in PD as well. By combining immunohistological and biochemical approaches, a profound layer-specific reduction of the serotonergic input to the prefrontal cortex (PFC) layers II and V/VI in aged mutant A53T alpha-synuclein-expressing mice (A53T mice) was detected. In addition, the altered fiber network was characterized by swollen axons and enlarged axonal varicosities within all PFC layers, but most pronounced in PFC layer I. Although prefrontal serotonin levels and synaptic protein expression were preserved, aged A53T mice showed increased levels of kinesin family member 1a and vesicular monoamine transporter 2. Together with increased tryptophan hydroxylase 2 mRNA levels in the raphe nuclei and an elevated serotonin receptor 1b expression in the PFC, these findings point to compensatory mechanisms within the serotonergic system to overcome the reduced neuritic input to the PFC in this transgenic animal model for PD. (C) 2019 Elsevier Inc. All rights reserved.
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