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Updated: Jun 13, 2025
Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
Activation of NMDAR/Ca2+/CaKMII/ROS pathway by Brucella induced neuronal cell apoptosis
Meiling Liu1, Hongfang Yu2, Yuzhe Wang2
1Department of Neurology, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Background:
Neurobrucellosis is an inflammatory disease of the central nervous system caused by brucellosis and is the most serious form of brucellosis. However, the pathogenesis of this disease is not well understood, and there are no suitable molecular markers for rapid diagnosis. In the present study, we infected neuronal cells and brain slices with cerebrospinal fluid from patients with bruceopathy.
Methods:
Neuron-specific enolase (NSE) levels were detected by immunofluorescence. Nissl staining, HE staining and transmission electron microscopy were used to observe nissl bodies and physiological. Calcium ion flow was detected by calcium ion fluorescence probe. The expression levels of related molecules were detected. Reactive oxygen species (ROS) levels and mitochondrial membrane potential were also measured.
Results:
The cerebrospinal fluid infected neurons and brain slice and activated kynurenine pathway (KP) lead to excessive activation of N-methyl-d-aspartate receptor (NMDAR), increased calcium flow, depolarization of mitochondrial membrane potential and increased ROS levels. This eventually leads to increased central nervous system (CNS) damage. The KP product quinolinic acid (QUIN) showed the same results as after infection with Brucella S2308.
Conclusion:
Collectively, our study supports that Brucella neurotype causes CNS damage via QUIN/NMDAR/Ca2+/CaKMII/ROS, which provides one possible therapeutic target for neurobrucellosis.
