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Neurotransmitter abnormalities in Borna disease.
W I Lipkin1, K M Carbone, M C Wilson
1Research Institute of Scripps Clinic, La Jolla, CA 92037.
Brain Research
|December 20, 1988
Summary
Borna disease (BD) infection in rats alters brain gene expression, affecting neuronal transcripts involved in behavior and persistently decreasing a specific transcript (MuBr8) throughout the infection course. This offers insights into inflammatory central nervous system (CNS) disease pathogenesis.
Area of Science:
- Neurovirology
- Molecular Neuroscience
- Pathogenesis of Infectious Diseases
Background:
- Borna disease (BD) is caused by an infectious agent leading to progressive central nervous system (CNS) dysfunction in vertebrates.
- BD in adult rats exhibits a biphasic course: an acute phase with aggression and brain inflammation, followed by a chronic phase with listlessness and inflammation resolution.
- BD antigens are found in neurons across various brain regions, including the hippocampus, neocortex, cerebellum, and brainstem, in both acute and chronic infections.
Purpose of the Study:
- To investigate changes in brain neuronal transcript levels during acute and chronic Borna disease infection in rats.
- To identify specific messenger RNAs (mRNAs) whose expression is altered by BD infection and correlate these changes with disease progression and antigen distribution.
Main Methods:
- Analysis of brain tissue from rats with experimentally induced acute and chronic Borna disease.
- Quantitative examination of neuronal transcript levels, including cholecystokinin, glutamic acid decarboxylase, somatostatin, and MuBr8 mRNA.
- Correlation of transcript level changes with the distribution of BD antigens in the CNS.
Main Results:
- Three neuronal transcripts (cholecystokinin, glutamic acid decarboxylase, somatostatin) showed decreased levels in acutely infected rats, with levels increasing towards normal in chronic infection.
- A fourth transcript, MuBr8, exhibited a distribution pattern similar to BD antigen and was persistently decreased throughout the course of infection.
- These transcript level changes suggest distinct molecular responses to acute versus chronic BD and a specific downregulation linked to viral presence.
Conclusions:
- Borna disease infection significantly alters the expression of specific neuronal transcripts in a manner that changes over the course of the disease.
- The persistent decrease in MuBr8 mRNA, correlating with BD antigen distribution, suggests its potential role in the pathogenesis of BD-induced neurological dysfunction.
- These findings contribute to understanding the molecular mechanisms underlying neurological disturbances in Borna disease and other inflammatory CNS diseases.