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Minocycline attenuates interferon-α-induced impairments in rat fear extinction

Overview of attention for article published in Journal of Neuroinflammation, January 2016
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Title
Minocycline attenuates interferon-α-induced impairments in rat fear extinction
Published in
Journal of Neuroinflammation, January 2016
DOI 10.1186/s12974-016-0638-z
Pubmed ID
Authors

Bi, Qiang, Shi, Lijuan, Yang, Pingting, Wang, Jianing, Qin, Ling

Abstract

Extinction of conditioned fear is an important brain function for animals to adapt to a new environment. Accumulating evidence suggests that innate immune cytokines are involved in the pathology of psychotic disorders. However, the involvement of cytokines in fear dysregulation remains less investigated. In the present study, we investigated how interferon (IFN)-α disrupts the extinction of conditioned fear and propose an approach to rescue IFN-α-induced neurologic impairment. We used a rat model of auditory fear conditioning to study the effect of IFN-α on the fear memory process. IFN-α was infused directly into the amygdala of rats and examined the rats' behavioral response (freezing) to fear-conditioned stimuli. Immunohistochemical staining was used to examine the glia activity status of glia in the amygdala. The levels of the proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the amygdala were measured by enzyme-linked immunosorbent assay. We also administrated minocycline, a microglial activation inhibitor, before the IFN-α infusion to testify the possibility to reverse the IFN-α-induced effects. Infusing the amygdala with IFN-α impaired the extinction of conditioned fear in rats and activated microglia and astrocytes in the amygdala. Administering minocycline prevented IFN-α from impairing fear extinction. The immunohistochemical and biochemical results show that minocycline inhibited IFN-α-induced microglial activation and reduced IL-1β and TNF-α production. Our findings suggest that IFN-α disrupts the extinction of auditory fear by activating glia in the amygdala and provides direction for clinical studies of novel treatments to modulate the innate immune system in patients with psychotic disorders.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 39 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 39 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 7 18%
Researcher 6 15%
Student > Ph. D. Student 6 15%
Lecturer 3 8%
Professor > Associate Professor 3 8%
Other 6 15%
Unknown 8 21%
Readers by discipline Count As %
Agricultural and Biological Sciences 6 15%
Neuroscience 5 13%
Psychology 4 10%
Medicine and Dentistry 4 10%
Immunology and Microbiology 3 8%
Other 7 18%
Unknown 10 26%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 02 July 2016.
All research outputs
#6,902,174
of 7,976,486 outputs
Outputs from Journal of Neuroinflammation
#882
of 1,017 outputs
Outputs of similar age
#218,885
of 260,708 outputs
Outputs of similar age from Journal of Neuroinflammation
#46
of 55 outputs
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