Chronic exposure to corticosterone enchances the neuroinflammatory and neurotoxic responses to methamphetamine

Kelly, Kimberly A.; Miller, Diane B.; Bowyer, John F.; O’Callaghan, James P.

doi:10.1111/j.1471-4159.2012.07864.x

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Chronic exposure to corticosterone enchances the neuroinflammatory and neurotoxic responses to methamphetamine

9 2012
By Kelly, Kimberly A. ; Miller, Diane B. ; Bowyer, John F. ; ...
http://dx.doi.org/10.1111/j.1471-4159.2012.07864.x
Source: J Neurochem. 122(5):995-1009

[PDF-1.98 MB]

English

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Details:

Alternative Title:

J Neurochem
Personal Author:

Kelly, Kimberly A. ; Miller, Diane B. ; Bowyer, John F. ; O’Callaghan, James P.

Kelly, Kimberly A. ; Miller, Diane B. ; Bowyer, John F. ; O’Callaghan, James P. Less -
Description:

Up-regulation of proinflammatory cytokines and chemokines in brain ("neuroinflammation") accompanies neurological disease and neurotoxicity. Previously, we documented a striatal neuroinflammatory response to acute administration of a neurotoxic dose of methamphetamine (METH), i.e. one associated with evidence of dopaminergic terminal damage and activation of microglia and astroglia. When we used minocycline to suppress METH-induced neuroinflammation, indices of dopaminergic neurotoxicity were not affected, but suppression of neuroinflammation was incomplete. Here, we administered the classic anti-inflammatory glucocorticoid, corticosterone (CORT), in an attempt to completely suppress METH-related neuroinflammation. METH alone caused large increases in striatal proinflammatory cytokine/chemokine mRNA and subsequent astrocytic hypertrophy, microglial activation, and dopaminergic nerve terminal damage. Pre-treatment of mice with acute CORT failed to prevent neuroinflammatory responses to METH. Surprisingly, when mice were pre-treated with chronic CORT in the drinking water, an enhanced striatal neuroinflammatory response to METH was observed, an effect that was accompanied by enhanced METH-induced astrogliosis and dopaminergic neurotoxicity. Chronic CORT pre-treatment also sensitized frontal cortex and hippocampus to mount a neuroinflammatory response to METH. Because the levels of chronic CORT used are associated with high physiological stress, our data suggest that chronic CORT therapy or sustained physiological stress may sensitize the neuroinflammatory and neurotoxicity responses to METH.
Subjects:

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Analysis Of Variance Animals Anti-Inflammatory Agents Body Weight Brain Central Nervous System Stimulants Chromatography, High Pressure Liquid Corticosterone Cytokines Disease Models, Animal Dopamine Dose-Response Relationship, Drug Drug Synergism Electrochemical Techniques Encephalitis Enzyme-Linked Immunosorbent Assay Glial Fibrillary Acidic Protein Lectins Male Methamphetamine Mice Mice, Inbred C57BL Microglia Time Factors Tyrosine 3-Monooxygenase Up-Regulation
Keywords:

[+]

Glucocorticoids Methamphetamine Microglial Activation Neuroinflammation Neurotoxicity Stress
Source:

J Neurochem. 122(5):995-1009
Pubmed ID:

22776046
Pubmed Central ID:

PMC4706460
Document Type:

Journal Article
Funding:

CC999999/Intramural CDC HHSUnited States/ ; ImNIH/Intramural NIH HHSUnited States/

CC999999/Intramural CDC HHSUnited States/ ; ImNIH/Intramural NIH HHSUnited States/ Less -
Volume:

122
Issue:

5
Collection(s):

CDC Public Access
Main Document Checksum:

[+]

urn:sha256:e9754483eba81c812374dff7e6423f9718bee965f6fa5245e8d6d13e1fb80cc1
Download URL:

https://stacks.cdc.gov/view/cdc/37377/cdc_37377_DS1.pdf
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