Journal
CNS & NEUROLOGICAL DISORDERS-DRUG TARGETS
Volume 14, Issue 2, Pages 282-294Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1871527314666150217121354
Keywords
Albumin leakage; blood-spinal cord barrier; brain; cellular damage; glial fibrillary acidic protein; hyperthermia; metabolic brain activation; spinal cord
Categories
Funding
- Intramural Research Program of NIDA-NIH
- Leaderal Foundation for Acute Medicine, Stavanger, Norway
- NIDA Distinguished International Scientist Collaboration Award (NIH)
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Acute methamphetamine (METH) intoxication induces metabolic brain activation as well as multiple physiological and behavioral responses that could result in life-threatening health complications. Previously, we showed that METH (9 mg/kg) used in freely moving rats induces robust leakage of blood-brain barrier, acute glial activation, vasogenic edema, and structural abnormalities of brain cells. These changes were tightly correlated with drug-induced brain hyperthermia and were greatly potentiated when METH was used at warm ambient temperatures (29 degrees C), inducing more robust and prolonged hyperthermia. Extending this line of research, here we show that METH also strongly increases the permeability of the blood-spinal cord barrier as evidenced by entry of Evans blue and albumin immunoreactivity in T9-12 segments of the spinal cord. Similar to the blood-brain barrier, leakage of bloodspinal cord barrier was associated with acute glial activation, alterations of ionic homeostasis, water tissue accumulation (edema), and structural abnormalities of spinal cord cells. Similar to that in the brain, all neurochemical alterations correlated tightly with drug-induced elevations in brain temperature and they were enhanced when the drug was used at 29 degrees C and brain hyperthermia reached pathological levels (>40 degrees C). We discuss common features and differences in neural responses between the brain and spinal cord, two inseparable parts of the central nervous system affected by METH exposure.
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