caa a22 4500 445376023 CHVBK 20180317143002.0 cr unu---uuuuu 170323e20110101xx s 000 0 eng 10.1007/s00702-010-0477-5 doi (NATIONALLICENCE)springer-10.1007/s00702-010-0477-5 Expression of heat shock protein (HSP 72kDa) during acute methamphetamine intoxication depends on brain hyperthermia: neurotoxicity or neuroprotection? [Elektronische Daten] [Eugene Kiyatkin, Hari Sharma] In the present study, light and electron microscopy were used to examine heat shock protein (HSP 72kD) expression during acute methamphetamine (METH) intoxication in rats and evaluate its relationships with brain temperature and alterations in a number of other histochemical and morphological parameters. Freely moving rats received METH at the same dose (9mg/kg, sc) but at different ambient temperatures (23 and 29°C), showing a wide range of brain temperature elevations (37.6-42.5°C); brains were taken for histochemical and morphological evaluations at peak of brain temperature increase. We found that acute METH intoxication induces massive and wide-spread HSP expression in neural and glial cells examined in detail in the cortex, hippocampus, thalamus, and hypothalamus. In each of these structures, the number of HSP-positive cells tightly correlated with brain temperature elevation. The changes in HSP immunoreactivity were also tightly related to alterations in permeability of the blood-brain barrier, acute glial activation, and brain edema assessed by albumin and GFAP immunoreactivity and measuring tissue water content, respectively. While robust and generalized HSP production normally appears to be the part of an adaptive brain response associated with METH-induced metabolic activation, activation of this protective mechanism has its natural limits and could not counteract the damaging effects of oxidative stress, high temperature, and edema—the leading factors of METH-induced neurotoxicity. Springer-Verlag (outside the USA), 2010 Metabolic activation nationallicence Blood-brain barrier nationallicence Neural and glial cells nationallicence Oxidative stress nationallicence Brain hyperthermia nationallicence Edema nationallicence Rats nationallicence Kiyatkin Eugene Behavioral Neuroscience Branch, National Institute on Drug Abuse-Intramural Research Program, NIH, 333 Cassell Drive, 21224, Baltimore, MD, USA aut Sharma Hari Laboratory of Cerebrovascular Research, Department of Surgical Sciences, University Hospital, Uppsala University, Uppsala, Sweden aut Journal of Neural Transmission Springer Vienna 118/1(2011-01-01), 47-60 0300-9564 118:1<47 2011 118 702 https://doi.org/10.1007/s00702-010-0477-5 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00702-010-0477-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Kiyatkin Eugene Behavioral Neuroscience Branch, National Institute on Drug Abuse-Intramural Research Program, NIH, 333 Cassell Drive, 21224, Baltimore, MD, USA aut NATIONALLICENCE 700 1- Sharma Hari Laboratory of Cerebrovascular Research, Department of Surgical Sciences, University Hospital, Uppsala University, Uppsala, Sweden aut NATIONALLICENCE 773 0- Journal of Neural Transmission Springer Vienna 118/1(2011-01-01), 47-60 0300-9564 118:1<47 2011 118 702 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer