Focussed microwave radiation: a technique to minimize post mortem changes of cyclic nucleotides, dopa and choline and to preserve brain morphology

Guidotti, Alessandro; Dl, Cheney; Trabucchi, M.; Doteuchi, Masami; Wang, C

doi:10.1016/0028-3908(74)90061-6

Cited by 312 publications

(56 citation statements)

References 14 publications

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“…Products of these PUFAs, including, E 2 /D 2 -IsoPs, TXB 2 , 5-HETE, 5-oxo-ETE, and 12-HETE, as well as mono-, di-and trihydroxy-DHA, were increased significantly as well. The brain was subjected to high-energy microwave irradiation to irreversibly inactivate enzymes in the entire brain within a few seconds (8,9,12,16,(28)(29)(30)(34)(35)(36)(37), which permitted comparison of fatty acid and metabolite levels in ischemic and control brain. A 5 min ischemia was chosen because it was used previously in our laboratory (30,31); this period includes a rapid phase followed by a much slower phase of fatty acid release from phospholipids (37,38).…”

Section: Discussionmentioning

confidence: 99%

Formation of eicosanoids, E2/D2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain

Farias

Basselin

Chang

et al. 2008

Journal of Lipid Research

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Inflammatory lipid mediators derived from arachidonic acid (AA) and docosahexaenoic acid (DHA) modify the pathophysiology of brain ischemia. The goal of this work was to investigate the formation of eicosanoids and docosanoids generated from AA and DHA, respectively, during noflow cerebral ischemia. Rats were subjected to head-focused microwave irradiation 5 min following decapitation (complete ischemia) or prior to decapitation (controls). Brain lipids were extracted and analyzed by reverse-phase liquid chromatography-tandem mass spectrometry. After complete ischemia, brain AA, DHA, and docosapentaenoic acid concentrations increased 18-, 5-and 4-fold compared with controls, respectively. Prostaglandin E 2 (PGE 2 ) and PGD 2 could not be detected in control microwaved rat brain, suggesting little endogenous PGE 2 /D 2 production in the brain in the absence of experimental manipulation. Concentrations of thromboxane B 2 , E 2 /D 2 -isoprostanes, 5-hydroxyeicosatetraenoic acid (5-HETE), 5-oxo-eicosatetraenoic acid, and 12-HETE were significantly elevated in ischemic brains. In addition, DHA products such as mono-, di-and trihydroxy-DHA were detected in control and ischemic brains. Monohydroxy-DHA, identified as 17-hydroxy-DHA and thought to be the immediate precursor of neuroprotectin D 1 , was 6.5-fold higher in ischemic than in control brain. The present study demonstrated increased formation of eicosanoids, E 2 /D 2 -IsoPs, and docosanoids following cerebral ischemia. A balance of these lipid mediators may mediate immediate events of ischemic injury and recovery.-Farias, S. E., M. Basselin, L. Chang, K. A. Heidenreich, S. I. Rapoport, and R. C. Murphy. Formation of eicosanoids, E 2 /D 2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain. J. Lipid Res.

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Section: Discussionmentioning

confidence: 99%

Formation of eicosanoids, E2/D2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain

Farias

Basselin

Chang

et al. 2008

Journal of Lipid Research

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“…The postmortem changes in concentration of inositol phosphates were studied by comparing tissue extracts from rats killed by decapitation with extracts from rats killed by focused microwave irradiation. This latter technique is accepted as the best available means of humanely killing the animals (<1 s) and rapidly blocking metabolism (8). The experiment was performed at the Laboratory of Preclinical Pharmacology, St. Elizabeths Hospital, National Institute of Mental Health, Washington, DC, using 300-g rats from Zivic-Miller (Pittsburgh).…”

mentioning

confidence: 99%

“…The distribution in various organs was examined initially. Since there is an extremely rapid change postmortem in another second messenger, cAMP (8), the method of obtaining tissues was then examined. After these studies were complete, the existence of inositol tetrakis(phosphate) (InsP4) was reported (5 (1,4,5)P3 was purchased from Amersham.…”

mentioning

confidence: 99%

Inositol bis-, tris-, and tetrakis(phosphate)s: analysis in tissues by HPLC.

Meek¹

1986

Proc. Natl. Acad. Sci. U.S.A.

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The concentration of isomers of inositol tris(phosphate) (InsP3) was measured in tissues of intact animals. The method employed involved anion-exchange HPLC with on-line enzymatic hydrolysis of the phosphate esters and detection of the inorganic phosphate formed. All seven organs tested from rats killed by decapitation contained Ins(1,4,5)P3 in concentrations of 1340 nmol/g; a distribution that bears no resemblance to that reported for its precursor [phosphatidylinositol bis(phosphate)]. A second InsP3 isomer [probably Ins(1,3,4)P3] was also detectable in brain and salivary gland. The content of Ins(1,4,5)P3 in brain and salivary gland from rats killed by decapitation was 10-60 times greater than that from rats killed by focused microwave irradiation to block postmortem metabolism. Inositol bis(phosphate) concentrations also changed dramatically postmortem.

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“…Group five was injected with sarin at dose of 0.5 x LD 50 and euthanized 30 min after injection. Animals were euthanized by a head-focused microwave device (3.0 kW, 2.45 MHz for 0.85 sec; GerlingMoore Metabostat System, Gerling-Moore, Inc., Santa Clara, CA) to arrest alterations of phosphorylation state in vivo at specified times after injection (Guidotti et al, 1974). Cerebral cortex, striatum and hippocampus were dissected rapidly after microwave procedure, immediately flash frozen, and then stored at -80 o C until phosphoprotein analysis.…”

Section: Methodsmentioning

confidence: 99%

The Role of DARPP-32, an Intracellular Signaling Molecule, in the Actions of the Nerve Agent Sarin

Shih¹,

Snyder²,

Fienberg³

et al. 2005

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information , 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY) ABSTRACTWe investigated the role of DARPP-32 in mediating changes in phosphorylation after sarin exposure. Wild type mice and mice bearing a targeted disruption of the gene for DARPP-32 were exposed to sarin; levels of brain phosphoproteins were measured. Mice receiving 1.0 x LD 50 dose of sarin displayed motor convulsions. No significant change in phosphorylation level of T75 DARPP-32 was observed in brains of wild type mice. Also, no significant changes in phosphorylation were observed in the brains of wild type or DARPP-32 knockout mice after 0.5 x LD 50 sarin. At a sarin dose of 1.0 x LD 50 a significant increase in CREB phosphorylation was observed. One difference was noted in brain phosphorylation between wild type and DARPP-32 knockout mice. The presence of DARPP-32 significantly affected the ability of sarin to alter phosphorylation of the AMPA receptor GluR1 at S831. An increase in phosphorylation measured in wild type mouse brain after sarin was significantly attenuated in the brain of DARPP-32 knockout mice, indicating that DARPP-32 may modulate the extent to which S831 responses are induced by sarin. The results of this study do not support the hypothesis that changes in phosphorylation levels of T75 DARPP-32 are necessary for phosphorylation changes observed in brain after a 1.0 x LD 50 dose of sarin. iii SUBJECT TERMS ACKNOWLEDGEMENTSThe expert advice and technical help of Dr. James O'Callaghan (CDC-NIOSH) in adapting the microwave applicator for use in mice is gratefully acknowledged. The excellent technical assistance of Peter Ingrassia (Rockefeller University) in the genotyping and shipment of mice for these studies is also gratefully acknowledged.v ABSTRACT Organophosphorus (OP) nerve agents exert acute effects by inhibiting the enzyme acetylcholinesterase in the central and peripheral nervous systems. Inhibition of acetylcholinesterase results in accumulation of acetylcholine and, which in turn causes overstimulation of nicotinic and muscarinic receptors. Previous study indicated that treatment of rats with the nerve agent sarin both at a convulsive dose (1.0 x LD 50 ) and a sub-convulsive threshold dose...

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Focussed microwave radiation: a technique to minimize post mortem changes of cyclic nucleotides, dopa and choline and to preserve brain morphology

Cited by 312 publications

References 14 publications

Formation of eicosanoids, E2/D2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain

Formation of eicosanoids, E2/D2 isoprostanes, and docosanoids following decapitation-induced ischemia, measured in high-energy-microwaved rat brain

Inositol bis-, tris-, and tetrakis(phosphate)s: analysis in tissues by HPLC.

The Role of DARPP-32, an Intracellular Signaling Molecule, in the Actions of the Nerve Agent Sarin

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