S I Rapoport

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. ncbi request reprint Osmotic opening of the blood-brain barrier: principles, mechanism, and therapeutic applications
    S I Rapoport
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Cell Mol Neurobiol 20:217-30. 2000
  2. pmc Dose-dependent changes in neuroinflammatory and arachidonic acid cascade markers with synaptic marker loss in rat lipopolysaccharide infusion model of neuroinflammation
    Matthew Kellom
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 9, 1S 126, Bethesda, MD, USA
    BMC Neurosci 13:50. 2012
  3. pmc Translational studies on regulation of brain docosahexaenoic acid (DHA) metabolism in vivo
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 88:79-85. 2013
  4. pmc Selective remodeling of cardiolipin fatty acids in the aged rat heart
    Ho Joo Lee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, USA
    Lipids Health Dis 5:2. 2006
  5. pmc Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain of HIV-1 transgenic rats
    Jagadeesh Sridhara Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, Bethesda, MD 20892, USA
    J Neuroinflammation 8:101. 2011
  6. pmc Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death
    Hyung Wook Kim
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    BMC Neurosci 10:123. 2009
  7. pmc Quantitative contributions of diet and liver synthesis to docosahexaenoic acid homeostasis
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 82:273-6. 2010
  8. ncbi request reprint Advances in osmotic opening of the blood-brain barrier to enhance CNS chemotherapy
    S I Rapoport
    Brain Physiology and Metabolism Section, Bldg 10, Rm 6N 202, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Expert Opin Investig Drugs 10:1809-18. 2001
  9. ncbi request reprint In vivo approaches and rationale for quantifying kinetics and imaging brain lipid metabolic pathways
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Prostaglandins Other Lipid Mediat 77:185-96. 2005
  10. ncbi request reprint In vivo fatty acid incorporation into brain phosholipids in relation to plasma availability, signal transduction and membrane remodeling
    S I Rapoport
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    J Mol Neurosci 16:243-61; discussion 279-84. 2001

Collaborators

Detail Information

Publications156 found, 100 shown here

  1. ncbi request reprint Osmotic opening of the blood-brain barrier: principles, mechanism, and therapeutic applications
    S I Rapoport
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Cell Mol Neurobiol 20:217-30. 2000
    ..The method also has been used together with anticancer drugs to treat patients with metastatic or primary brain tumors, with some success and minimal morbidity...
  2. pmc Dose-dependent changes in neuroinflammatory and arachidonic acid cascade markers with synaptic marker loss in rat lipopolysaccharide infusion model of neuroinflammation
    Matthew Kellom
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 9, 1S 126, Bethesda, MD, USA
    BMC Neurosci 13:50. 2012
    ..5 ng/h) and a high-dose (250 ng/h) of LPS on neuroinflammatory, AA cascade, and pre- and post-synaptic markers in rat brain. We used artificial cerebrospinal fluid-infused brains as controls...
  3. pmc Translational studies on regulation of brain docosahexaenoic acid (DHA) metabolism in vivo
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 88:79-85. 2013
    ..In humans, regional rates of brain DHA metabolism can be quantitatively imaged with positron emission tomography following intravenous injection of [1-¹¹C]DHA...
  4. pmc Selective remodeling of cardiolipin fatty acids in the aged rat heart
    Ho Joo Lee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, USA
    Lipids Health Dis 5:2. 2006
    ..We therefore measured the fatty acid concentration of cardiolipin in hearts of 4, 12 and 24 month old rats that consumed one diet, adequate in fatty acids for the duration of their life...
  5. pmc Increased neuroinflammatory and arachidonic acid cascade markers, and reduced synaptic proteins, in brain of HIV-1 transgenic rats
    Jagadeesh Sridhara Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, Bethesda, MD 20892, USA
    J Neuroinflammation 8:101. 2011
    ..We recently reported upregulated brain AA metabolism in 7- to 9-month-old HIV-1 Tg rats. We hypothesized that these HIV-1 Tg rats also would show upregulated brain inflammatory and AA cascade markers and a deficit of synaptic proteins...
  6. pmc Chronic NMDA administration to rats increases brain pro-apoptotic factors while decreasing anti-Apoptotic factors and causes cell death
    Hyung Wook Kim
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    BMC Neurosci 10:123. 2009
    ..In this study, we determined if chronic NMDA administration (25 mg/kg i.p., 21 days) to rats would alter expression of pro- and anti-apoptotic factors in frontal cortex, compared with vehicle control...
  7. pmc Quantitative contributions of diet and liver synthesis to docosahexaenoic acid homeostasis
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 82:273-6. 2010
    ..A noninvasive intravenous [U-(13)C]alpha-LNA infusion method that produces steady-state liver tracer metabolism gives exact liver DHA synthesis-secretion rates and could be extended for human studies...
  8. ncbi request reprint Advances in osmotic opening of the blood-brain barrier to enhance CNS chemotherapy
    S I Rapoport
    Brain Physiology and Metabolism Section, Bldg 10, Rm 6N 202, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Expert Opin Investig Drugs 10:1809-18. 2001
    ..However, controlled clinical trials are critical to see if the osmotic procedure with intra-arterial drugs enhances survival in brain tumour patients compared with intra-arterial drug alone...
  9. ncbi request reprint In vivo approaches and rationale for quantifying kinetics and imaging brain lipid metabolic pathways
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Prostaglandins Other Lipid Mediat 77:185-96. 2005
    ..Cases that are discussed are arachidonic acid turnover and imaging of neuroreceptor-initiated phospholipase A2 activation, ether phospholipid biosynthesis, and kinetics of the phosphatidylinositol cycle...
  10. ncbi request reprint In vivo fatty acid incorporation into brain phosholipids in relation to plasma availability, signal transduction and membrane remodeling
    S I Rapoport
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    J Mol Neurosci 16:243-61; discussion 279-84. 2001
    ....
  11. pmc Bipolar disorder and mechanisms of action of mood stabilizers
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Brain Res Rev 61:185-209. 2009
    ..This review presents ways to test these suggestions...
  12. ncbi request reprint Functional brain imaging in the resting state and during activation in Alzheimer's disease. Implications for disease mechanisms involving oxidative phosphorylation
    S I Rapoport
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 893:138-53. 1999
    ....
  13. ncbi request reprint [In vivo imaging for evaluating synaptic integrity in Alzheimer disease]
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA
    Psychol Neuropsychiatr Vieil 3:97-106. 2005
    ....
  14. pmc Brain metabolism of nutritionally essential polyunsaturated fatty acids depends on both the diet and the liver
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 77:251-61. 2007
    ..These changes, plus reduced levels of brain derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB) in n-3 PUFA diet deficient rats, likely render their brain more vulnerable to neuropathological insults...
  15. ncbi request reprint Do lithium and anticonvulsants target the brain arachidonic acid cascade in bipolar disorder?
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, Bldg 10, Room 6N202, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Arch Gen Psychiatry 59:592-6. 2002
    ..Lithium and certain anticonvulsants, including carbamazepine and valproic acid, are effective antimanic drugs for treating bipolar disorder, but their mechanisms of action remain uncertain...
  16. pmc Can the rat liver maintain normal brain DHA metabolism in the absence of dietary DHA?
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, 9000 Rockville Pike, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 81:119-23. 2009
    ..Docosahexaenoic acid (DHA) is required for normal brain function. The concentration of DHA in the brain depends on both diet and liver metabolism...
  17. ncbi request reprint Hydrogen magnetic resonance spectroscopy in Alzheimer's disease
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Lancet Neurol 1:82. 2002
  18. ncbi request reprint Coupled reductions in brain oxidative phosphorylation and synaptic function can be quantified and staged in the course of Alzheimer disease
    Stanley I Rapoport
    Brain Physiology and Metabolism Sections, Bldg 10, Rm 6N202, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neurotox Res 5:385-98. 2003
    ..In this second stage, severe energy depletion and other pathological processes associated with irreversibly downregulated OXPHOS lead to cell death, and the brain cannot normally respond to functional stimulation...
  19. ncbi request reprint Reduced brain delivery of homovanillic acid to cerebrospinal fluid during human aging
    Stanley I Rapoport
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Arch Neurol 61:1721-4. 2004
    ..However, the cerebrospinal fluid (CSF) concentration of homovanillic acid (HVA), a major dopamine metabolite, is reported to not change or to increase in elderly individuals...
  20. pmc Arachidonic acid and the brain
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    J Nutr 138:2515-20. 2008
    ..8 and 4.6 mg/d, whereas in patients with Alzheimer disease, AA consumption is elevated. In the future, PET could be used to relate human brain rates of AA and DHA consumption to liver PUFA metabolism and dietary PUFA intake...
  21. doi request reprint Brain arachidonic and docosahexaenoic acid cascades are selectively altered by drugs, diet and disease
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, 9 Memorial Drive, Bethesda, MD 20892, USA
    Prostaglandins Leukot Essent Fatty Acids 79:153-6. 2008
    ..6 mg/day, respectively, of AA and DHA, and that brain AA consumption is increased in Alzheimer disease patients. In the future, PET could help to determine how human brain AA or DHA consumption is influenced by diet, aging or disease...
  22. ncbi request reprint In vivo PET imaging and postmortem studies suggest potentially reversible and irreversible stages of brain metabolic failure in Alzheimer's disease
    S I Rapoport
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Eur Arch Psychiatry Clin Neurosci 249:46-55. 1999
    ..A later irreversible stage of AD is accompanied by marked synaptic loss, accumulation of intracellular neurofibrillary tangles, reduced general transcriptional capacity, and death of neurons...
  23. ncbi request reprint How did the human brain evolve? A proposal based on new evidence from in vivo brain imaging during attention and ideation
    S I Rapoport
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Brain Res Bull 50:149-65. 1999
    ....
  24. ncbi request reprint In vivo imaging of fatty acid incorporation into brain to examine signal transduction and neuroplasticity involving phospholipids
    S I Rapoport
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Ann N Y Acad Sci 820:56-73; discussion 73-4. 1997
    ....
  25. ncbi request reprint In vivo fatty acid incorporation into brain phospholipids in relation to signal transduction and membrane remodeling
    S I Rapoport
    Laboratory of Neurosciences National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Neurochem Res 24:1403-15. 1999
    ....
  26. ncbi request reprint Brain energy metabolism, cognitive function and down-regulated oxidative phosphorylation in Alzheimer disease
    S I Rapoport
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neurodegeneration 5:473-6. 1996
    ..Such down-regulation may occur when neuronal energy demand is first reduced by synaptic dysfunction or loss...
  27. ncbi request reprint Delivery and turnover of plasma-derived essential PUFAs in mammalian brain
    S I Rapoport
    Brain Physiology and Metabolism Section, University of Iowa, Iowa City, IA 52242, USA
    J Lipid Res 42:678-85. 2001
    ..Dietary supplementation, by altering plasma unesterified PUFA concentrations, can regulate brain PUFA content and may help to treat brain diseases involving PUFA imbalance...
  28. doi request reprint Biomarkers and evolution in Alzheimer disease
    Stanley I Rapoport
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S 126, Bethesda, MD 20892, USA
    Prog Neurobiol 95:510-3. 2011
    ....
  29. ncbi request reprint Chronic valproate treatment decreases the in vivo turnover of arachidonic acid in brain phospholipids: a possible common effect of mood stabilizers
    M C Chang
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 7965, USA
    J Neurochem 77:796-803. 2001
    ..Thus, both mood stabilizers, Li(+) and VPA have a common action in reducing AA turnover in brain phospholipids, albeit by different mechanisms...
  30. ncbi request reprint Nutritional deprivation of alpha-linolenic acid decreases but does not abolish turnover and availability of unacylated docosahexaenoic acid and docosahexaenoyl-CoA in rat brain
    M A Contreras
    Section on Brain Physiology and Metabolism, National Institute on Aging, Bethesda 20892, USA
    J Neurochem 75:2392-400. 2000
    ..We propose that functional brain effects of n-3 deficiency reflect altered ratios of n-6 to n-3 fatty acids...
  31. ncbi request reprint Frequency variation of a pattern-flash visual stimulus during PET differentially activates brain from striate through frontal cortex
    M J Mentis
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Neuroimage 5:116-28. 1997
    ..The reproducibility and systematically changing rCBF responses to this passive stimulus suggest that it could be successfully used as a disease probe to evaluate neural function and drug effects in cognitively impaired patients...
  32. ncbi request reprint Dietary n-3 PUFA deprivation alters expression of enzymes of the arachidonic and docosahexaenoic acid cascades in rat frontal cortex
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 12:151-7. 2007
    ....
  33. ncbi request reprint Increasing required neural response to expose abnormal brain function in mild versus moderate or severe Alzheimer's disease: PET study using parametric visual stimulation
    M J Mentis
    Laboratory of Neurosciences, National Institute on Aging, Bethesda, MD, USA
    Am J Psychiatry 155:785-94. 1998
    ..The authors examined the interaction of Alzheimer's disease severity and visual stimulus complexity in relation to regional brain function...
  34. ncbi request reprint Lithium decreases turnover of arachidonate in several brain phospholipids
    M C Chang
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892 1582, USA
    Neurosci Lett 220:171-4. 1996
    ..The effect may be secondary to the known action of lithium on the phosphoinositide cycle, by inhibiting the activity of inositol monophosphatase...
  35. ncbi request reprint n-3 polyunsaturated fatty acid deprivation in rats decreases frontal cortex BDNF via a p38 MAPK-dependent mechanism
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 12:36-46. 2007
    ..DHA's ability to regulate BDNF via a p38 MAPK-dependent mechanism may contribute to its therapeutic efficacy in brain diseases having disordered cell survival and neuroplasticity...
  36. pmc Cholinergic stimulation alters performance and task-specific regional cerebral blood flow during working memory
    M L Furey
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 94:6512-6. 1997
    ..These results suggest that enhancement of cholinergic function can improve processing efficiency and thus reduce the effort required to perform a WM task, and that activation of right prefrontal cortex is associated with task effort...
  37. ncbi request reprint Chronic fluoxetine upregulates arachidonic acid incorporation into the brain of unanesthetized rats
    Ying Qu
    Brain Physiology and Metabolism Section, Building 9, Room 1S128, National Institute on Aging, National Institutes of Health, 9 Memorial Drive, Bethesda, MD 20892, USA
    Eur Neuropsychopharmacol 16:561-71. 2006
    ..Such upregulation may contribute to fluoxetine's efficacy against human depression...
  38. ncbi request reprint Chronic nutritional deprivation of n-3 alpha-linolenic acid does not affect n-6 arachidonic acid recycling within brain phospholipids of awake rats
    M A Contreras
    Brain Physiology and Metabolism Section, National Institute on Aging, NIH, Bethesda, Maryland 20892, USA
    J Neurochem 79:1090-9. 2001
    ....
  39. ncbi request reprint Haloperidol downregulates phospholipase A(2) signaling in rat basal ganglia circuits
    C S Myers
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Brain Res 896:96-101. 2001
    ..These results suggest that one mechanism by which haloperidol exerts its effect is by downregulating D(2)-mediated PLA(2) signaling involving AA release in basal ganglia-frontal cortex circuitry...
  40. ncbi request reprint Association between brain functional failure and dementia severity in Alzheimer's disease: resting versus stimulation PET study
    P Pietrini
    Laboratory of Neurosciences, National Institute on Aging, NIH, Bethesda, MD 20892, USA
    Am J Psychiatry 156:470-3. 1999
    ..This study tested the hypothesis that regional cerebral glucose metabolism during neuronal activation is a more sensitive index of neuronal dysfunction and clinical severity in Alzheimer's disease than is glucose metabolism at rest...
  41. ncbi request reprint High brain myo-inositol levels in the predementia phase of Alzheimer's disease in adults with Down's syndrome: a 1H MRS study
    W Huang
    Laboratory of Neurosciences, National Institute on Aging, Clinical Center, NIH, Bethesda, MD, USA
    Am J Psychiatry 156:1879-86. 1999
    ..The authors investigated whether abnormal brain levels of myo-inositol and other metabolites occur in the preclinical stages of Alzheimer's disease associated with Down's syndrome...
  42. ncbi request reprint Corpus callosum atrophy is a possible indicator of region- and cell type-specific neuronal degeneration in Alzheimer disease: a magnetic resonance imaging analysis
    H Hampel
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Arch Neurol 55:193-8. 1998
    ..Pathological studies in Alzheimer disease indicate the specific loss of layer III and V large pyramidal neurons in association cortex. These neurons give rise to long corticocortical connections within and between the cerebral hemispheres...
  43. ncbi request reprint Region-specific corpus callosum atrophy correlates with the regional pattern of cortical glucose metabolism in Alzheimer disease
    S J Teipel
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Arch Neurol 56:467-73. 1999
    ..Atrophy of the corpus callosum as the major tract of intracortical connective fibers may reflect decreased cortical functional integration in AD...
  44. ncbi request reprint Increased expression of voltage-activated calcium channels in cultured hippocampal neurons from mouse trisomy 16, a model for Down syndrome
    Z Galdzicki
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Brain Res Mol Brain Res 56:200-6. 1998
    ....
  45. ncbi request reprint Ts65Dn mouse, a Down syndrome model, exhibits elevated myo-inositol in selected brain regions and peripheral tissues
    H U Shetty
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 1582, USA
    Neurochem Res 25:431-5. 2000
    ..In all tissues, concentrations of polyol internal controls were normal. The Ts65Dn mouse is useful to study the possible effect of elevated myo-inositol on cellular processes...
  46. pmc Altered expression of apoptotic factors and synaptic markers in postmortem brain from bipolar disorder patients
    Hyung Wook Kim
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neurobiol Dis 37:596-603. 2010
    ..These differences may contribute to brain atrophy and progressive cognitive changes in BD...
  47. ncbi request reprint In vivo imaging detects a transient increase in brain arachidonic acid metabolism: a potential marker of neuroinflammation
    Helen Lee
    Brain Physiology and Metabolism Section, National Institutes on Aging, National Institutes of Health, Bethesda, Maryland, USA
    J Neurochem 91:936-45. 2004
    ..These results confirm that brain AA metabolism is disturbed after 6 days of LPS exposure, show this increase is transient, and that these changes can be detected and localized using in vivo imaging with radiolabeled AA...
  48. ncbi request reprint Chronic carbamazepine decreases the incorporation rate and turnover of arachidonic acid but not docosahexaenoic acid in brain phospholipids of the unanesthetized rat: relevance to bipolar disorder
    Richard P Bazinet
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 59:401-7. 2006
    ..One hypothesis is that, similar to lithium and valproate (antibipolar drugs), carbamazepine might selectively decrease the kinetics of arachidonic acid (AA) in brain phospholipids...
  49. ncbi request reprint In vivo approaches to quantifying and imaging brain arachidonic and docosahexaenoic acid metabolism
    Stanley I Rapoport
    National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Pediatr 143:S26-34. 2003
    ..The in vivo fatty method is being extended for human studies using positron emission tomography...
  50. doi request reprint Mode of action of mood stabilizers: is the arachidonic acid cascade a common target?
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Mol Psychiatry 13:585-96. 2008
    ..Targeting the AA cascade with drugs or diet may be a useful therapeutic approach in bipolar disorder, and examining the AA cascade in patients might help in better understanding the disease...
  51. pmc Altered neuroinflammatory, arachidonic acid cascade and synaptic markers in postmortem Alzheimer's disease brain
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Transl Psychiatry 1:e31. 2011
    ..These results indicate that increased AA cascade and inflammatory markers could contribute to AD pathology. Altered brain AA cascade enzymes could be considered therapeutic targets for future drug development...
  52. pmc Altered arachidonic acid cascade enzymes in postmortem brain from bipolar disorder patients
    H W Kim
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Mol Psychiatry 16:419-28. 2011
    ..An upregulated cascade should be considered as a target for drug development and for neuroimaging in BD...
  53. pmc Chronic imipramine but not bupropion increases arachidonic acid signaling in rat brain: is this related to 'switching' in bipolar disorder?
    H J Lee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Mol Psychiatry 15:602-14. 2010
    ..Mania in bipolar disorder thus may involve upregulated brain AA metabolism...
  54. ncbi request reprint Intravenously injected [1-14C]arachidonic acid targets phospholipids, and [1-14C]palmitic acid targets neutral lipids in hearts of awake rats
    E J Murphy
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 1582, USA
    Lipids 35:891-8. 2000
    ..Thus, in rat heart, [1-14C]20:4n-6 was primarily targeted for esterification into phospholipids, while [1-14C]16:0 was targeted for esterification into TG or metabolized into nonvolatile aqueous components...
  55. ncbi request reprint No association between Alzheimer plaques and decreased levels of cytochrome oxidase subunit mRNA, a marker of neuronal energy metabolism
    K Hatanpaa
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892 1582, USA
    Brain Res Mol Brain Res 59:13-21. 1998
    ..Cytochrome oxidase enzyme activity in neuronal processes also showed no local reduction around neuritic plaques. These results suggest that neuritic plaques do not contribute to reduced neuronal energy metabolism in Alzheimer disease...
  56. ncbi request reprint Chronic valproate does not alter the kinetics of docosahexaenoic acid within brain phospholipids of the unanesthetized rat
    Richard P Bazinet
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 1S 128, Bethesda, MD 20892, USA
    Psychopharmacology (Berl) 182:180-5. 2005
    ..It is also known that lithium and carbamazepine do so without decreasing the turnover of docosahexaenoic acid (DHA, 22:6n-3)...
  57. ncbi request reprint Chronic carbamazepine selectively downregulates cytosolic phospholipase A2 expression and cyclooxygenase activity in rat brain
    Sandra Ghelardoni
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biol Psychiatry 56:248-54. 2004
    ....
  58. ncbi request reprint Parametric analysis of functional neuroimages: application to a variable-rate motor task
    J W VanMeter
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Neuroimage 2:273-83. 1995
    ..Habituation of responses was not observed...
  59. ncbi request reprint Chronic lithium downregulates cyclooxygenase-2 activity and prostaglandin E(2) concentration in rat brain
    Frances Bosetti
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 10 Rm 6N202, Bethesda, MD 20892, USA
    Mol Psychiatry 7:845-50. 2002
    ..These and prior results indicate that lithium targets a part of the AA cascade that involves cPLA(2) and COX-2. This effect may contribute to lithium's therapeutic action in bipolar disorder...
  60. ncbi request reprint Mitochondrial cytochrome c oxidase subunit III is selectively down-regulated by aluminum exposure in PC12S cells
    F Bosetti
    Section on Brain Physiology and Metabolism, National Institute on Aging, NIH, Bethesda, MD 20892, USA
    Neuroreport 12:721-4. 2001
    ..Higher concentrations of AlCl3 did not show a significant further effect. These results suggest that Al neurotoxicity involves a specific impairment of cytochrome c oxidase...
  61. ncbi request reprint Brain lipid metabolism in the cPLA2 knockout mouse
    Thad A Rosenberger
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    J Lipid Res 44:109-17. 2003
    ....
  62. ncbi request reprint alpha-Linolenic acid does not contribute appreciably to docosahexaenoic acid within brain phospholipids of adult rats fed a diet enriched in docosahexaenoic acid
    James C DeMar
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Neurochem 94:1063-76. 2005
    ..Thus, in rats fed a diet containing large amounts of both alpha-LNA and DHA, the alpha-LNA that enters brain from plasma largely undergoes beta-oxidation, and is not an appreciable source of DHA within brain phospholipids...
  63. ncbi request reprint Brain incorporation of 11C-arachidonic acid, blood volume, and blood flow in healthy aging: a study with partial-volume correction
    Giampiero Giovacchini
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892 1180, USA
    J Nucl Med 45:1471-9. 2004
    ..Animal studies suggest reduction in the activity of this signaling system with age. The aim of this study was to evaluate the effect of healthy aging on brain incorporation of 11C-AA, before and after partial-volume correction (PVC)...
  64. ncbi request reprint Chronic treatment with mood stabilizers increases membrane GRK3 in rat frontal cortex
    Renee N Ertley
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Biol Psychiatry 61:246-9. 2007
    ..G-protein coupled receptor supersensitivity, possibly as a result of decreased GRK, has been suggested in affective disorders...
  65. ncbi request reprint Valproic acid selectively inhibits conversion of arachidonic acid to arachidonoyl-CoA by brain microsomal long-chain fatty acyl-CoA synthetases: relevance to bipolar disorder
    Richard P Bazinet
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Psychopharmacology (Berl) 184:122-9. 2006
    ..0 to 1.5 mM, inhibition of arachidonoyl-CoA formation can occur at brain concentrations that are therapeutically relevant to this disease. Furthermore, brain microsomal Acsl did not produce valproyl-CoA...
  66. ncbi request reprint Imaging of brain serotonergic neurotransmission involving phospholipase A2 activation and arachidonic acid release in unanesthetized rats
    Ying Qu
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 10, Rm 6N202, Bethesda, MD 20892, USA
    Brain Res Brain Res Protoc 12:16-25. 2003
    ..The detailed method is described...
  67. ncbi request reprint Selective dopamine receptor stimulation differentially affects [3H]arachidonic acid incorporation, a surrogate marker for phospholipase A2-mediated neurotransmitter signal transduction, in a rodent model of Parkinson's disease
    T Hayakawa
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Pharmacol Exp Ther 296:1074-84. 2001
    ..Butaclamol blocked this effect. The data suggest up-regulation in basal ganglia and cortical dopamine circuits mediated by phospholipase A(2) ipsilateral to the substantia nigra lesion...
  68. ncbi request reprint Measurement of myo-inositol turnover in phosphatidylinositol: description of a model and mass spectrometric method for cultured cortical neurons
    E G Chikhale
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Biochemistry 40:11114-20. 2001
    ..3%/h in this in vitro system. The mathematical model and the stable isotope method described here should allow assessment of the dynamics of PtdIns signaling altered in certain diseases or by agents...
  69. pmc Cerebral cortical astroglia from the trisomy 16 mouse, a model for down syndrome, produce neuronal cholinergic deficits in cell culture
    P G Nelson
    Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA
    Proc Natl Acad Sci U S A 94:12644-8. 1997
    ..The Ts16 glia could lack a cholinergic supporting factor present in normal glia or contain a factor that down-regulates cholinergic function...
  70. ncbi request reprint Chronic fluoxetine increases cytosolic phospholipase A(2) activity and arachidonic acid turnover in brain phospholipids of the unanesthetized rat
    Ho Joo Lee
    Brain Physiology and Metabolism Section National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Psychopharmacology (Berl) 190:103-15. 2007
    ..We hypothesized that chronic fluoxetine would increase the brain activity of PLA(2) and the turnover rate of arachidonic acid (AA) in phospholipids of the unanesthetized rat...
  71. pmc Chronic administration of mood stabilizers upregulates BDNF and bcl-2 expression levels in rat frontal cortex
    Yunyoung C Chang
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 9, 1S 126, Bethesda, MD 20892, USA
    Neurochem Res 34:536-41. 2009
    ..A common mechanism of action of mood stabilizers in the treatment of bipolar disorder may involve neuroprotection mediated by upregulation of brain BDNF and Bcl-2 expression...
  72. pmc Chronic NMDA administration increases neuroinflammatory markers in rat frontal cortex: cross-talk between excitotoxicity and neuroinflammation
    Yunyoung C Chang
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 9, 1S 126, Bethesda, MD, 20892, USA
    Neurochem Res 33:2318-23. 2008
    ..As both processes have been reported in a number of human brain diseases, NMDA receptor inhibitors might be of use in treating neuroinflammation in these diseases...
  73. pmc Imaging signal transduction via arachidonic acid in the human brain during visual stimulation, by means of positron emission tomography
    Giuseppe Esposito
    Brain Physiology and Metabolism Section, Bldg 9, Rm 1S128, National Institute on Aging, National Institutes of Health, 9 Memorial Drive, Bethesda, MD 20892, USA
    Neuroimage 34:1342-51. 2007
    ..This signaling process can be imaged in brain as a regional brain AA incorporation coefficient K*...
  74. ncbi request reprint Brain incorporation of [11C]arachidonic acid in young healthy humans measured with positron emission tomography
    Giampiero Giovacchini
    Brain Physiology and Metabolism Section, National Institute on Aging, Bethesda, Maryland, U S A
    J Cereb Blood Flow Metab 22:1453-62. 2002
    ..As brain incorporation of labeled AA has been shown in awake rats to be increased by pharmacological activation associated with phospholipase A2-signaling, PET and [11C]AA may be useful to measure signal transduction in the human brain...
  75. pmc Epigenetic modifications in frontal cortex from Alzheimer's disease and bipolar disorder patients
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Transl Psychiatry 2:e132. 2012
    ..These epigenetic modifications involving neuroinflammatory, AA cascade and synaptic markers may contribute to progression in AD and BD and identify new targets for drug development...
  76. pmc Increased excitotoxicity and neuroinflammatory markers in postmortem frontal cortex from bipolar disorder patients
    J S Rao
    Brain Physiology and Metabolism Section, NIA, NIH Bethesda, Bethesda, MD 20892, USA
    Mol Psychiatry 15:384-92. 2010
    ..The changes may account for reported evidence of disease progression in BD and be a target for future therapy...
  77. ncbi request reprint Reduced palmitate turnover in brain phospholipids of pentobarbital-anesthetized rats
    M A Contreras
    Laboratory of Neurosciences, NIA, National Institutes of Health, Bethesda, MD 20892, USA
    Neurochem Res 24:833-41. 1999
    ..Thus, pentobarbital decreases, in a dose-dependent manner, the turnover of palmitate in brain phospholipids. This suggests that palmitate turnover is closely coupled to brain functional activity...
  78. ncbi request reprint ATP synthesis is coupled to rat liver mitochondrial RNA synthesis
    S F DasGupta
    Section on Brain Physiology and Metabolism, NIA, NIH, Bethesda, MD, USA
    Mol Cell Biochem 221:3-10. 2001
    ..At ADP concentrations above 2 mM, RNA synthesis decreased. These results demonstrate that mitochondrial transcription is tightly coupled to ATP levels...
  79. ncbi request reprint Energy consumption by phospholipid metabolism in mammalian brain
    A D Purdon
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    Neurochem Res 27:1641-7. 2002
    ..This new estimate is consistent with recent evidence that phospholipids actively participate in brain signaling and membrane remodeling, among other processes...
  80. ncbi request reprint Blood-brain barrier transport of kynurenines: implications for brain synthesis and metabolism
    S Fukui
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892
    J Neurochem 56:2007-17. 1991
    ..In contrast, QUIN, KYNA, and 3-HANA cross the blood-brain barrier poorly, and therefore are not expected to contribute significantly to brain pools under normal conditions...
  81. ncbi request reprint The effect of brain atrophy on cerebral hypometabolism in the visual variant of Alzheimer disease
    A L Bokde
    Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Arch Neurol 58:480-6. 2001
    ..The different patterns of hypometabolism indicate the differential development of the lesions between the AD and AD + VS groups...
  82. ncbi request reprint Chronic administration of lamotrigine downregulates COX-2 mRNA and protein in rat frontal cortex
    Ho Joo Lee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 9, 1S 126, Bethesda, MD 20892, USA
    Neurochem Res 33:861-6. 2008
    ..Consistent with the hypothesis, lamotrigine and other mood-stabilizers have a common downregulatory action on COX-2 expression in rat brain, which may account in part for their efficacy in bipolar disorder...
  83. ncbi request reprint One generation of n-3 polyunsaturated fatty acid deprivation increases depression and aggression test scores in rats
    James C DeMar
    Brain Physiology and Metabolism Section, National Institute on Aging, and Child Psychiatry Branch, National Institutes of Health Bethesda, MD, 20892, USA
    J Lipid Res 47:172-80. 2006
    ....
  84. pmc Imaging neuroinflammation in Alzheimer's disease with radiolabeled arachidonic acid and PET
    Giuseppe Esposito
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Nucl Med 49:1414-21. 2008
    ..Data also indicate that neuroinflammation contributes to Alzheimer's disease (AD). On the basis of these observations, K* for AA was hypothesized to be elevated in patients with AD...
  85. ncbi request reprint 5-HT2A/2C receptor signaling via phospholipase A2 and arachidonic acid is attenuated in mice lacking the serotonin reuptake transporter
    Ying Qu
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Building 9, Room 1S128, Bethesda, MD, 20892, USA
    Psychopharmacology (Berl) 180:12-20. 2005
    ..To further understand SERT function, we measured a marker of regional brain phospholipase A2 (PLA2) activation in SERT knockout mice (SERT-/-) and their littermate controls (SERT+/+)...
  86. ncbi request reprint Lithium chloride, administered chronically to rats, does not affect the fractional phosphorylation of brain cytosolic phospholipase A2, while reducing its net protein level
    Gayani R Weerasinghe
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Brain Res Bull 59:303-6. 2003
    ..Thus, decreased brain PLA(2) enzyme activity caused by chronic lithium is likely a consequence only of lithium's downregulation of cPLA(2) transcription...
  87. ncbi request reprint Imaging brain phospholipase A2-mediated signal transduction in response to acute fluoxetine administration in unanesthetized rats
    Ying Qu
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neuropsychopharmacology 28:1219-26. 2003
    ..The results show that it is possible to image quantitatively PLA(2)-mediated signal transduction in vivo in response to fluoxetine...
  88. ncbi request reprint The effect of chronic lithium on arachidonic acid release and metabolism in rat brain does not involve secretory phospholipase A2 or lipoxygenase/cytochrome P450 pathways
    Gayani R Weerasinghe
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Brain Res Bull 63:485-9. 2004
    ..These results indicate that the effect of lithium selectively involves the cPLA2/COX-2 pathway, which might be responsible for the therapeutic effect in bipolar disorder...
  89. ncbi request reprint Topiramate does not alter expression in rat brain of enzymes of arachidonic acid metabolism
    Sandra Ghelardoni
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg 10, Rm 6N202, Bethesda, MD 20892, USA
    Psychopharmacology (Berl) 180:523-9. 2005
    ..Phase II clinical trials with the anticonvulsant topiramate [2,3:4,5-bis-O-(1-methylethylidene)-beta-D-fructopyranose sulfamate] suggest that this drug may also be effective for bipolar disorder...
  90. ncbi request reprint Muscarinic versus nicotinic modulation of a visual task. a pet study using drug probes
    M J Mentis
    Laboratory of Neurosciences, NIA NIH, Bethesda, MD, USA
    Neuropsychopharmacology 25:555-64. 2001
    ..A parsimonious reconciliation of these results with functional anatomy suggests that muscarinic action modulates visual attribute processing, while nicotinic action modulates arousal and selective attention to the visual task...
  91. ncbi request reprint Chronic fluoxetine upregulates activity, protein and mRNA levels of cytosolic phospholipase A2 in rat frontal cortex
    J S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Pharmacogenomics J 6:413-20. 2006
    ..Chronic fluoxetine's effect on cPLA(2) expression was opposite to the effect reported with chronic lithium or carbamazepine administration, and may be part of fluoxetine's mode of action...
  92. ncbi request reprint Beta-amyloid induced increase in choline flux across PC12 cell membranes
    D D Allen
    Laboratory of Neurosciences, NIA, NIH, Bethesda, MD 20892, USA
    Neurosci Lett 234:71-3. 1997
    ....
  93. ncbi request reprint Phospholipid composition and levels are not altered in fibroblasts bearing presenilin-1 mutations
    E J Murphy
    Section on Brain Physiology and Metabolism, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Brain Res Bull 52:207-12. 2000
    ..However, these results do not preclude the possible use of other fibroblasts bearing AD-related mutations, e.g., APP mutations, to examine AD-related changes in brain lipid metabolism, or of these fibroblasts under different conditions...
  94. ncbi request reprint Striate cortex in humans demonstrates the relationship between activation and variations in visual form
    L L Beason-Held
    Laboratory of Neurosciences, NIA, National Institutes of Health, Bethesda, MD 20892, USA
    Exp Brain Res 130:221-6. 2000
    ..This finding suggests that a special subpopulation of striate cortical neurons participates in the ability to extract and process structural continuity within visual stimuli...
  95. ncbi request reprint Flurbiprofen, a cyclooxygenase inhibitor, reduces the brain arachidonic acid signal in response to the cholinergic muscarinic agonist, arecoline, in awake rats
    Mireille Basselin
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg 9, Room 1S126, MSC 0947, 9 Memorial Drive, Bethesda, MD 20892, USA
    Neurochem Res 32:1857-67. 2007
    ....
  96. ncbi request reprint Chronic treatment of rats with sodium valproate downregulates frontal cortex NF-kappaB DNA binding activity and COX-2 mRNA
    Jagadeesh S Rao
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Bipolar Disord 9:513-20. 2007
    ..VPA shares many cellular and molecular targets with lithium, including reducing arachidonic acid turnover in rat brain phospholipids and cyclooxygenase-2 (COX-2) protein level and activity in rat brain...
  97. pmc Quantifying conversion of linoleic to arachidonic and other n-6 polyunsaturated fatty acids in unanesthetized rats
    Fei Gao
    Brain Physiology and Metabolism Section, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, MD, USA
    J Lipid Res 51:2940-6. 2010
    ..The heavy-isotope intravenous infusion method could be used to quantify steady-state liver synthesis-secretion of AA from LA under different conditions in rodents and in humans...
  98. pmc In vivo imaging of disturbed pre- and post-synaptic dopaminergic signaling via arachidonic acid in a rat model of Parkinson's disease
    Abesh Kumar Bhattacharjee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg 9, Room 1S126, Bethesda, MD 20892, USA
    Neuroimage 37:1112-21. 2007
    ..Parkinson's disease involves loss of dopamine (DA)-producing neurons in the substantia nigra, associated with fewer pre-synaptic DA transporters (DATs) but more post-synaptic dopaminergic D2 receptors in terminal areas of these neurons...
  99. ncbi request reprint Dietary n-3 PUFA deprivation for 15 weeks upregulates elongase and desaturase expression in rat liver but not brain
    Miki Igarashi
    Brain Physiology and Metabolism Section, National Institute on Aging, NIH, Bethesda, MD 20892, USA
    J Lipid Res 48:2463-70. 2007
    ..These data suggest that liver n-3 PUFA metabolism determines DHA availability to the brain when DHA is absent from the diet...
  100. pmc Brain arachidonic acid cascade enzymes are upregulated in a rat model of unilateral Parkinson disease
    Ho Joo Lee
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, MD 20892, USA
    Neurochem Res 35:613-9. 2010
    ..Thus, the tonically increased ipsilateral AA signal in the lesioned rat corresponds to upregulated cPLA(2) and COX-2 expression within the AA metabolic cascade, which may contribute to symptoms and pathology in Parkinson disease...
  101. pmc Acute but not chronic donepezil increases muscarinic receptor-mediated signaling via arachidonic acid in unanesthetized rats
    Mireille Basselin
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg 9, Room 1S126, Bethesda, MD 20892, USA
    J Alzheimers Dis 17:369-82. 2009
    ..In contrast, the AA signal in response to arecoline was not altered following donepezil...