TRADITIONAL POSTER - ismrm

Poster Sessions
2396. Protective Actions of L-Carnitine in Ammonia-Precipitated Hepatic Encephalopathy
Jane Missler 1,2 , Wenlei Jiang 3 , Dieter Leibfritz 2 , Claudia Zwingmann 1
1 Département de médicine, Centre de Recherche, Hôpital Saint-Luc, Université de Montréal, Montréal, Quebec, Canada; 2 Department
of Chemistry, University of Bremen, Bremen, Germany; 3 Département de médicine , Centre de Recherche, Hôpital Saint-Luc,
Université de Montréal, Montréal, Quebec, Canada
Hepatic Encephalopathy is associated with hyperammonemia and energetic changes in brain. In animal models and patients with mild HE, L-carnitine has
been shown to be protective. In order to investigate the effect of L-carnitine on brain energy-metabolism, multinuclear NMR was used to measure metabolic
pathways in brain following administration of [U-13C]glucose in ammonia-treated rats with PCA. In ammonia-precipitated encephalopathy, L-carnitine
considerably delayed the time to coma, concomitantly to enhanced ammonia detoxification via astrocytic glutamine synthesis and attenuation of lactate
accumulation. These results indicate to cell-specific actions of L-carnitine which might explain its therapeutic effect in ammonia-precipitated HE in cirrhotic
patients.
2397. Effects of Desipramine Pretreatment on Behavioral and Regional Neurochemical Responses in the
Mouse Forced Swimming Test: A High Resolution in Vivo 1H-MRS Study at 9.4 Tesla
Sang-Young Kim 1,2 , Chi-Bong Choi 3 , Yun-Jung Lee 4 , Hyeonjin Kim 4 , Do-Wan Lee 1,2 , Dong-Cheol Woo 1,2 ,
Jeong-Ho Chae 5 , Bo-Young Choe 1,2
1 Department of Biomedical Engineering, The Catholic University of Korea, Seoul, Korea, Republic of; 2 Research Institute of
Biomedical Engineering, Seoul, Korea, Republic of; 3 Department of Radiology, Kyunghee University Medical Center, Seoul, Korea,
Republic of; 4 Gachon University of Medicine and Science, Incheon, Korea, Republic of; 5 Department of Psychiatry, The Catholic
University of Korea, Seoul, Korea, Republic of
Until recently, no data are available about the behavioral and simultaneous non-invasive measurements of neurochemial responses following antidepressant
treatment in mice FST model. In this study, in vivo 1H-MRS at 9.4 T was used to examine the effects of desipramine (DMI) pretreatment on behavioral and
regional neurocheimal responses of C57BL/6 mice brain. We found significant behavioral changes as well as metabolic alterations of glutamate and myoinositol
by the DMI pretreatment. Our results suggest that glutamatergic activity and glial cell dysfunction contribute to pathophysiological mechanisms
underlying depression and that modulation of synaptic neurotransmitter concentrations represent invaluable targets for antidepressant drug development.
2398. Implication of Myo-Inositol Metabolic Level in an Animal Model of Depression
Sang-Young Kim 1,2 , Chi-Bong Choi 3 , Hyun-Sung Lee 4 , Sung-Ho Lee 5 , Dong-Cheol Woo 1,2 , Bo-Young
Choe 1,2
1 Department of Biomedical Engineering, The Catholic University of Korea, Seoul, Korea, Republic of; 2 Research Institute of
Biomedical Engineering, Seoul, Korea, Republic of; 3 Department of Radiology, Kyunghee University Medical Center, Seoul, Korea,
Republic of; 4 Korea Basic Science Institute, Korea, Republic of; 5 Department of Veterinary Surgery, Konkuk University, Seoul,
Korea, Republic of
Animal models for depression are indispensable tools in the search to identify new antidepressant drugs. The forced swimming test (FST) is the most widely
used tool for assessing antidepressant activity in rodents. Few studies have been performed proton spectroscopy to assess antidepressant effects on brain
metabolism of rat exposed to the FST. The in vivo proton spectra quantified by LCModel revealed that myo-inositol metabolic level in left dorsolateral
prefrontal cortex of rat was significantly altered in both FST and desipramine treated group. Our findings suggest a possible role of myo-inositol within the
left DLPFC of rat model for depression.
2399. Effect of Morphine Exposure on Developing Rat Hippocampus
Christopher M. Traudt 1 , Kathleen M. Ennis 1 , Raghu Rao 1 , Ivan Tkac 2
1 Dept. of Pediatrics, University of Minnesota, Minneapolis, MN, United States; 2 University of Minnesota, Center for Magnetic
Resonance Research, Minneapolis, MN, United States
In vivo 1 H NMR NMR spectroscopy at 9.4T was used to investigate effects of morphine on the neurochemical profile of the developing rat hippocampus.
Significant differences between pup exposed to the morphine (2 mg/kg/, twice a day, P3 – P7) and their littermate controls were observed for multiple brain
metabolites on postnatal day 8. These changes had resolved by P29. Biochemical changes indicated effects of morphine on inhibitory neurotransmission
(GABA, Tau), glial development and myelination (Gln, myo-Ins), osmoregulation (myo-Ins, Tau) and antioxidant processes (GSH).These results indicate
that morphine exposure during hippocampal development may lead to hippocampal-dependant cognitive deficits in premature infants.
2400. NAA as a Non-Invasive Biomarker in Traumatic Brain Injury: Neuroprotective Effects of
Cyclosporine A
Janna L. Harris 1 , Henry Yeh 2 , Nancy E. Berman 3 , William M. Brooks 1
1 Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas City, KS, United States; 2 Department of Biostatistics,
University of Kansas Medical Center, Kansas City, KS, United States; 3 Department of Anatomy & Cell Biology, University of Kansas
Medical Center, Kansas City, KS, United States
N-acetylaspartate (NAA), a metabolite synthesized in neuronal mitochondria and detected by proton magnetic resonance spectroscopy (MRS), might serve
as a non-invasive biomarker of mitochondrial integrity after traumatic brain injury (TBI). Previous studies in human survivors of TBI have linked NAA with
cognitive recovery, although the specific mechanism has not been elucidated. We have examined a time course of changes in NAA and behavioral
impairment after TBI in a well-characterized animal model. We then investigated whether these NAA changes are sensitive to manipulation of mitochondrial
status by cyclosporine A (CsA), an experimental neuroprotective agent that inhibits mitochondrial permeability transition after TBI.