Neurochemical adaptation to cocaine abuse: reduction of N-acetyl aspartate in thalamus of human cocaine abusers
Identifieur interne : 002F46 ( Main/Merge ); précédent : 002F45; suivant : 002F47Neurochemical adaptation to cocaine abuse: reduction of N-acetyl aspartate in thalamus of human cocaine abusers
Auteurs : Shi-Jiang Li [États-Unis] ; Yonker Wang [États-Unis] ; John Pankiewicz [États-Unis] ; Elliot A. Stein [États-Unis]Source :
- Biological Psychiatry [ 0006-3223 ] ; 1999.
English descriptors
- KwdEn :
- Teeft :
- Abuser, Acute cocaine administration, Aids dementia, Anatomic localizer image, Basal, Basal ganglia, Biol, Biol psychiatry, Biophysics research institute, Cerebral atrophy, Cerebral metabolites, Cerebral vasculitis, Chronic cocaine, Chronic cocaine users, Cocaine, Cocaine abuse, Cocaine abusers, Cocaine addiction, Cocaine dependence, Cocaine group, Cocaine user, Cocaine users, Control group, Control subjects, Control volunteer, Detoxified subjects, Dopamine, Early withdrawal, Ganglion, Habitual cocaine abusers, Human brain, Imaging, Internal capsule, Localized, Localized proton, Magn, Magn reson, Magnetic resonance spectroscopic imaging, Magnetic resonance spectroscopy, Medical college, Metabolic, Metabolic concentrations, Metabolic ratios, Metabolism, Multiple sclerosis, Neurochemical, Neuron, Neuronal, Neuronal dysregulation, Neuronal loss, Neuronal viability, Neurosci biobehav, Normal control subjects, Normal volunteer, Polydrug abusers, Polysubstance abusers, Possible mechanisms, Present study, Proton, Psychiatry, Receptor availability, Reson, Resonance spectroscopy, Smrm meeting, Social phobia, Spectroscopy, Spgr images, Spgr surface coil image, Striatal dopaminergic responsiveness, Synaptic density, Thalamus, Tomography study, User, Vivo proton, Volkow, Water signal.
Abstract
Abstract: Background: The aim of this study was to determine the existence of, and possible mechanisms for, chronic cocaine use-induced neurotoxicity in the human brain. Because in vivo magnetic resonance spectroscopy (MRS) provides a noninvasive way to detect biochemical and physiological changes in the brain, we sought to specifically determine the neurochemical adaptations in chronic cocaine-dependent subjects.Methods: Twenty-one cocaine users and 13 non–drug-using, age-matched normal volunteers were recruited for an in vivo proton MRS study. Following screening that included physical examination, histories, and blood testing, cocaine group subjects received a spectral scan on a 1.5-T GE Signa scanner. Spectra were obtained from the left basal ganglia and/or the left thalamus from subjects in both groups using an rf bird-cage type head coil with single-voxel localization.Results: The level of N-acetyl aspartate in the region of left thalamus was lower (17%) in the chronic cocaine user group but not in the region of left basal ganglia, compared with the control group.Conclusions: These results suggest that chronic cocaine use may induce abnormal neurochemical activity and a state of neuronal dysregulation and/or neurotoxicity. It will now be important to determine if these alterations are reversible during withdrawal and what the functional implications of this observation are with respect to cognitive function and drug relapse.
Url:
DOI: 10.1016/S0006-3223(98)00230-3
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ISTEX:D70EFA9BCF79CC65D1C5ABCF3836DB2EAA93B029Le document en format XML
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<wicri:cityArea>Address reprint requests to Dr. Shi-Jiang Li, Biophysics Research Institute, Medical College of Wisconsin, 8701 Watertown Plank Road, P.O. Box 26509, Milwaukee</wicri:cityArea>
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<term>creatine</term>
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<term>Acute cocaine administration</term>
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<term>Biol psychiatry</term>
<term>Biophysics research institute</term>
<term>Cerebral atrophy</term>
<term>Cerebral metabolites</term>
<term>Cerebral vasculitis</term>
<term>Chronic cocaine</term>
<term>Chronic cocaine users</term>
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<term>Cocaine abuse</term>
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<term>Dopamine</term>
<term>Early withdrawal</term>
<term>Ganglion</term>
<term>Habitual cocaine abusers</term>
<term>Human brain</term>
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<term>Internal capsule</term>
<term>Localized</term>
<term>Localized proton</term>
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<term>Magn reson</term>
<term>Magnetic resonance spectroscopic imaging</term>
<term>Magnetic resonance spectroscopy</term>
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<term>Metabolic concentrations</term>
<term>Metabolic ratios</term>
<term>Metabolism</term>
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<term>Neurochemical</term>
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<term>Neurosci biobehav</term>
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<term>Normal volunteer</term>
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<term>Possible mechanisms</term>
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<term>Spgr images</term>
<term>Spgr surface coil image</term>
<term>Striatal dopaminergic responsiveness</term>
<term>Synaptic density</term>
<term>Thalamus</term>
<term>Tomography study</term>
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<front><div type="abstract" xml:lang="en">Abstract: Background: The aim of this study was to determine the existence of, and possible mechanisms for, chronic cocaine use-induced neurotoxicity in the human brain. Because in vivo magnetic resonance spectroscopy (MRS) provides a noninvasive way to detect biochemical and physiological changes in the brain, we sought to specifically determine the neurochemical adaptations in chronic cocaine-dependent subjects.Methods: Twenty-one cocaine users and 13 non–drug-using, age-matched normal volunteers were recruited for an in vivo proton MRS study. Following screening that included physical examination, histories, and blood testing, cocaine group subjects received a spectral scan on a 1.5-T GE Signa scanner. Spectra were obtained from the left basal ganglia and/or the left thalamus from subjects in both groups using an rf bird-cage type head coil with single-voxel localization.Results: The level of N-acetyl aspartate in the region of left thalamus was lower (17%) in the chronic cocaine user group but not in the region of left basal ganglia, compared with the control group.Conclusions: These results suggest that chronic cocaine use may induce abnormal neurochemical activity and a state of neuronal dysregulation and/or neurotoxicity. It will now be important to determine if these alterations are reversible during withdrawal and what the functional implications of this observation are with respect to cognitive function and drug relapse.</div>
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