Brain glucose metabolism in chronic marijuana users at baseline and during marijuana intoxication.
Identifieur interne : 000A14 ( PubMed/Corpus ); précédent : 000A13; suivant : 000A15Brain glucose metabolism in chronic marijuana users at baseline and during marijuana intoxication.
Auteurs : N D Volkow ; H. Gillespie ; N. Mullani ; L. Tancredi ; C. Grant ; A. Valentine ; L. HollisterSource :
- Psychiatry research [ 0165-1781 ] ; 1996.
English descriptors
- KwdEn :
- Basal Ganglia (diagnostic imaging), Basal Ganglia (metabolism), Brain (metabolism), Cerebellum (diagnostic imaging), Cerebellum (metabolism), Chronic Disease, Dronabinol (blood), Frontal Lobe (diagnostic imaging), Frontal Lobe (metabolism), Humans, Marijuana Abuse (complications), Marijuana Abuse (metabolism), Paleopathology, Psychomotor Disorders (chemically induced), Tomography, Emission-Computed.
- MESH :
- chemical , blood : Dronabinol.
- chemically induced : Psychomotor Disorders.
- complications : Marijuana Abuse.
- diagnostic imaging : Basal Ganglia, Cerebellum, Frontal Lobe.
- metabolism : Basal Ganglia, Brain, Cerebellum, Frontal Lobe, Marijuana Abuse.
- Chronic Disease, Humans, Paleopathology, Tomography, Emission-Computed.
Abstract
Despite the widespread abuse of marijuana, knowledge about its effects in the human brain is limited. Brain glucose metabolism with and without delta 9 tetrahydrocannabinol (THC) (main psychoactive component of marijuana) was evaluated in eight normal subjects and eight chronic marijuana abusers with positron emission tomography. At baseline, marijuana abusers showed lower relative cerebellar metabolism than normal subjects. THC increased relative cerebellar metabolism in all subjects, but only abusers showed increases in orbitofrontal cortex, prefrontal cortex, and basal ganglia. Cerebellar metabolism during THC intoxication was significantly correlated with the subjective sense of intoxication. The decreased cerebellar metabolism in marijuana abusers at baseline could account for the motor deficits previously reported in these subjects. The activation of orbitofrontal cortex and basal ganglia by THC in the abusers but not in the normal subjects could underlie one of the mechanisms leading to the drive and the compulsion to self-administer the drug observed in addicted individuals.
PubMed: 8797240
Links to Exploration step
pubmed:8797240Le document en format XML
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<author><name sortKey="Volkow, N D" sort="Volkow, N D" uniqKey="Volkow N" first="N D" last="Volkow">N D Volkow</name>
<affiliation><nlm:affiliation>Medical Department, Brookhaven National Laboratory, Upton, NY 11973, USA.</nlm:affiliation>
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<author><name sortKey="Gillespie, H" sort="Gillespie, H" uniqKey="Gillespie H" first="H" last="Gillespie">H. Gillespie</name>
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<author><name sortKey="Mullani, N" sort="Mullani, N" uniqKey="Mullani N" first="N" last="Mullani">N. Mullani</name>
</author>
<author><name sortKey="Tancredi, L" sort="Tancredi, L" uniqKey="Tancredi L" first="L" last="Tancredi">L. Tancredi</name>
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<author><name sortKey="Grant, C" sort="Grant, C" uniqKey="Grant C" first="C" last="Grant">C. Grant</name>
</author>
<author><name sortKey="Valentine, A" sort="Valentine, A" uniqKey="Valentine A" first="A" last="Valentine">A. Valentine</name>
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<author><name sortKey="Hollister, L" sort="Hollister, L" uniqKey="Hollister L" first="L" last="Hollister">L. Hollister</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Brain glucose metabolism in chronic marijuana users at baseline and during marijuana intoxication.</title>
<author><name sortKey="Volkow, N D" sort="Volkow, N D" uniqKey="Volkow N" first="N D" last="Volkow">N D Volkow</name>
<affiliation><nlm:affiliation>Medical Department, Brookhaven National Laboratory, Upton, NY 11973, USA.</nlm:affiliation>
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<author><name sortKey="Gillespie, H" sort="Gillespie, H" uniqKey="Gillespie H" first="H" last="Gillespie">H. Gillespie</name>
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<author><name sortKey="Mullani, N" sort="Mullani, N" uniqKey="Mullani N" first="N" last="Mullani">N. Mullani</name>
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<author><name sortKey="Tancredi, L" sort="Tancredi, L" uniqKey="Tancredi L" first="L" last="Tancredi">L. Tancredi</name>
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<author><name sortKey="Grant, C" sort="Grant, C" uniqKey="Grant C" first="C" last="Grant">C. Grant</name>
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<author><name sortKey="Valentine, A" sort="Valentine, A" uniqKey="Valentine A" first="A" last="Valentine">A. Valentine</name>
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<author><name sortKey="Hollister, L" sort="Hollister, L" uniqKey="Hollister L" first="L" last="Hollister">L. Hollister</name>
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<series><title level="j">Psychiatry research</title>
<idno type="ISSN">0165-1781</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal Ganglia (diagnostic imaging)</term>
<term>Basal Ganglia (metabolism)</term>
<term>Brain (metabolism)</term>
<term>Cerebellum (diagnostic imaging)</term>
<term>Cerebellum (metabolism)</term>
<term>Chronic Disease</term>
<term>Dronabinol (blood)</term>
<term>Frontal Lobe (diagnostic imaging)</term>
<term>Frontal Lobe (metabolism)</term>
<term>Humans</term>
<term>Marijuana Abuse (complications)</term>
<term>Marijuana Abuse (metabolism)</term>
<term>Paleopathology</term>
<term>Psychomotor Disorders (chemically induced)</term>
<term>Tomography, Emission-Computed</term>
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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Dronabinol</term>
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<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Psychomotor Disorders</term>
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<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Marijuana Abuse</term>
</keywords>
<keywords scheme="MESH" qualifier="diagnostic imaging" xml:lang="en"><term>Basal Ganglia</term>
<term>Cerebellum</term>
<term>Frontal Lobe</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Basal Ganglia</term>
<term>Brain</term>
<term>Cerebellum</term>
<term>Frontal Lobe</term>
<term>Marijuana Abuse</term>
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<keywords scheme="MESH" xml:lang="en"><term>Chronic Disease</term>
<term>Humans</term>
<term>Paleopathology</term>
<term>Tomography, Emission-Computed</term>
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<front><div type="abstract" xml:lang="en">Despite the widespread abuse of marijuana, knowledge about its effects in the human brain is limited. Brain glucose metabolism with and without delta 9 tetrahydrocannabinol (THC) (main psychoactive component of marijuana) was evaluated in eight normal subjects and eight chronic marijuana abusers with positron emission tomography. At baseline, marijuana abusers showed lower relative cerebellar metabolism than normal subjects. THC increased relative cerebellar metabolism in all subjects, but only abusers showed increases in orbitofrontal cortex, prefrontal cortex, and basal ganglia. Cerebellar metabolism during THC intoxication was significantly correlated with the subjective sense of intoxication. The decreased cerebellar metabolism in marijuana abusers at baseline could account for the motor deficits previously reported in these subjects. The activation of orbitofrontal cortex and basal ganglia by THC in the abusers but not in the normal subjects could underlie one of the mechanisms leading to the drive and the compulsion to self-administer the drug observed in addicted individuals.</div>
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<Title>Psychiatry research</Title>
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<ArticleTitle>Brain glucose metabolism in chronic marijuana users at baseline and during marijuana intoxication.</ArticleTitle>
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<Abstract><AbstractText>Despite the widespread abuse of marijuana, knowledge about its effects in the human brain is limited. Brain glucose metabolism with and without delta 9 tetrahydrocannabinol (THC) (main psychoactive component of marijuana) was evaluated in eight normal subjects and eight chronic marijuana abusers with positron emission tomography. At baseline, marijuana abusers showed lower relative cerebellar metabolism than normal subjects. THC increased relative cerebellar metabolism in all subjects, but only abusers showed increases in orbitofrontal cortex, prefrontal cortex, and basal ganglia. Cerebellar metabolism during THC intoxication was significantly correlated with the subjective sense of intoxication. The decreased cerebellar metabolism in marijuana abusers at baseline could account for the motor deficits previously reported in these subjects. The activation of orbitofrontal cortex and basal ganglia by THC in the abusers but not in the normal subjects could underlie one of the mechanisms leading to the drive and the compulsion to self-administer the drug observed in addicted individuals.</AbstractText>
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