Glutamic Acid Decarboxylase and Glutamate Receptor Changes during Tolerance and Dependence to Benzodiazepines
Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. In contrast, signs o...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 98; no. 6; pp. 3483 - 3488 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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United States
National Academy of Sciences
13.03.2001
National Acad Sciences The National Academy of Sciences |
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Abstract | Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. In contrast, signs of dependence such as decrease in open-arm entries on an elevated plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (but not 12, 24, or 48 h) after diazepam withdrawal. During the first 72 h of withdrawal, tolerance is associated with changes in the expression of GABAA (γ-aminobutyric acid type A) receptor subunits (decrease in γ2 and α1; increase in α5) and with an increase of mRNA expression of the most abundant form of glutamic acid decarboxylase (GAD), GAD67. In contrast, DL-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam withdrawal. Immuno-histochemical studies of GluR1 subunit expression with gold-immunolabeling technique reveal that the increase of GluR1 subunit protein is localized to layer V pyramidal neurons and their apical dendrites in the cortex, and to pyramidal neurons and in their dendritic fields in hippocampus. The results suggest an involvement of GABA-mediated processes in the development and maintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via AMPA receptors) may be involved in the expression of signs of dependence after withdrawal. |
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AbstractList | Protracted administration of diazepam elicits tolerance, whereas
discontinuation of treatment results in signs of dependence. Tolerance
to the anticonvulsant action of diazepam is present in an early phase
(6, 24, and 36 h) but disappears in a late phase (72–96 h) of
withdrawal. In contrast, signs of dependence such as decrease in
open-arm entries on an elevated plus-maze and increased susceptibility
to pentylenetetrazol-induced seizures were apparent 96 h (but not
12, 24, or 48 h) after diazepam withdrawal. During the first
72 h of withdrawal, tolerance is associated with changes in the
expression of GABA
A
(γ-aminobutyric acid type A) receptor
subunits (decrease in γ
2
and α
1
; increase
in α
5
) and with an increase of mRNA expression of the
most abundant form of glutamic acid decarboxylase (GAD),
GAD
67
. In contrast,
dl
-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid
(AMPA) receptor GluR1 subunit mRNA and cognate protein, which are
normal during the early phase of diazepam withdrawal, increase by
approximately 30% in cortex and hippocampus in association with the
appearance of signs of dependence 96 h after diazepam withdrawal.
Immunohistochemical studies of GluR1 subunit expression with
gold-immunolabeling technique reveal that the increase of GluR1 subunit
protein is localized to layer V pyramidal neurons and their apical
dendrites in the cortex, and to pyramidal neurons and in their
dendritic fields in hippocampus. The results suggest an involvement of
GABA-mediated processes in the development and maintenance of tolerance
to diazepam, whereas excitatory amino acid-related processes
(presumably via AMPA receptors) may be involved in the expression
of signs of dependence after withdrawal. Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. In contrast, signs of dependence such as decrease in open-arm entries on an elevated plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (but not 12, 24, or 48 h) after diazepam withdrawal. During the first 72 h of withdrawal, tolerance is associated with changes in the expression of GABAA (γ-aminobutyric acid type A) receptor subunits (decrease in γ2 and α1; increase in α5) and with an increase of mRNA expression of the most abundant form of glutamic acid decarboxylase (GAD), GAD67. In contrast, DL-α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam withdrawal. Immuno-histochemical studies of GluR1 subunit expression with gold-immunolabeling technique reveal that the increase of GluR1 subunit protein is localized to layer V pyramidal neurons and their apical dendrites in the cortex, and to pyramidal neurons and in their dendritic fields in hippocampus. The results suggest an involvement of GABA-mediated processes in the development and maintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via AMPA receptors) may be involved in the expression of signs of dependence after withdrawal. Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. tolerance to the anticovulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72–96 h) of withdrawal. In contrast, signs of dependence such as decrease in open-arm entries on an elevated plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (but not 12, 24, or 48 h) after diazepam withdrawal. During the first 72 h of withdrawal, tolerance is associated with changes in the expression of GABA A (γ-aminobutyric acid type A) receptor subunits (decrease in γ 2 and α 1 ; increase in α 5 ) and with an increase of mRNA expression of the most abundant form of glutamic acid decarboxylase (GAD), GAD 67 . In contrast, dl -α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam withdrawal. Immunohistochemical studies of GluR1 subunit expression with gold-immunolabeling technique reveal that the increase of GluR1 subunit protein is localized to layer V pyramidal neurons and their apical dendrites in the cortex, and to pyramidal neurons and in their dendritic fields in hippocampus. The results suggest an involvement of GABA-mediated processes in the development and maintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via AMPA receptors) may be involved in the expression of signs of dependence after withdrawal. Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. In contrast, signs of dependence such as decrease in open-arm entries on an elevated plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (but not 12, 24, or 48 h) after diazepam withdrawal. During the first 72 h of withdrawal, tolerance is associated with changes in the expression of GABA(A) (gamma-aminobutyric acid type A) receptor subunits (decrease in gamma(2) and alpha(1); increase in alpha(5)) and with an increase of mRNA expression of the most abundant form of glutamic acid decarboxylase (GAD), GAD(67). In contrast, dl-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam withdrawal. Immunohistochemical studies of GluR1 subunit expression with gold-immunolabeling technique reveal that the increase of GluR1 subunit protein is localized to layer V pyramidal neurons and their apical dendrites in the cortex, and to pyramidal neurons and in their dendritic fields in hippocampus. The results suggest an involvement of GABA-mediated processes in the development and maintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via AMPA receptors) may be involved in the expression of signs of dependence after withdrawal. Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant action of diazepam is present in an early phase (6, 24, and 36 h) but disappears in a late phase (72-96 h) of withdrawal. In contrast, signs of dependence such as decrease in open-arm entries on an elevated plus-maze and increased susceptibility to pentylenetetrazol-induced seizures were apparent 96 h (but not 12, 24, or 48 h) after diazepam withdrawal. During the first 72 h of withdrawal, tolerance is associated with changes in the expression of GABA sub(A) ( gamma -aminobutyric acid type A) receptor subunits (decrease in gamma sub(2) and alpha sub(1); increase in alpha sub(5)) and with an increase of mRNA expression of the most abundant form of glutamic acid decarboxylase (GAD), GAD sub(67). In contrast, DL- alpha -amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor GluR1 subunit mRNA and cognate protein, which are normal during the early phase of diazepam withdrawal, increase by approximately 30% in cortex and hippocampus in association with the appearance of signs of dependence 96 h after diazepam withdrawal. Immunohistochemical studies of GluR1 subunit expression with gold-immunolabeling technique reveal that the increase of GluR1 subunit protein is localized to layer V pyramidal neurons and their apical dendrites in the cortex, and to pyramidal neurons and in their dendritic fields in hippocampus. The results suggest an involvement of GABA-mediated processes in the development and maintenance of tolerance to diazepam, whereas excitatory amino acid-related processes (presumably via AMPA receptors) may be involved in the expression of signs of dependence after withdrawal. |
Author | Pesold, Christine Guidotti, Alessandro Auta, James Costa, Erminio Izzo, Emanuela Impagnatiello, Francesco |
AuthorAffiliation | Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois, Chicago, IL 60612 |
AuthorAffiliation_xml | – name: Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois, Chicago, IL 60612 |
Author_xml | – sequence: 1 givenname: Emanuela surname: Izzo fullname: Izzo, Emanuela – sequence: 2 givenname: James surname: Auta fullname: Auta, James – sequence: 3 givenname: Francesco surname: Impagnatiello fullname: Impagnatiello, Francesco – sequence: 4 givenname: Christine surname: Pesold fullname: Pesold, Christine – sequence: 5 givenname: Alessandro surname: Guidotti fullname: Guidotti, Alessandro – sequence: 6 givenname: Erminio surname: Costa fullname: Costa, Erminio |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/11248104$$D View this record in MEDLINE/PubMed |
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Notes | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 To whom reprint requests should be addressed at: 1601 West Taylor Street, M/C 912, Psychiatric Institute, University of Illinois, Chicago, IL 60612. E-mail: Costa@psych.uic.edu. Contributed by Erminio Costa |
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Snippet | Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant... Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. Tolerance to the anticonvulsant... Protracted administration of diazepam elicits tolerance, whereas discontinuation of treatment results in signs of dependence. tolerance to the anticovulsant... |
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SubjectTerms | Animals Antibodies Biological Sciences Brain - drug effects Brain - metabolism Dendrites Diazepam - pharmacology Drug therapy Drug Tolerance Frontal Lobe - drug effects Frontal Lobe - metabolism GABA Modulators - pharmacology Gene Expression Profiling Glutamate Decarboxylase - genetics Glutamate Decarboxylase - metabolism Hippocampus Hippocampus - drug effects Hippocampus - metabolism Isoenzymes - genetics Isoenzymes - metabolism Ligands Male Messenger RNA N methyl D aspartate receptors Neurological disorders Neurology Occipital Lobe - drug effects Occipital Lobe - metabolism Rats Rats, Inbred F344 Receptors Receptors, AMPA - genetics Receptors, AMPA - metabolism RNA, Messenger Seizures Substance-Related Disorders Time Factors Vehicles |
Title | Glutamic Acid Decarboxylase and Glutamate Receptor Changes during Tolerance and Dependence to Benzodiazepines |
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