[3H]-flunitrazepam -labeled benzodiazepine binding sites in the hippocampal formation in autism : A multiple concentration autoradiographic study

Increasing evidence indicates that the GABAergic system in cerebellar and limbic structures is affected in autism. We extended our previous study that found reduced [(3)H]flunitrazepam-labeled benzodiazepine sites in the autistic hippocampus to determine whether this reduction was due to a decrease...

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Bibliographic Details
Published in:Journal of autism and developmental disorders 2007-05, Vol.37 (5), p.911-920
Main Authors: GUPTILL, Jeffrey T, BOOKER, Anne B, GIBBS, Terrell T, KEMPER, Thomas L, BAUMAN, Margaret L, BLATT, Gene J
Format: Article
Language:English
Subjects:
Adolescent
Adult
Adult and adolescent clinical studies
Affinity
Anatomy
Attention Span
Autism
Autistic Disorder - diagnosis
Autistic Disorder - pathology
Autoradiography - instrumentation
Benzodiazepines
Benzodiazepines - pharmacokinetics
Binding sites
Binding Sites - drug effects
Biological and medical sciences
Brain
Cerebellum
Cerebellum - metabolism
Cerebellum - pathology
Death
Developmental Delays
Developmental disorders
Expressive Language
Flunitrazepam
Flunitrazepam - pharmacokinetics
GABA Modulators - pharmacokinetics
Gamma-aminobutyric acid
Hippocampus
Hippocampus - metabolism
Hippocampus - pathology
Humans
Information Processing
Inhibitory processing
Intellectual Disability
Language Skills
Male
Males
Medical sciences
Miscellaneous
Motor Development
Nerve Net - metabolism
Nerve Net - pathology
Nissl Bodies - metabolism
Nissl Bodies - pathology
Pregnancy
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Quantitation
Receptors, GABA - metabolism
Seizures
Speech
Stimuli
Verbal Ability
Verbal Communication
γ-Aminobutyric acid A receptors
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Description
Summary:Increasing evidence indicates that the GABAergic system in cerebellar and limbic structures is affected in autism. We extended our previous study that found reduced [(3)H]flunitrazepam-labeled benzodiazepine sites in the autistic hippocampus to determine whether this reduction was due to a decrease in binding site number (B (max)) or altered affinity (K (d)) to bind to the ligand. Quantitation of hippocampal lamina demonstrated a 20% reduction in B (max) indicating a trend toward a decreased number of benzodiazepine binding sites in the autistic group but normal K (d) values. A reduction in the number of hippocampal benzodiazepine binding sites suggests alterations in the modulation of GABA(A) receptors in the presence of GABA in the autistic brain, possibly resulting in altered inhibitory functioning of hippocampal circuitry.
ISSN:0162-3257
1573-3432
DOI:10.1007/s10803-006-0226-7