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dc.contributor.authorMoratalla, Rosario-
dc.contributor.authorBarth TM-
dc.contributor.authorBowery, N. G.-
dc.date.accessioned2017-05-30T09:55:31Z-
dc.date.available2017-05-30T09:55:31Z-
dc.date.issued1989-
dc.identifierissn: 0028-3908-
dc.identifier.citationNeuropharmacology 28: 893- 900 (1989)-
dc.identifier.urihttp://hdl.handle.net/10261/150638-
dc.description.abstractIt has previously been shown that diazepam impairs behavioural recovery from partial unilateral ablation of the cerebral cortex in rats. The present study confirmed this in rats with large unilateral lesions of the frontal cortex and showed that diazepam (5 mg/kg i.p. daily for 14 days immediately after surgery) prevented recovery from sensory asymmetry even after 120 days. In saline-treated rats greater than 80% recovery had occurred by this time. A study of binding to benzodiazepine receptors, using an in vitro autoradiographic technique, was performed to determine whether the lack of recovery after administration of diazepam was associated with any long-term receptor changes on the damaged side of the brain. Binding of [3H]Ro15-1788 was increased by up to 40% in the caudate putamen on the decorticated side at 14-120 days. This was not significantly altered by treatment with diazepam. Binding of [3H]Ro15-1788 in the nucleus accumbens was not altered by lesion of the frontal cortex alone or after treatment with diazepam. It is concluded that the lack of recovery from sensory asymmetry, produced by diazepam after lesion of the frontal cortex cannot be correlated with any change in binding to benzodiazepine receptors within the corpus striatum.-
dc.publisherPergamon Press-
dc.rightsclosedAccess-
dc.titleBenzodiazepine receptor autoradiography in corpus striatum of rat after large frontal cortex lesions and chronic treatment with diazepam-
dc.typeartículo-
dc.date.updated2017-05-30T09:55:31Z-
dc.description.versionPeer Reviewed-
dc.language.rfc3066eng-
dc.relation.csic-
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