Alterations of GABA-A and dopamine D-2 brain receptors in dogs with portal-systemic encephalopathy
| Autor: | Ezio Ventura, I. Casciarri, M. Germini, Odoardo Tofanetti, Mario Baraldi, C. Vezzelli, M.L. Zeneroli |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
medicine.medical_specialty
Dopamine Glutamate decarboxylase Encephalopathy Stimulation Biology Inhibitory postsynaptic potential General Biochemistry Genetics and Molecular Biology Dimethylnitrosamine Receptors Dopamine Norepinephrine Radioligand Assay Dogs Internal medicine medicine Animals General Pharmacology Toxicology and Pharmaceutics Receptor Octopamine Diazepam GABAA receptor Glutamate Decarboxylase Brain General Medicine medicine.disease Receptors GABA-A Disease Models Animal Kinetics Endocrinology Dopamine receptor Hepatic Encephalopathy Synapses medicine.drug |
| Zdroj: | Life sciences. 48(1) |
| ISSN: | 0024-3205 |
| Popis: | The binding characteristics of gamma-aminobutyric acid-A (GABA-A) receptors and the kinetic characteristics of the target enzyme of GABA synthesis in nerve terminals, glutamic acid decarboxylase (GAD), were studied in a dog model of portal-systemic encephalopathy obtained by porta-caval shunt performed in dimethylnitrosamine pretreated animals. Furthermore the properties of dopamine receptors and the levels of catecholamines of encephalopathic dogs were investigated. The mild stage of encephalopathy was characterized by an up-regulation of the inhibitory GABA-A receptors probably related to a decrease of GABA in nerve terminals since GAD was decreased and by a slight decrease of catecholamines and by an increased synthesis of octopamine associated with a decreased affinity of dopamine receptors. In the severe stage there was a selection of high affinity GABA-A receptors with an increased number of benzodiazepine recognition sites which were supersensitive to GABA stimulation, a decreased number of Dopamine D-2 receptors and a marked reduction of catecholamines. These data seem to suggest that the neurological disturbances of experimental portal-systemic encephalopathy might be the result of an imbalance between inhibitory and excitatory systems leading to a prevalence of the first one. |
| Databáze: | OpenAIRE |
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