Changes in striatal electroencephalography and neurochemistry induced by kainic acid seizures are modified by dopamine receptor antagonists
| Autor: | Paul Fosbraey, James A. Bourne, John Halliday |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Kainic acid
medicine.medical_specialty Dopamine Guinea Pigs Glutamic Acid chemistry.chemical_compound Dopamine receptor D1 Seizures Internal medicine Dopamine receptor D2 medicine Excitatory Amino Acid Agonists Animals gamma-Aminobutyric Acid Pharmacology SCH-23390 Aspartic Acid Kainic Acid Chemistry Receptors Dopamine D2 Receptors Dopamine D1 Glutamate receptor Electroencephalography Homovanillic Acid Neurochemistry Benzazepines Corpus Striatum Dopamine D2 Receptor Antagonists Endocrinology Dopamine receptor 3 4-Dihydroxyphenylacetic Acid Dopamine Antagonists Sulpiride medicine.drug |
| Zdroj: | European journal of pharmacology. 413(2-3) |
| ISSN: | 0014-2999 |
| Popis: | We investigated the involvement of striatal dopamine release in electrographic and motor seizure activity evoked by kainic acid in the guinea pig. The involvement of the dopamine receptor subtypes was studied by systemic administration of the dopamine D(1) receptor antagonist, R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrochloride (SCH 23390; 0.5 mg kg(-1)), or the dopamine D(2) antagonist, (5-aminosulphonyl)-N-[(1-ethyl-2-pyrrolidinyl)-methyl]-2-methoxybenzamide (sulpiride, 30 mg kg(-1)). Microdialysis and high performance liquid chromatography were used to monitor changes in extracellular levels of striatal dopamine and its metabolites, glutamate, aspartate and gamma-amino-butyric acid (GABA). These data were correlated with changes in the striatal and cortical electroencephalographs and clinical signs. We found that, although neither dopamine receptor antagonist inhibited behavioural seizure activity, blockade of the dopamine D(1)-like receptor with SCH 23390 significantly reduced both the 'power' of the electrical seizure activity and the associated change in extracellular striatal concentration of glutamate, whilst increasing the extracellular striatal concentration of GABA. In contrast, blockade of the dopamine D(2)-like receptor with sulpiride significantly increased the extracellular, striatal content of glutamate and the dopamine metabolites. These results confirm previous evidence in other models of chemically-evoked seizures that antagonism of the dopamine D(1) receptor tends to reduce motor and electrographic seizure activity as well as excitatory amino-acid transmitter activity, while antagonism of the dopamine D(2) receptor has relatively less apparent effect. |
| Databáze: | OpenAIRE |
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