Glycine stimulates the release of labeled acetylcholine but not dopamine nor glutamate from superfused rat striatal tissue
Autor: | Leandro de Magalhães, Marina S. Hernandes, Lanfranco R.P. Troncone |
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Rok vydání: | 2007 |
Předmět: |
Male
Agonist medicine.medical_specialty N-Methylaspartate Time Factors medicine.drug_class Dopamine Glycine Glutamic Acid Tetrodotoxin In Vitro Techniques Biology Tritium chemistry.chemical_compound Internal medicine Excitatory Amino Acid Agonists medicine Animals Drug Interactions Rats Wistar Molecular Biology Glycine receptor Analysis of Variance Dose-Response Relationship Drug General Neuroscience Glycine Agents Glycine receptor antagonist Strychnine Acetylcholine Corpus Striatum Rats Endocrinology chemistry Haloperidol NMDA receptor Cholinergic Calcium Neurology (clinical) Antipsychotic Agents Sodium Channel Blockers Developmental Biology medicine.drug |
Zdroj: | Brain Research. 1168:32-37 |
ISSN: | 0006-8993 |
Popis: | Glycine is known as an inhibitory neurotransmitter in the spinal cord and forebrain but its precise role in the forebrain is largely overlooked. This investigation evaluated whether glycine alters acetylcholine, glutamate or dopamine release from striatal tissue using an in vitro approach. We observed that while glycine induced a robust (3)H-acetylcholine release ((3)H-ACh) from superfused striatal tissue, it failed at releasing (3)H-glutamate or (3)H-dopamine. Glycine stimulated (3)H-ACh release in a dose- and calcium-dependent manner (EC(50)=69 microM). Tetrodotoxin (1 microM) inhibited about 75% of the release demonstrating a predominant dendritic and cell body location of glycine receptors. The prototypical glycine receptor antagonist strychnine at 10 microM completely abolished (3)H-ACh release. To further characterize the role of striatal glycine receptors in (3)H-ACh release we examined glycine effects after in vivo treatment with Haloperidol-decanoate (HD). Treatment for 30 days or more with HD decreased maximal glycine-stimulated release of (3)H-ACh suggesting a non-competitive inhibition. After 30 days of washout release parameters did not return to vehicle-treated levels. The glutamate agonist NMDA also stimulated acetylcholine release but showed slightly different behavior in HD-treated striatal tissue. These effects could be attributed to changes in chloride transporters expressed in the giant striatal cholinergic cell as well as glycine receptor subunit composition and finally, GABA/glycine co-release in this tissue. |
Databáze: | OpenAIRE |
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