Receptor systems participating in nicotine-specific effects.

摘要: It is generally accepted that self-administration of drugs prompted primarily by a reward system driven an increase in extracellular dopamine the nucleus accumbens. Recent findings accumbens can be caused many other factors, among them stress, suggest more complex mechanism, and possibly differences for different compounds. In present paper we compare effects receptor-specific antagonists on induced nicotine with cocaine conscious rats. The compounds alone or together were injected intravenously, level changes measured via microdialysis. When administered effect was additive. Apparently there some interaction between two compounds, since had no after combined administration. Perhaps available pool exhausted prior nicotinic antagonist mecamylamine, muscarinic atropine, NMDA glutamate receptor MK-801 each blocked nicotine-induced release accumbens, indicating participation than single effect. These three did not inhibit cocaine-induced lack role these receptors under our experimental conditions. SCH-23390, D1 antagonist, both nicotine- effects, possible this effects. results indicate are mediating central examined, cocaine, although influences levels, interact.