Skip to main content
Login | Suomeksi | På svenska | In English

Browsing by Subject "opioidi-nikotiini-interaktiot"

Sort by: Order: Results:

  • Leino, Sakari (2013)
    Nicotinic acetylcholine receptors are ion channel receptors that consist of five subunits and have an important role in modulating neurotransmitter release in the central nervous system. The literature review part of this thesis presents an overview of the structure, function and diverse subunit composition of nicotinic receptors and reviews the scientific literature on their function as modulators of neurotransmitter release. Relevant literature on the role of the nicotinic receptors of the striatum, the hippocampus and the prefrontal cortex in the modulation of the release of dopamine, glutamate, GABA, acetylcholine, noradrenalin and serotonin is reviewed. Finally, a summary for each of the brain areas and some conclusions are presented. The experimental part of this thesis consists of a series of experiments, where the ability of morphine to activate the presynaptic nicotinic receptors modulating dopamine release in the mouse striatum was investigated based on opioid-nicotine-interactions reported earlier. The possible effect of morphine was studied by measuring the release of radiolabeled dopamine from perfused synaptosomes prepared from mouse striatum. In addition, the effect of nicotine was studied to confirm the correct functioning of the method and to obtain data for comparison with the morphine results. Both nicotine and morphine elicited the release of [3H]dopamine from striatal synaptosomes. The release of [3H]dopamine elicited by morphine was blocked by nicotinic antagonists, suggesting that the effect of morphine was mediated by nicotinic receptors. Use of the selective antagonist α-conotoxin MII revealed that the effect of morphine, similar to nicotine, was mediated in part by α6β2* receptors and in part by other receptors, possibly α4β2*. In addition, the opioid antagonist naloxone blocked the effects of both nicotine and morphine, likely via direct antagonism of nicotinic receptors. However, the concentrations of morphine and naloxone needed for affecting [3H]dopamine release were very high, which suggests that the clinical relevance of the effects described here is likely to be small. The involvement of opioid receptors was deemed to be unlikely but, along with possible non-specific effects by high concentrations, could not be completely ruled out.