1,721,084 research outputs found
Nicotine pre-exposure modulates NMDA receptors function in dopaminergic terminals of the rat nucleus accumbens
Derangements in neurotransmission and their correlate in behavioural alterations during aging: rescue from nutraceuticals and nutrition supplements
A new specific neuronal modulatory effect of nicotine: the functional cross talk between nicotinic and glutamate receptors
Somatostatin inhibits glutamate release from mouse cerebrocortical nerve endings through presynaptic sst2 receptors linked to the adenylyl cyclase-protein kinase A pathway
Presynaptic nicotinic receptors modulating neurotransmitter release in the Central Nervous System: Functional interactions with other coexisting receptors
NMDA-mediated modulation of dopamine release is modified in rat prefrontal cortex and nucleus accumbens after chronic nicotine treatment
Chronic nicotine treatment differentially affects the function of presynaptic NMDA receptors modulating dopamine release from rat prefrontal cortex and nucleus accumbens
Chronic nicotine differentially affects the function of nicotinic receptor subtypes regulating neurotransmitter release
It is known that nicotine can activate several subtypes of release-regulating presynaptic nicotinic receptors (nAChRs) including those situated on central noradrenergic, dopaminergic, cholinergic and glutamatergic axon terminals. The objective of this study was to investigate the effects of chronic administration of (–)nicotine on the function of the above autoreceptors and heteroreceptors using rat superfused synaptosomes. In hippocampal synaptosomes prelabelled with [3H]noradrenaline (NA) the nicotine-evoked overflow of [3H]NA was higher in rats treated with nicotine for 10 days (via osmotic mini-pumps) than in vehicle-treated rats. In striatal synaptosomes, prelabelled with [3H]dopamine (DA), chronic nicotine did not modify the releasing effect of nicotine. No significant change was observed in experiments with synaptosomes from nucleus accumbens prelabelled with [3H]DA. Exposure of hippocampal synaptosomes prelabelled with [3H]choline to nicotine elicited release of [3H]acetylcholine; this effect was almost abolished in synaptosomes from animals administered nicotine for 10 days, suggesting downregulation of nicotinic autoreceptors. In hippocampal synaptosomes prelabelled with [3H]D-aspartate, the releasing effect of epibatidine following chronic nicotine treatment did not differ from that in controls. The K+-evoked exocytotic release of the neurotransmitters tested was not modified by long-term nicotine administration. The results show that chronic nicotine differentially affects the function of releaseregulating nAChR subtypes
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