Pharmacological characterization of dopamine, norepinephrine and serotonin release in the rat prefrontal cortex by neuronal nicotinic acetylcholine receptor agonists
Autor: | Tadimeti S. Rao, Lucia Correa, P. Adams, Emily M. Santori, Aida I. Sacaan |
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Rok vydání: | 2003 |
Předmět: |
Male
Agonist Nicotine Serotonin medicine.medical_specialty Pyridines medicine.drug_class Dopamine Prefrontal Cortex Nicotinic Antagonists Tetrodotoxin In Vitro Techniques Mecamylamine Receptors Nicotinic Rats Sprague-Dawley Norepinephrine chemistry.chemical_compound Cytisine Alkaloids Internal medicine medicine Animals Nicotinic Agonists Nicotinic Antagonist Neurotransmitter Molecular Biology Neurons Dose-Response Relationship Drug General Neuroscience Dihydro-beta-Erythroidine Bridged Bicyclo Compounds Heterocyclic Azocines Rats Nicotinic acetylcholine receptor Nicotinic agonist Endocrinology chemistry Epibatidine Calcium Neurology (clinical) Dimethylphenylpiperazinium Iodide Quinolizines Developmental Biology medicine.drug |
Zdroj: | Brain Research. 990:203-208 |
ISSN: | 0006-8993 |
Popis: | Neuronal nicotinic acetylcholine receptors (nAChRs) modulate synaptic transmission by regulating neurotransmitter release, an action that involves multiple nAChRs. The effects of four nAChR agonists, nicotine (NIC), 1,1-dimethyl-4-phenylpiperzinium iodide (DMPP), cytisine (CYT) and epibatidine (EPI) were investigated on [3H]-norepinephrine (NE), [3H]-dopamine (DA) and [3H]-serotonin (5-HT) release from rat prefrontal cortical (PFC) slices. All four agonists evoked [3H]-DA release to a similar magnitude but with a differing rank order of potency of EPI>>DMPP approximately NIC approximately CYT. Similarly, all four agonists also increased [3H]-NE release, but with a differing rank order of potency of EPI>>CYT approximately DMPP>NIC. NIC-induced [3H]-NE and [3H]-DA release responses were both calcium-dependent and attenuated by the sodium channel antagonist, tetrodotoxin (TTX) and by the nAChR antagonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbetaE), but not by D-tubocurare (D-TC). The modulation of [3H]-5-HT release by nAChR agonists was distinct from that seen for catecholamines. DMPP produced robust increases with minimal release observed with other agonists. DMPP-induced [3H]-5-HT release was neither sensitive to known nAChR antagonists nor dependent on external calcium. The differences between nicotinic agonist induced catecholamine and serotonin release suggest involvement of distinct nAChRs. |
Databáze: | OpenAIRE |
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