Frequency-Dependent Modulation of Dopamine Release by Nicotine and Dopamine D1 Receptor Ligands: An In Vitro Fast Cyclic Voltammetry Study in Rat Striatum

• Published in: Neurochemical research 2016-05, Vol.41 (5), p.945-950
• Main Authors: Goutier, W., Lowry, J. P., McCreary, A. C., O’Connor, J. J.
• Format: Article
• Language: English
• Subjects: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine - pharmacology; Animals; Benzazepines - pharmacology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Corpus Striatum - drug effects; Corpus Striatum - metabolism; Dopamine - metabolism; Electric Stimulation; In Vitro Techniques; Ligands; Male; Neurochemistry; Neurology; Neurosciences; Nicotine - pharmacology; Rats, Wistar; Receptors, Dopamine D1 - agonists; Receptors, Dopamine D1 - antagonists & inhibitors; Receptors, Dopamine D1 - metabolism; Short Communication
• ISSN: 0364-3190; 1573-6903
• DOI: 10.1007/s11064-015-1786-8

Nicotine is a highly addictive drug and exerts this effect partially through the modulation of dopamine release and increasing extracellular dopamine in regions such as the brain reward systems. Nicotine acts in these regions on nicotinic acetylcholine receptors. The effect of nicotine on the frequency dependent modulation of dopamine release is well established and the purpose of this study was to investigate whether dopamine D 1 receptor (D 1 R) ligands have an influence on this. Using fast cyclic voltammetry and rat corticostriatal slices, we show that D 1 R ligands are able to modulate the effect of nicotine on dopamine release. Nicotine (500 nM) induced a decrease in dopamine efflux at low frequency (single pulse or five pulses at 10 Hz) and an increase at high frequency (100 Hz) electrical field stimulation. The D 1 R agonist SKF-38393, whilst having no effect on dopamine release on its own or on the effect of nicotine upon multiple pulse evoked dopamine release, did significantly prevent and reverse the effect of nicotine on single pulse dopamine release. Interestingly similar results were obtained with the D 1 R antagonist SCH-23390. In this study we have demonstrated that the modulation of dopamine release by nicotine can be altered by D 1 R ligands, but only when evoked by single pulse stimulation, and are likely working via cholinergic interneuron driven dopamine release.