Serotonin modifies the spontaneous spiking activity of gracile nucleus neurons in rats: role of 5-HT1A and 5-HT2 receptors

• Published in: Archives italiennes de biologie Vol. 154; no. 2-3; p. 39
• Main Authors: Grasso, C, Li Volsi, G, Barresi, M
• Format: Journal Article
• Language: English
• Published: Italy 01.06.2016
• Subjects: 8-Hydroxy-2-(di-n-propylamino)tetralin - pharmacology; Action Potentials - drug effects; Animals; Iontophoresis; Ketanserin - pharmacology; Male; Medulla Oblongata - cytology; Neurons - drug effects; Piperazines - pharmacology; Pyridines - pharmacology; Rats; Rats, Wistar; Receptor, Serotonin, 5-HT1A; Receptors, Serotonin, 5-HT2; Serotonin - analogs & derivatives; Serotonin - pharmacology; Serotonin 5-HT1 Receptor Agonists - pharmacology; Serotonin 5-HT1 Receptor Antagonists - pharmacology; Serotonin 5-HT2 Receptor Agonists - pharmacology; Serotonin 5-HT2 Receptor Antagonists - pharmacology
• ISSN: 0003-9829
• DOI: 10.4449/aib.v154i2/3.3430

We tested the effects of microiontophoretic application of serotonin (5-HT) on the firing rate of neurons located in the gracile nucleus (GN) of rats. Application of 5-HT1A and 5-HT2 agonists and antagonists respectively mimicked/ modulated and blocked the effects produced by the amine, respectively. Among the tested neurons, 88.2% modified their background firing activity in the presence of 5-HT. Responsive neurons decreased their mean firing activity (MFA) in 56.7% of cases and increased it in the remaining 43.3%. To ascertain the specificity of the effects induced by 5-HT, we utilized 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) and alpha-methyl-5-hydroxytryptamine (α-MET-5-HT), agonists for 5-HT1A and 5-HT2 receptors, respectively. The microiontophoresis of 8-OH-DPAT modified the background firing rate of all GN neurons (100% of tested neurons) mimicking the decrease of MFA evoked by 5-HT. The application of a-MET-5-HT modified the MFA in 76.9% of tested neurons, decreasing it in 61.5% of cases and increasing in the remaining 23.1%. The decrease of MFA induced by 8-OH-DPAT was antagonized by application of the 5-HT1A receptor antagonist N-[2-[-(2-Methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate salt (WAY100635), while application of 5-HT2 receptor antagonist ketanserine tartrate (KET) antagonized only the increase of MFA induced by a-MET-5-HT. These results indicate that 5-HT is able to modulate the background firing activity of GN neurons by 5-HT1A and 5-HT2 receptors.