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Persistent rhythmic oscillations induced by nicotine on neonatal rat hypoglossal motoneurons in vitro.
Eur J Neurosci. 2006 Nov; 24(9):2543-56.EJ

Abstract

Patch-clamp recording from hypoglossal motoneurons in neonatal Wistar rat brainstem slices was used to investigate the electrophysiological effects of bath-applied nicotine (10 microm). While nicotine consistently evoked membrane depolarization (or inward current under voltage clamp), it also induced electrical oscillations (3-13 Hz; lasting for >/= 8.5 min) on 40% of motoneurons. Oscillations required activation of nicotinic receptors sensitive to dihydro-beta-erythroidine (0.5 microm) or methyllycaconitine (5 nm), and were accompanied by enhanced frequency of spontaneous glutamatergic events. The slight voltage dependence of oscillations and their block by the gap junction blocker, carbenoxolone, suggest they originate from electrically coupled neurons. Network nicotinic receptors desensitized more slowly than motoneuron ones, demonstrating that network receptors remained active longer to support heightened release of the endogenous glutamate necessary for enhancing the network excitability. The ionotropic glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and the group I metabotropic receptor antagonist, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), suppressed oscillations, while the NMDA receptor antagonist, d-amino-phosphonovaleriate (APV), produced minimal depression. Nicotine-evoked oscillations constrained spike firing at low rates, although motoneurons could still generate high-frequency trains of action potentials with unchanged gain for input depolarization. This is the first demonstration that persistent activation of nicotinic receptors could cause release of endogenous glutamate to evoke sustained oscillations in the theta frequency range. As this phenomenon likely represented a powerful process to coordinate motor output to tongue muscles, our results outline neuronal nicotinic acetylcholine receptors (nAChRs) as a novel target for pharmacological enhancement of motoneuron output in motor dysfunction.

Authors+Show Affiliations

Neurobiology Sector and CNR-INFM DEMOCRITOS National Simulation Center, International School for Advanced Studies (SISSA), Via Beirut 4, 34014 Trieste, Italy.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17100842

Citation

Lamanauskas, Nerijus, and Andrea Nistri. "Persistent Rhythmic Oscillations Induced By Nicotine On Neonatal Rat Hypoglossal Motoneurons in Vitro." The European Journal of Neuroscience, vol. 24, no. 9, 2006, pp. 2543-56.
Lamanauskas N, Nistri A. Persistent rhythmic oscillations induced by nicotine on neonatal rat hypoglossal motoneurons in vitro. Eur J Neurosci. 2006;24(9):2543-56.
Lamanauskas, N., & Nistri, A. (2006). Persistent rhythmic oscillations induced by nicotine on neonatal rat hypoglossal motoneurons in vitro. The European Journal of Neuroscience, 24(9), 2543-56.
Lamanauskas N, Nistri A. Persistent Rhythmic Oscillations Induced By Nicotine On Neonatal Rat Hypoglossal Motoneurons in Vitro. Eur J Neurosci. 2006;24(9):2543-56. PubMed PMID: 17100842.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Persistent rhythmic oscillations induced by nicotine on neonatal rat hypoglossal motoneurons in vitro. AU - Lamanauskas,Nerijus, AU - Nistri,Andrea, PY - 2006/11/15/pubmed PY - 2007/1/20/medline PY - 2006/11/15/entrez SP - 2543 EP - 56 JF - The European journal of neuroscience JO - Eur. J. Neurosci. VL - 24 IS - 9 N2 - Patch-clamp recording from hypoglossal motoneurons in neonatal Wistar rat brainstem slices was used to investigate the electrophysiological effects of bath-applied nicotine (10 microm). While nicotine consistently evoked membrane depolarization (or inward current under voltage clamp), it also induced electrical oscillations (3-13 Hz; lasting for >/= 8.5 min) on 40% of motoneurons. Oscillations required activation of nicotinic receptors sensitive to dihydro-beta-erythroidine (0.5 microm) or methyllycaconitine (5 nm), and were accompanied by enhanced frequency of spontaneous glutamatergic events. The slight voltage dependence of oscillations and their block by the gap junction blocker, carbenoxolone, suggest they originate from electrically coupled neurons. Network nicotinic receptors desensitized more slowly than motoneuron ones, demonstrating that network receptors remained active longer to support heightened release of the endogenous glutamate necessary for enhancing the network excitability. The ionotropic glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), and the group I metabotropic receptor antagonist, (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA), suppressed oscillations, while the NMDA receptor antagonist, d-amino-phosphonovaleriate (APV), produced minimal depression. Nicotine-evoked oscillations constrained spike firing at low rates, although motoneurons could still generate high-frequency trains of action potentials with unchanged gain for input depolarization. This is the first demonstration that persistent activation of nicotinic receptors could cause release of endogenous glutamate to evoke sustained oscillations in the theta frequency range. As this phenomenon likely represented a powerful process to coordinate motor output to tongue muscles, our results outline neuronal nicotinic acetylcholine receptors (nAChRs) as a novel target for pharmacological enhancement of motoneuron output in motor dysfunction. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/17100842/Persistent_rhythmic_oscillations_induced_by_nicotine_on_neonatal_rat_hypoglossal_motoneurons_in_vitro_ L2 - https://doi.org/10.1111/j.1460-9568.2006.05137.x DB - PRIME DP - Unbound Medicine ER -