Effects of nicotine on cortical high voltage spindles in rats

• Published in: Brain research Vol. 625; no. 1; pp. 23 - 28
• Main Author: Radek, Richard J.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 15.10.1993; Amsterdam Elsevier; New York, NY
• Subjects: Action Potentials - drug effects; Animals; Biological and medical sciences; Central nervous system; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Cotinine; Cotinine - pharmacology; Dose-Response Relationship, Drug; EEG; Electroencephalography; Electrophysiology; Fundamental and applied biological sciences. Psychology; High voltage spindle; HVS; Male; Mecamylamine; Mecamylamine - pharmacology; Nicotine; Nicotine - pharmacology; Rat; Rats; Rats, Wistar; Spike wave discharge; Vertebrates: nervous system and sense organs; High voltage spindle; Spike wave discharge; HVS; Rat; EEG; Cotinine; Nicotine; Mecamylamine; Cholinergic receptor; Vertebrata; Mammalia; Rodentia; Discharge pattern; Electrophysiology; Electroencephalography; Nicotinic receptor
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(93)90133-8

Cholinergic systems have been shown to modulate 6–10 Hz immobility-related cortical spike wave discharges (high voltage spindles - HVS) in rats. This study reports that activation of central nicotinic receptors inhibits HVS identified from cortical EEG recordings. Nicotine (0.19–1.9 μmol/kg i.p.) significantly reduced the summed duration of HVS bursts during 20 min of waking immobility. The nicotinic antagonist mecamylamine (5.0 μmol/kg i.p.) blocked the effect of nicotine (0.62 μmol/kg i.p.) without itself significantly affecting HVS. At higher doses, mecamylamine (15.0 and 25.0 μmol/kg i.p.) increased HVS activity. Dimethylphenylpiperazinium (0.62–6.2 μmol/kg i.p.), a nicotinic agonist which does not cross the blood-brrrier, did not affect HVS, consistent with the idea that the effect of nicotine on HVS is due to an action in the central nervous system. Cotinine, the major metabolite of nicotine, did not affect HVS at doses similar to or higher than those tested for nicotine. Cotinine also did not block the effect of nicotine, indicating that this metabolite does not interfere with the modulatory effect of nicotine on HVS. These results suggest a role for nicotinic regulation of the neuronal substrates involved in the generation of HVS.