Critical role of peripheral actions of intravenous nicotine in mediating its central effects.

ABSTRACT: In addition to its direct action on central neurons, nicotine (NIC) activates multiple nicotinic acetylcholine receptors localized on afferent terminals of sensory nerves at the sites of its administration. Although the activation of these receptors is important in mediating the primary sensory and cardiovascular effects of NIC, their role in triggering and maintaining the neural effects of NIC remains unclear. Using high-speed electroencephalography (EEG) and electromyography (EMG) recordings in freely moving rats, we showed that NIC at low intravenous (i.v.) doses (10-30 μg/kg) induced rapid, strong, and prolonged EEG desynchronization both in the cortex and ventral tegmental area (with decreases in α and robust increases in β and γ frequencies) and neck EMG activation that began during

SUBMITTER: Lenoir M 

PROVIDER: S-EPMC3158310 | biostudies-literature | 2011 Sep

REPOSITORIES: biostudies-literature