Effects of nicotine on electrocortical activity and acetylcholine release from the cat cerebral cortex

Abstract

The effects of small amounts of nicotine on electrocortical activity and central acetylcholine (ACh) release have been studied on anaesthetized cats. The most common effect of nicotine given intravenously in a dose of 2 μg/kg every 30 sec for 20 min was to cause desynchronization of the electrocorticogram, indicating cortical activation, and an increase in the release of cortical ACh. A larger dose given less frequently (4 μg/kg every min for 20 min) caused, in some experiments, an increase and in others a decrease in cortical activity. Such changes were accompanied respectively by an increase or decrease in cortical ACh output. The amounts of nicotine that affected the electrocorticogram and ACh release are probably similar to those absorbed by the cigarette smoker who inhales. The effects of nicotine on the electrocorticogram were transient, but the effects on ACh were prolonged. This suggests that at least two pathways are involved in the nicotine response.

Cholinergic Control in Developing Prefrontal–Hippocampal Networks

“…These findings are surprising, especially in light of the previously reported ability of nAChR-mediated excitability to interfere with the oscillatory activity of the adult neocortex (Armitage et al, 1969;Siok et al, 2006;Lu and Henderson, 2010). One possible explanation for the inability of nAChRs to contribute to the cholinergic control of prefrontal SB and NG might be their functional absence in the neonatal PFC.…”

“…The main frequency remained constant before and after nicotine application, but the relative power shifted from slow theta band to fast beta-gamma band. Similar effects of nicotine on the neocortical EEG patterns have been reported in adult cats and humans (Armitage et al, 1969;Knott, 1988), suggesting that the ability of nAChRs to mediate the cholinergic control of the PFC maturates during the second postnatal week. In contrast, MLA had less prominent effects on the continuous Cg and PL activity (Table 4).…”

Biphasic dose‐related responses of the CNV (contingent negative variation) to I.V. nicotine in man.

“…Armitage, Hall & Sellers (1969) have shown in animals that intravenous nicotine can mimic the effects of cigarette smoking but only if the drug is given as intermittent 'shots'; comparable effects are not obtained if the nicotine is administered as a continuous infusion. In the present work the effects of intravenous nicotine on the CNV were studied in human volunteers who received the drug as intermittent 'shots' as used by Armitage and his colleagues (1969) in animals.…”

Plasma nicotine levels after cigarette smoking and chewing nicotine gum.

“…The increases produced within two minutes of finishing each cigarette were: 30-6, 26-2, 30 0, 26-6, 22-2, 27-1, and 31-9 ng/ml (mean 27-8 1-2 ng/ml). The maximal increases in plasma nicotine produced by each piece of 4-mg nicotine chewing-gum took [15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30] minutes to develop and were 12-8, 9-6, 8-3, 12-4, 12-8, 11-7, and 15-7 ng/ml (mean 11 9±0 9 ng/ml). The difference between these two means was more than twofold and was statistically significant (t= 10 3; P < 0-001).…”