Nicotine, Smoking and Cortical Activation

Abstract

EVIDENCE has recently been presented which suggests that acetylcholine (ACh) is an inhibitory synaptic transmitter in the feline cerebral cortex^1,2. Nicotine and tobacco smoke, in addition to ACh, have now been shown to depress cortical neurones³, and as a result of this finding Phillis and York have suggested that “the actions of nicotine on humans are a result, at least in part, of an action on cortical neurones”. It should be emphasized, however, that the doses of nicotine (100–1,000 µg/kg injected intravenously or 1–20 µg close arterially) used in the experiments of Phillis and York are far in excess of those likely to be attained during cigarette smoking. The crucial point in any study concerning the relevance of the pharmacological properties of nicotine to human tobacco smoking is the dose of nicotine necessary to produce the pharmacological response⁴. Armitage, Hall and Morrison⁵ have calculated that each time a cigarette smoker inhales a puff of tobacco smoke he can be expected to receive a dose of nicotine roughly equivalent to between 1 and 2 µg/kg administered intravenously. They have also shown that forty such injections given at 30 s intervals consistently desynchronized the electrocorticogram in cats and increased the amount of acetylcholine collected in a cup placed on the exposed cortex.