Chapter 14 Effect of nicotine on the release of acetylcholine and amino acids in the brain

Abstract

The central effects of nicotine are mainly due to its interaction with specific brain receptors. Their stimulation increases the firing rate of many neurons and, consequently, the release of the respective transmitters. Since these receptors are also present on the nerve endings, including cholinergic nerve endings, their stimulation does enhance the neurosecretory process, independently of the axonal impulse flow. This chapter determines the influence of nicotine on D-[ 3 H]aspartate, endogenous gamma-aminobutyric acid GABA and acetylcholine (ACh) release in brain slices and in freely moving rats and guinea-pigs. The possible alterations in the cholinergic secretory response and in nicotinic receptors following chronic nicotine treatment are checked. Nicotine evokes in unanaesthetized animals a series of complex neuronal responses represented by increased ACh release, increased D-[ 3 H] aspartate and reduced GABA outflow. Such an imbalance between excitatory and inhibitory signals certainly increases cortical excitability, possibly even leading to toxicological consequences. In fact, the suppression of GABA control, together with increased glutamatergic activity, might promote cellular damage when concomitant metabolic or blood supply troubles are present. On the other hand, the increased efficacy of the excitatory inputs may explain the favorable effects of nicotine in maintaining and facilitating the memory processes.