Breathing is an involuntary and automatic process initiated by a network of neurons within the brainstem. These neurons are affected by a number of factors (mechanical, electrical and chemical) that help modulate the frequency and pattern of breathing. Three respiratory chemosensitive sites have traditionally been described on the ventral medullary surface. These sites are affected by the pH of the cerebrospinal fluid (CSF) bathing the brain and by chemicals dissolved within the CSF. More recently, additional sites have been described with chemosensitive activity and of these the medullary raphé has received the most attention.

Although the dangers of smoking is well known, people have continued with this habit. Of concern are women who smoke and of particular concern are pregnant women who continue to smoke during their pregnancy. This is of concern because of the many chemicals contained within cigarette smoke, nicotine is particularly potent at affecting the health and well-being of the mother and fetus (and infant) because nicotine can enter the circulation within minutes of ingesting cigarette smoke. I am interested in how nicotine affects breathing. I therefore looked at the effects of nicotine on the caudal raphé, the raphé magnus.

Nicotine injected into the raphé magnus did not affect the animal's respiratory activity, even in pharmacological doses (P > 0.05). Neither respiratory frequency, amplitude, as well as inspiratory or expiratory time were affected. Administration of increasing levels of carbon dioxide before and after nicotine injections caused vigorous changes in respiratory activity. I tested the effectiveness of the drug by injecting it into a known nicotine-sensitive region (the caudal chemosensitive region) which resulted in respiratory stimulation. It appears that the raphé magnus is not responsive to nicotine. Immunohistomical studies should now be undertaken to determine if there are indeed nicotinic receptors at this location.