This week’s article will focus predominantly on the drastic effects of nicotine on the central nervous system, and consequently why you may be accustomed to your addicted friend promising that this will be their last ever cigarette. Everyone is aware of the chemically addictive nature of nicotine, but seldom do people wonder what processes occur at their synapses when deprived of their beloved ciggy. As a member of the school biology society, my interest in this topic was sparked proceeding an experiment we conducted to investigate the effect of nicotine on the heart rate of Daphnia. Shockingly, the heart rate was initially raised considerably by a count of 80 beats per minute before plummeting to a count 40 beats per minute less than the resting rate, reducing the Daphnia to an almost comatose state. Such emphatic results proposed the question of what processes cause this to occur?
Once within the bloodstream, nicotine may circulate around the body until it reaches the brain. This can occur in as little as 7 seconds. When in the brain, it binds to and activates receptors called the cholinergic receptors. These cholinergic receptors are also abundant in other areas of the body such as the muscles, heart, adrenal glands and other vital organs. Normally, these receptors are activated when they bind to a neurotransmitter called acetylcholine, which is produced at nerve endings in the brain and in the nerves of the peripheral nervous system. Stimulation of the receptors by acetylcholine is important in maintaining healthy respiration, heart function and muscle movement, as well as cognitive function. Acetylcholine binds to the cholinergic receptors of neurones resulting the opening of protein channels that allow Na+ ions to diffuse into the neurone. Na+ ions are instrumental in initiating new electrical impulses.
Since nicotine has a similar structure to acetylcholine, it can activate the cholinergic receptors. However, unlike acetylcholine, nicotine enters the brain and disrupts its normal functioning. Regular use of cigarettes leads to an increase in the number of cholinergic receptors and changes in the sensitivity of these receptors which may lead to nicotine tolerance. A smoker then needs to maintain a regular supply of nicotine to maintain normal brain function and the habit becomes addictive. I personally find it incredibly ironic when considering the premiss behind the primary reason to smoke; to calm the nerves. Nicotine simply maintains normal synaptic function, thus the ‘pleasure’ of nicotine to an addict is simply a state of normality for a non-addict. However, nicotine does also stimulate the release of several neurotransmitters such as norepinephrine, epinephrine, vasopressin, dopamine, arginine and beta-endorphin. Pain, anxiety and other negative symptoms are relieved and positive pleasant sensations are increased.
Nicotine intake also increases blood glucose levels, which is generally thought to be the result of the increased adrenalin levels that occur with nicotine intake. Adrenaline binds to receptors causing a g-protein to activate enzymes in the Islets of Langerhans’ cells to break down glycogen into glucose. The increased availability of glucose along with adrenalin is thought to be responsible for the increased learning ability, memory and alertness that has been associated with smoking. An increase in the rise of blood glucose also reduces appetite, which raises metabolic rate and eventually causes weight loss in the long term.