?Nicotine is an alkaloid present in plants of the Family Solanaceae. Most commonly found in tobacco (Nicotiana tabacum), nicotine serves as a plant secondary chemical to protect plants against insects and other herbivores. Nicotine is an addictive stimulant in mammals, and is commonly used in cigarettes, cigars, pipes, and chewing tobacco. Nicotine can be administered to the body in many ways: orally through smoking tobacco, inhaling vaporized nicotine, or ingesting nicotine substances such as gum or lozenges; nasally via snuff or nasal spray; and transdermal modes such as patches or topical gels.
Nicotine quickly crosses the blood brain barrier, typically in under 20 seconds, and has a half-life of around 2 hours. Nicotine acts on nicotinic acetylcholine receptors, affecting multiple bodily systems including the sympathetic nervous system, and many isolated areas in the brain, including the thalamus, amygdala, hippocampus basal ganglia, and the cerebral cortex. By binding to nicotinic acetylcholine receptors (nAChRs), nicotine controls the release of neurotransmitters such as acetylcholine, dopamine, norepinephrine, and serotonin.
Nicotine interacts directly with the mesolimbic system, which leads to addiction. Nicotine can act on presynaptic AChRs to induce an increased release of acetylcholine, or postsynaptically to create an excitatory postsynaptic potential. By binding to a receptor, nicotine opens the ligand-gated channel and allows ions to flow through it. The ions create an excitatory postsynaptic potential, leading to a depolarization of neurotransmitters. Nicotine also inhibits acetylcholinesterase (AChE), which hydrolyzes acetylcholine, terminating it in the synaptic cleft.
Nicotine increases neurotransmission of other neurotransmitters, most notably glutamate, in the hippocampus, the region associated with memory and learning, by increasing synaptic firing and inducing Long Term Potentiation (LTP), thereby increasing task learning and memory formation. In mesolimbic and striatal dopaminergic pathways, nicotine induces the release of dopamine. This reactive increase in dopamine release is a main factor in the addictiveness of nicotine, but also serves to reduce stress, elevate mood, and increase cognition.
In the thalamus, nicotine induces neurotransmission at glutamate synapses, which leads to increased performance in attention, sensory-gating, and spatial memory tasks. By directly influencing the release of neurotransmitters, nicotine has a significant nootropic effect on the brain and body. The most notable nootropic effects of nicotine are particularly striking in neurological diseases. Nicotine has a pronounced effect on patients with Alzheimer’s disease (AD), Parkinson’s disease (PD), and attention related disorders such as Attention Deficit Disorder (ADD), and Attention Deficit Hyperactive Disorder (ADHD).
These diseases involve decreased cognitive activity associated with senescence. AD is associated with neurofibrillary tangles and neuritic plaques in regions governing learning and memory. Nicotine interferes with the formation of plaques, leading to studies of nicotine as a preventative agent in patients with AD. PD is characterized by damage to dopaminergic nigrostriatal neurons, which decreases dopamine transmission in the midbrain.
Nicotine stimulates dopaminergic pathways by increasing the amount of dopamine produced and acting as a neuroprotective agent, thereby leading to a decrease in PD symptoms. A significant number of patients with ADHD tend to self-medicate themselves with nicotine by smoking. ADHD patients have underdeveloped or under responsive cholinergic systems. The direct stimulation of nAChRs has been shown to increase cognitive performance in areas requiring intense processing, detail recovery, and sensory-gating.
Sensory-gating is governed by a nicotinic receptor in the hippocampus, and is linked to learning and memory. Although nicotine has many beneficial effects, the deleterious effects of cigarette smoke overshadow them. Additional chemicals in cigarettes can lead to vessel restriction and cell death, causing cognitive deficiencies. In most studies, the benefits of nicotine are dose dependent and are most beneficial when administered in small to moderate doses of 0. 2 – 0. 9mg. Cigarettes and cigars typically contain 1 – 1.
7mg of nicotine, which is enough to saturate and desensitize nAChRs. Some benefits of nicotine, such as increased learning performance and working memory enhancement, are state dependent. In studies using the Morris Water Maze and Radial Arm Maze, mice were given an initial acute dose of nicotine while learning the maze. When forced to navigate the maze again, mice given nicotine initially and again during the second test performed better than mice that were either given no nicotine, or only the initial dose.
The state dependent benefits are not as pronounced in humans. Given the observable benefits of nicotine on neurological organs and related diseases, nicotine is considered an acceptable agent to treat symptoms of, and in some cases prevent, neurological diseases. Though nicotine has a more obvious effect on non-smokers, it is not recommendable as a nootropic drug to increase cognitive performance in everyday tasks due to the highly addictive nature of nicotine. References 1. Potter, Alexandra S. , and Paul A. Newhouse.
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