Conclusions and Future Work

Conclusions and Proposals for future work:

Nicotine has been a part of human culture in some shape or form for hundreds of years, and remains highly present through tobacco consumption in cultures worldwide. While the addictive nature of nicotine is well known, and the health effects of tobacco exposure widely exposed to consumers, it does not appear that there will be a significant reduction in nicotine exposure within the next several years. In light of the novel nicotine delivery systems without tobacco, such as electronic cigarettes, the possibility of increased exposure to nicotine by recreational users is a possibility. With the lack of knowledge regarding potential nicotine toxicity, there exists the possibility for accidental poisonings until proper handling of nicotine products and liquids is more commonly understood within the public sphere. Additionally, the risk of chronic exposure to nicotine beyond that of addiction is less well understood, with the majority of knowledge resting in neuroscience regarding the role of increased dopamine levels.

 

Figure 1: An example of commercial nicotine products occurring at extraordinarily high concentrations. (Google images 2015)
Figure 1: An example of commercial nicotine products occurring at dangerously high concentrations. (Google images 2015)

Possible areas of research going forward include:

 

  1. Further examination of binding sites within the nAChR complex, and experimentation seeking to discern whether the presence of terminal groups on neonicotinoids benefits or inhibits binding in all cases. The role of pesticides and wide use of neonicotinoids presents this as both a mechanism to better understand nicotine toxicity as well as manage the public health concerns regarding nicotine-like chemicals in wider dispersal through crops and water supplies.  (Fassa 2014)

    Figure 2: neonicotinoid pesticdes are indicated as a possible responsible agent for colony collapse disorder, which results in widespread death among honeybee populations (Google Images 2014)
    Figure 2: neonicotinoid pesticdes are indicated as a possible responsible agent for colony collapse disorder, which results in widespread death among honeybee populations (Google Images 2014)
  2. Examination of further genetic data which seeks to determine if there is any heritable traits which affect either the short term response to nicotine through the acetylcholine binding mechanisms, or that correlate with propensities for addictive behavior overall. This would hopefully allow for further examination not just directly relevant to acute poisoning, but also serve to examine the genetics of addiction more closely through a well-known model. (Saccone 2007)
  3. Examining the role of medical treatments to directly counteract or limit the effects of nicotine upon the nAChR complex, including modifying end groups in such a way as to create a less potent neonicotinoid alternative without any additional detrimental effects upon human health. This could allow for a reduction in accidental acute cases of nicotine poisoning, as decreasing the binding affinity for the nicotine molecule would correlate directly with less overstimulation and resulting cascade block of the nAChR complexes. (Schep 2009)

 

2 Replies to “Conclusions and Future Work”

  1. Hey Anthony, great job overall, I thought it your pages were well-organized and interesting. So, since neurons and neuron receptor proteins are involved in nicotine toxicity, and neuroplasticity is known to take place in many cases (when part of the brain re-configures its neurons to make up for trauma or other injury), are you aware of any instances of neuroplasticity in terms of cigarette use or nicotine toxicity? Does the acute nature of the toxicity and its symptoms cause enough stress that the neurons change their nature? In terms of e-cigarettes (and related products), is some sort of placebo effect possible, where because of neuroplasticity, the same effects of nicotine use occur regardless of nicotine use? Thanks!

    1. Hi Besher,
      In regards to neuroplasticity of nicotine affected subjects, it appears that nicotine stimulation of non-smokers leads to a degree of neural stimulation consistent with most stimulant drugs. There have been some studies performed on the different effects of taking nicotine spray as compared to smokers whom have engaged in nicotine behavior for a long duration to time. These studies seem to indicate that long duration effects of nicotine exposure ultimately result in some manipulation of signalling pathways, which coheres with what we know about addiction mechanisms. As far as the placebo effect is concerned, it appears that it does indeeed play a role in terms of neuroplasticity when treating addictive patients using nicotine replacment therapy. I cannot however find information which demonstrates that placebo effects alone can stimulate the same neuroplasticicty seen in nicotine addiction without the actual alteration of the process at the nAChR receptor groups.

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