Drug Reactivity: The Cannabis Debate


by Jen L’Insalata

From the earliest of records human have utilized substances in nature such as seeds, leaves, roots, and animal products for their medicinal qualities. Many of these substances were discovered to promote healing, prevent infection, reduce pain, and promote sleep. Some of the same substances which hold medicinal properties were also discovered to hold recreational properties educing euphoria, relaxation, and psychotropic qualities.

Cannabis is such a substance that in recent years has entered the public spotlight. Typically considered a recreational substance, the primary active ingredient Tetrahydrocannabinol or THC acts directly on the endogenous cannabinoid receptor CB1 located throughout the basal ganglia, limbic system, and hippocampus. Agonistic qualities of THC increases dopamine levels while blocking the CB1 receptors responsible for decreasing the reinforcement effect of dopamine (Pacher, Bátkai, & Kunos, 2006).

From a recreational standpoint, users seek out the various relaxation and psychoactive effects achieved most frequently by smoking. Effects are felt quickly and reinforced thorough he dopomergenic system. It is recognized that approximately 1/3 of individuals self-administer cannabis to cope with pain, anxiety, depression, and other stress and mood related disorders (Buckner, Heimberg, Matthews, & Silgado, 2012).

Cannabidiol or CBD; another active compound found in cannabis has shown to have a wider medicinal use with marked antiemetic properties, pain reduction properties, and anti-aggression and anti-anxiety properties. Current studies are exploring the use of CBD in treatment for PTSD, multiple sclerosis-, and other neurodegenerative disorders despite the rise in concern for cannabis dependency. In many cases studies show a marginal increase (0.997) cannabis use disorders among individuals utilizing it for medical purposes (Kevorkian, Bonn-Miller, Belendiuk, Carney, Roberson-Nay, & Berenz, 2015).

In many states cannabis has become legalized or decriminalized for recreational use and a growing number of recreational users seek a variety of THC and CBD effects. As with most substances cannabis users develop a tolerance to its effects and in turn may utilize the substance more frequently or in higher quantities to achieve the desired effect. The relationship between dose and effect is difficult to measure in that the dose being administered relies not only on the potency level of THC but also the individual’s inhalation strength. The size and strength of the inhalation combined with the extended length of time the smoke is held within the user’s lungs increased the dose administered.

In laboratory studies, dosage is monitored by computerized mechanism and have observed effects on THC content ranging from 0.2% to 4.0%. The subjective effects have been measured and vary depending on the individual. Individuals are asked to use a visual analog scale consisting of 44 descriptors to describe the dosage effect on medicinal aspects including stomachache, headache and pain, mood, aspects such as anxiety levels, depression, and feeling of content (Ramesh, Haney, & Cooper, 2013).

Regulating dosage effects becomes difficult in social situation in that social stimuli may alter the individuals intended dosage. As dosage and frequency increases individuals may build up a tolerance to both the impairitive and the desired effects. As dependence is brought about by the reinforcement through the dopomergenic system, individual susceptibility relies heavily on multiple aspects from both biological and environmental components. In many cases the individual must experience a positive effect and be willing to smoke again in order to develop necessary reinforcement.

The perception that cannabis is relatively easy to find and attain has also increased its social acceptance. Examining behavioral economic reinforcement surrounding the cost of cannabis must also be considered. Use as an economic reinforcement follows similar patterns to other substances and individuals are willing to continue to purchase cannabis until a breaking point. Examining the average cost of a cannabis joint being between $7 to $9, the breaking point appears to be approximately $38 per joint. Regular users are estimated to consume approximate 20 joints per week to attain a moderate high. Regular users express comfort in spending between $100 and $200 a month on cannabis and would be willing to pay slightly more for what is perceived as higher quality (Collins, Vincent, Yu, Liu, & Epstein, 2014).  Legislation can be established using tax to increase the price of cannabis and in turn decrease its use in legal states in a similar manor to what is done with tobacco.




Buckner, J. D., Heimberg, R. G., Matthews, R. A., & Silgado, J. (2012). Marijuana-related problems and social anxiety: The role of marijuana behaviors in social situations. Psychology Of Addictive Behaviors, 26(1),

Collins, R. L., Vincent, P. C., Yu, J., Liu, L., & Epstein, L. H. (2014). A behavioral economic approach to assessing demand for marijuana. Experimental And Clinical Psychopharmacology, 22(3), 211-221. doi:10.1037/a0035318

Kevorkian, S., Bonn-Miller, M. O., Belendiuk, K., Carney, D. M., Roberson-Nay, R., & Berenz, E. C. (2015). Associations among trauma, posttraumatic stress disorder, cannabis use, and cannabis use disorder in a nationally representative epidemiologic sample. Psychology Of Addictive Behaviors, 29(3), 633-638. doi:10.1037/adb0000110

Pacher, P., Bátkai, S, & Kunos, G. (2006). “The Endocannabinoid System as an Emerging Target of Pharmacotherapy”. Pharmacological Reviews 58 (3): 389–462. doi:10.1124/pr.58.3.2PMC 2241751.PMID 16968947.

Ramesh, D., Haney, M., & Cooper, Z. D. (2013). Marijuana’s dose-dependent effects in daily marijuana smokers. Experimental And Clinical Psychopharmacology, 21(4), 287-293. doi:10.1037/a0033661


Artwork by Toby Allen
By Jen L’Insalata

Stress has been cited for many adverse physical and mental health conditions and is linked to the proliferation of non-communicable disease epidemics in recent years. During the 1800’s most deaths were related to poor sanitary and hygienic conditions. Most deaths were attributed to outbreaks of cholera, Influenza, typhoid, and tuberculosis spread through unsanitary drinking water (Shern, Blanch, & Steverman, 2016).

In the 21st century, public health is still at risk. The US ranked 36th out of 194 for life expectancy in 2012 with the vast majority of deaths related to obesity, coronary heart disease, lung disease, and substance abuse. Most contemporary chronic illness has its roots in stress and it is estimated that nearly half of Americans will develop resulting mental health and addiction issues at some point during their lifetime (Shern, Blanch, & Steverman, 2016).

It is widely understood that a combination of genetic predisposition coupled with environmental influence shape over all human development. Many alterations in genetic material correlate with environmental stressors. In other words, genetic mutation and expression is strongly influenced by the environments which people are exposed to.

While manageable stress is considered important for healthy human development, toxic stress is not. Frequent, intense, and prolonged exposure to adversity including but not limited to physical and emotional abuse or violence, neglect, and economic hardship account for the source of much toxic stress. Acute or chronic exposure to traumatic events including death and sexual abuse also fall into the toxic stress category as does the persistence of less sever stressors including family instability and income insecurity (Shern, Blanch, & Steverman, 2016).

Stress alters development   over the course of a lifetime. Prenatal exposure to stress impacts developing structures of the fetus leading to adverse effects on memory and cognition. Early childhood stress often results in diminished behavioral, emotional, and impulse control. Individuals exposed to toxic stress during late adolescence and early adulthood develop a heightened fear response and are hyper responsive to stress stimuli (Shern, Blanch, & Steverman, 2016). Additionally, stress amplifies the aging process on both the brain and the body as a whole.

Stress causes structural remodeling of the brain and weakens neuro-connections within in the brain. Exposure to stress activates stress hormones and raises cortisol levels. Persistent elevation of cortisol levels increases the adverse effects on the connective structures within the amygdala; a structure commonly linked to cognitive and emotional regulation (Shern, Blanch, & Steverman, 2016 & Pagliaccio, Luby, & … Barch, 2015).

Genetic mutations occur throughout the short alleles of the serotonin transport promoter and produced heightened monoamine oxidise A activity. Heightened activity along the Hypothalamic-Pituitary-Adrenal Axis greatly effects the monoamine/serotonin structures and leads to additional cortisol release. It is the relationship between cortisol and amygdala connectivity that is believed to be a foundational component of internalizing pathology (Pagliaccio, Luby, & … Barch, 2015).

Internalizing pathology such and depression and anxiety contribute additional stress to an individual’s life. Symptoms of both disorders have dehabilitating effects on one’s ability to function in a socioeconomic capacity and produce feeling of dependency on unhealthy relationships and substances. Thus the cycle of stress, cell malfunction, and disorder is perpetuated.



Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey, M. S., Belden, A. C., & … Barch, D. M. (2015). Amygdala functional connectivity, HPA axis genetic variation, and life stress in children and relations to anxiety and emotion regulation. Journal Of Abnormal Psychology, 124(4), 817-833. doi:10.1037/abn0000094

Shern, D. L., Blanch, A. K., & Steverman, S. M. (2016). Toxic stress, behavioral health, and the next major era in public health. American Journal Of Orthopsychiatry, 86(2), 109-123. doi:10.1037/ort0000120


A Brief Overview of Neurons and Neurotransmission

neuronsJen L’Insalata

Preston, O’Neal, & Talaga (2013), presented the comparison of neural transmission to a telephone switchboard. In many ways, that analogy is accurate since neurotransmitters are essentially messages being sent from one nerve to another. Neurons utilize electrical and chemical stimulation to communicate and ultimately control human behavior.

To understand how transmissions are passed between neural pathways, one must first understand the basic structure of a nerve cell. The main body of the nerve cell or neuron is known as the soma. Its shape differs depending on its specific function but is contains the structures universal to all cells such as the nucleus, mitochondria, and cytoplasm. The axon is a slender tube like structure that emanates from the soma. It is often covered by a myelin sheath which aids in the conduction of information from one neuron to another; known as an action potential. Terminal buttons are the end points of axons which secrete hormones known as neurotransmitters. To do this an action potential must travel down the axon and reach the terminal buttons. The neurotransmitter either excites or inhibits the action potential allowing it to continue or cease its communication with the neighboring neuron. The dendrites of the neighboring neuron receive the transmission from the terminal button across a fluid filled gap called a synapse. The dendrite resembles the branches of a tree and allow the transmission to continue along the neural pathway (Carlson, 2014. & Saladin, 2012).


Neural transmission and action potentials are governed by the balance of positively and negatively charged ions such as sodium, potassium, and chloride. Polarization of the intracellular fluid by salutatory conduction and diffusions allows the transmission of the action potential down the length of the axon until it reaches the terminal buttons. If the action potential is strong enough at the terminal button, synaptic vesicles containing neurotransmitters are able to bind with the presynaptic membrane of the terminal button. This membrane essentially separates the end of the terminal button from the synaptic cleft. The synaptic vesicle is then able to release the neurotransmitter across the intracellular fluid which fills the gap, or synapse, between the terminal button and the opposing dendrite (Carlson, 2014. & Saladin, 2012).


Neurotransmitters are transported from the cell body to the terminal button by sac-like structures called vesicles. The vesicles bind to the membrane of the terminal button ans create tiny opening from which the neurotransmitter is released from the presynaptic neuron. Neurotransmitters are then ale to cross they synapse and bind with receptors on the dendrites of the postsynaptic neuron facilitating communication. While some neurotransmitters bind with the receptor sites on the post synaptic neuron, others are destroyed, or reabsorbed by the terminal button of the presynaptic neuron (Reed, Carlson, Quale, 2016).




Carlson, N. R. (2014). Foundations of behavioral neuroscience (9th ed.). Boston, MA: Pearson. ISBN: 9780205940240.

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Reed, L., Carlson, L, Quale, S. (2016). Capella University Neurotransmission Retrieved from http://media.capella.edu/course media/PSY7330/animation/transcript.htm1

Saladin. K.S. (2012). Anatomy and Physiology: The Unity of Form and Function. 6th ed. Mcgraw-Hill. New York, NY. ISBN978-0-07-337825-1.