Neurotransmitters are chemical messengers that play an integral role in cellular communication as they transmit signals across synapses allowing for rapid communication between cells. Due to their vital role in signal transduction, it is important that these transmitters function properly (Sapolsky, 2005). While all humans possess these neurotransmitters it is possible that there can be person to person differences in these transmitters.
Due to their vital role in communication, when there is differences in the levels of neurotransmitters this can drastically alter several processes including behavior. Neurotransmitters influence different parts of the brain, therefore if there is an excess or a deficit in one of these transmitters this can lead to a deviation from normal behavior (Sapolsky, 2005). Three examples of neurotransmitters which have been shown to alter behavior are that of acetylcholine, dopamine and serotonin.

Acetylcholine is realized by the brain and is involved in voluntary movement, memory and learning (Sapolsky, 2005). When a person has high levels of this neurotransmitter this is associated with an increased risk of depression (Higley & Picciotto, 2014). Like acetylcholine dopamine is also involved in learning and movement (Sapolsky, 2005). In contrast to acetylcholine, low levels of dopamine have been linked to an increased risk of depression (Aarsland, Påhlhagen, Ballard, Ehrt, & Svenningsson, 2012). As well low levels of dopamine can cause muscle tremors, which are seen in Parkinson’s disease.

Finally serotonin, which is involved in mood, sleep and aggressive behavior, can also drastically affect a person’s behavior (Sapolsky, 2005). Like dopamine, low levels have been associated with increased risk of depression or anxiety disorders. In persons with depression, serotonin receptors are a popular target of antidepressant medications to help reverse these symptoms (Pehrson et al., 2015).

Overall, it is clear that person to person differences in neurotransmitters can lead to substantial negative changes in a person’s behavior.

References
• Aarsland, D., Påhlhagen, S., Ballard, C. G., Ehrt, U., & Svenningsson, P. (2012). Depression in Parkinson disease—epidemiology, mechanisms and management. Nature Reviews Neurology, 8(1), 35-47.
• Higley, M. J., & Picciotto, M. R. (2014). Neuromodulation by acetylcholine: examples from schizophrenia and depression. Current opinion in neurobiology, 29, 88-95.
• Pehrson, A. L., Leiser, S. C., Gulinello, M., Dale, E., Li, Y., Waller, J. A., & Sanchez, C. (2015). Treatment of cognitive dysfunction in major depressive disorder—a review of the preclinical evidence for efficacy of selective serotonin reuptake inhibitors, serotonin–norepinephrine reuptake inhibitors and the multimodal-acting antidepressant vortioxetine. European journal of pharmacology, 753, 19-31.
• Sapolsky, R. M. (2005). Biology and human behavior: The neurological origins of individuality: Teaching Company.