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What is neuropharmacology?

Neuropharmacology is a field related to how medications influence neuron function (molecular neuropharmacology) and human behavior (behavioral neuropharmacology).


Scientists who do this type of research often start by testing drugs on animals to look for drug mechanisms of action (i.e., how are the medication's molecules binding to receptors, what impact are they having on neuron communication, etc.). If animal studies seem to produce enough positive symptom effects in animals without severe negative side effects, then drug development can move on to small clinical trials in humans. From there, promising drugs are put through the test in large clinical trials before they can be approved by government agencies to be released for actual patient use.

What kinds of mechanisms of action are there?

When we want to a group of neurons carry out a biological response, we're looking for a ligand called an "agonist." When we want to stop a group of neurons from carrying out a biological response, we're looking for a ligand called an "antagonist." 


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Substances that bind to a receptor to promote a biological response.


Substances that block the receptor's binding site to prevent a biological response. 

Partial Agonist/Antagonist

Substances that bind to a receptor that are intended to cause a smaller effect of promotion/prevention of a biological response. 

Allosteric Modulator

Substances that bind to secondary sites that are distinct from an endogenous agonist's primary binding site. Their binding to this secondary site changes the shape of the primary binding site. They can be used to promote or prevent a biological response in combination with another ligand.

Let's say the tuna nigiri here is a type of receptor called a nicotinic acetylcholine receptor (nAChR), where nicotine can bind. When someone smokes a cigarette, nicotine is introduced into his/her body and binds to nAChRs, causing their associated neurons to activate. When someone wants to quit smoking, therapies can help by applying a nicotine agonist or an antagonist.


First, a person could use a different source than a cigarette to provide a nicotine agonist. This nicotine is delivered through a patch or gum, meaning it doesn't come with all of the harmful carcinogens that are found in cigarettes. Over time, a person is weaned off of this nicotine and cravings are reduced.


Second, a person could take a nicotine antagonist to block the nAChR, such as bupropion. Because the receptor is blocked, nicotine isn't able to bind to the receptor. As a result, the person doesn't experience the typical feeling associated with smoking their cigarette and desires them less and less over time. 

Synaptogenesis - Potential MoA from Depression Research

For a long time, scientists have viewed neuropharmacological approaches as a way of making neurotransmitters/hormones more or less available in synapses. But, emerging research is questioning whether there might be some other process that makes medications useful for some people.


One area of research looking for alternative treatment mechanisms of action is in depression. Although people with mild symptoms benefit most from evidence-based psychotherapies, a combination of psychotherapy and antidepressants are recommended for people with moderate to severe depression.

In the US, selective serotonin reuptake inhibitors (SSRIs) are most commonly prescribed for depression. Serotonin reuptake happens when a neuron releasing serotonin takes it


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back, decreasing the amount of available serotonin. Scientists once thought that inhibiting, or blocking, reuptake improved mood by making serotonin more available.

But, there were problems with this model: 1) patients’ serotonin levels increased soon after taking SSRIs, but their symptoms didn’t change until weeks later, 2) we learned that neuron communication, or signaling, is too complex for this explanation.

Newer research suggests that some people with depression have fewer neurons and synapses in brain regions related to emotion, learning, and memory. Increasing serotonin might indirectly improve mood by

contributing to changes in neuron signaling. Evidence shows that signaling changes can produce new neurons, new synapses (synaptogenesis), and/or change synaptic strength. We might see the time lag between taking SSRIs and mood improvements because these processes don’t just happen overnight.


Because SSRIs are only somewhat effective for ~60-70% of people who take them, ongoing research is aiming to more directly target neuron signaling as a pharmacological approach to depression treatment.

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[1] Abdel-Magid, A. F. (2015). Allosteric modulators: an emerging concept in drug discovery.

[2] Nestler, E. J., Hyman, S. E., & Malenka, R. C. (2001). Molecular basis of neuropharmacology: a foundation for clinical neuroscience. East Norwalk, Conn: Appleton & Lange.

[3] Bauer, M., Pfennig, A., Severus, E., Whybrow, P. C., Angst, J., Möller, H. J., & Šon behalf of the Task Force on Unipolar Depressive Disorders. (2013). World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders, part 1: update 2013 on the acute and continuation treatment of unipolar depressive disorders. The World Journal of Biological Psychiatry, 14(5), 334-385.

[4] Duman, R. S., & Voleti, B. (2012). Signaling pathways underlying the pathophysiology and treatment of depression: novel mechanisms for rapid-acting agents. Trends in neurosciences, 35(1), 47-56.

[5] Castrén, E., & Hen, R. (2013). Neuronal plasticity and antidepressant actions. Trends in neurosciences, 36(5), 259-267.

[6] Oved, K., Morag, A., Pasmanik-Chor, M., Rehavi, M., Shomron, N., & Gurwitz, D. (2013). Genome-wide expression profiling of human lymphoblastoid cell lines implicates integrin beta-3 in the mode of action of antidepressants. Translational psychiatry, 3(10), e313.

[7] Bambico, F. R., & Belzung, C. (2012). Novel insights into depression and antidepressants: a synergy between synaptogenesis and neurogenesis?. In Neurogenesis and Neural Plasticity (pp. 243-291). Springer, Berlin, Heidelberg.

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