Have you ever thought about how you recall information from something you learned in the past? Or why stressful situations can affect your mood or behavior?

These changes do not just happen. They occur in part because of communication signals that alter activity in your nervous system.

Your nervous system is a complex network of nerve cells called neurons that comprise your brain, spinal cord, and peripheral nervous system. Your brain contains more than 100 billion neurons that are constantly communicating with one another by releasing chemical messengers called neurotransmitters.

This communication occurs at a region between two neurons called a synapse. The neurotransmitters are released from communicating neurons through synaptic terminals where they move across to the other end of the synapse and interact with receptors on the neuron receiving the message. When these receptors receive these neurotransmitters, they cause the neuron to increase or decrease its activity.

It is through this process that the nervous system is able to coordinate your movement, your thoughts, and your actions. For example, as you are reading the words of this article, neurons near your eyes are releasing neurotransmitters to neuronal circuits that control visual and language centers in your brain, which decode the words you are reading into a context that you can understand.

Researchers have discovered that the activity of neurons can be strengthened or weakened by adjusting the size of the neuron’s synaptic terminal or the amount of neurotransmitters released from it. Additionally, neurons can adjust their response to neurotransmitters by altering the amount of their receptors. This ability of neurons to alter their synaptic strength is called synaptic plasticity, which is important to understand because it has been implicated in learning, pain, and stress.

Research conducted in the department of Neurosciences in the University of Toledo College of Medicine and Life Sciences, seeks to understand the mechanisms by which synaptic plasticity occurs in the nervous system.

Our lab has demonstrated that a signaling molecule named pituitary adenylate cyclase-activating polypeptide, or PACAP, can induce synaptic plasticity. PACAP regulates social, motor, and stress behaviors and has been implicated in psychological disorders such as post-traumatic stress disorder. By understanding how PACAP causes synaptic plasticity, we can find clues as to how disruptions in its signaling can lead to the development of such disorders.

One focus of our lab has been to better understand how PACAP induces synaptic plasticity in neurons. Using techniques to measure synaptic activity, we have learned that PACAP can immediately cause synaptic plasticity in a subset of neurons in the peripheral nervous system by robustly increasing their activity. PACAP causes this short-term synaptic plasticity by increasing the amount of neurotransmitters that these neurons release from their synaptic terminals.

In addition to this short-term plasticity, we have discovered that when we wait 48 hours following PACAP treatment, neuronal activity is even higher. 

Coined as long-term PACAP-induced plasticity, we have demonstrated that this synaptic plasticity also is associated with an increase in the amount of neurotransmitters released from synaptic terminals. However, unlike in the short-term, this long-term PACAP-induced synaptic plasticity also is associated with an increase in the size of synaptic terminals and an increase in the amount of receptors that neurotransmitters can bind to.

In addition, we have recently discovered that the long-term PACAP-induced synaptic plasticity is mediated by mechanisms that are distinct from the short-term effects. For example, unlike the short-term effects, the long-term requires the synthesis of new proteins that we plan to investigate further.

We are currently researching how PACAP can sustainably alter neuronal communication. Studies are under way investigating the contribution of individual proteins that PACAP can potentially recruit to cause this long-term synaptic plasticity.

These discoveries are exciting because they reveal novel ways your nervous system works to cause synaptic plasticity. By understanding synaptic plasticity, we can better understand the role of synaptic communication in the context of human behavior and disease.

Eric Starr is a PhD student in the department of neurosciences in the University of Toledo college of medicine and life sciences biomedical science program, formerly the Medical College of Ohio. Mr. Starr is doing his research in the laboratory of Dr. Joseph Margiotta. For more information, contact Eric.Starr@rockets.utoledo.edu or go to utoledo.edu/​med/​grad/​biomedical.

First Published July 4, 2016, 4:00 a.m.