The University of Texas at Dallas School of Behavioral and Brain Sciences

Neurobiology of Memory Lab

Lab Research

The past is never dead. It’s not even past.
William Faulkner (1951)

Our research examines the effects of stress on memory. We study the interactions of stress hormones in the peripheral nervous system with synaptic plasticity and responding in brain circuits. As we gain an understanding of how these processes interact to influence memory, we hope to develop approaches to treat disorders of memory.

Synaptic Consolidation

An experience may be so exciting emotionally as almost to leave a scar on the cerebral tissues.
William James (1884)

It’s not difficult to understand why we have evolved in such a way that we are able to remember important, life-altering events better than insignificant experiences. Much like the thirsty lion remembers the location of a watering hole in the expansive desert, we humans remember to drive slowly when approaching a treacherous turn where we once nearly had an accident. How these memories are formed, on the other hand, is not as obvious. We are studying a gene that is expressed in the brain immediately following new experiences. The immediate early gene Arc is transcribed in the neuronal nucleus and transported to activated synapses upon experiencing a novel context. When translated to protein, Arc contributes to synapse-specific plasticity that underlies long-term memory. But, we don’t remember every new situation for the long term. Instead, we specifically remember those that are meaningful. Now suppose you trip and break your ankle as you cross the threshold of an unfamiliar room. You might remember some of the details of the room that you would never have remembered if you passed through uneventfully. According to our model, release of stress hormones engages the amygdala which modulates the translation of Arc mRNA that is poised in the appropriate synapses throughout the brain to store the memory of the event.

We stand to benefit from this research not only by gaining an understanding of how memories are formed in the brain but we also hope that this information will assist in treatment approaches when memory proves to be dysfunctional, such as in post-traumatic stress disorder.

Dentate 20x

Our Model

Vagus Nerve Stimulation and Extinction

The most beautiful experience we can have is the mysterious…the fundamental emotion which stands at the cradle of true art and true science.
Albert Einstein

Information acquired during daily encounters is not readily encoded into memory, but requires some effort or rehearsal to be preserved. In contrast, experiences that are stressful or emotionally meaningful in content are stored, without conscious effort, as life-long memories. This memory modulation occurs as a result of adrenaline release initiated by the sympathetic nervous system. In the classic “fight or flight” response, adrenaline increases heart rate and diverts blood flow away from internal organs and toward striated muscles. Adrenaline assists in meeting the physical requirements for coping with danger while also enhancing psychological features such as alertness and memory consolidation. Although adrenaline does not freely cross the blood-brain barrier, it must interact with the brain in some way. One potential pathway involves adrenaline binding to receptors on the vagus nerve, which in turn produces an increase in noradrenaline in the brain. Thus, the vagus nerve can be thought of as a string that nature pulls to momentarily make the brain impressionable at times when rapid plasticity is advantageous for later survival.