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The Memory Center is a national reference in research on the cellular, molecular and pharmacological mechanisms involved in mnemonic processing. It was pioneer in demonstrating that the extinction of aversive memory can be facilitated by exposure to something new, and that the learning of extinction of fear memory occurs without evocation of the original memory. Formed by PUCRS researchers and professors, the MC counts on the participation of scientific initiation (undergraduate), master’s and doctoral students, who have the opportunity to access high-tech laboratories. Interaction allows the expansion of knowledge and the participation of these students in national and international publications.

The Memory Center is headed by renowned researcher Dr. Ivan Izquierdo, who is the recipient of more than 60 national and international prizes and awards, including Grã-Cruz da Ordem do Mérito Científico (1996), Prêmio Conrado Wessel (2007), Prêmio Almirante Alvaro Alberto (2010), Honoris Causa Doctor of Universidade Federal do Paraná and Universidad de Córdoba, and Professor Emeritus at Universidade Federal do Rio Grande do Sul (2014). He discovered a phenomenon known as endogenous state-dependency and the functional separation between short- and long-term memories.

To contact the Memory Center, call 55(51) 3320.3000, extension 2532.

Lines of Research

Get to know some of the current projects of our researchers:

Structures and mechanisms involved in the extinction of aversive memories.

Traumatic events can lead to the formation of recurrent involuntary memories, causing anxiety disorders, panic attacks, and, in some cases, post-traumatic stress disorder. One way to deal with the unnecessary expression of traumatic memories is through the extinguishing process, in which an individual learns to inhibit evocation of the corresponding memory. Researchers at the Memory Center have recently demonstrated that the extinction of fear memories can be modulated by different systems, including the histaminergic, the dopaminergic and the noradrenergic ones. Besides the CA1 region of the dorsal hippocampus, the basolateral amygdala and the ventromedial prefrontal cortex participate in the consolidation of memory. Knowing the brain structures and mechanisms involved in the formation and expression memory extinction can aid in the treatment of disorders triggered by aversive memories.

Published articles:

PACAP modulates the consolidation and extinction of the contextual fear conditioning through NMDA receptors

Modulation of the extinction of two different fear-motivated tasks in three distinct brain areas

Histamine in the basolateral amygdala promotes inhibitory avoidance learning independently of hippocampus


Behavioral Tagging: induction of extinction by exposure to something new.

Experiencing an extremely stressful, potentially life-threatening event, such as a violent assault or natural disasters, can lead to the formation of traumatic memories, which are unlikely to be forgotten. Despite the indisputable importance of this type of memory for survival, its recurring evocation at inappropriate places and times may have devastating effects on the individual’s daily life and trigger anxiety disorders such as panic disorder and Post-Traumatic Stress Disorder. One way of inhibiting the expression of this type of memory is through the process of extinction, or exposure therapy, as it is clinically called. Extinction does not consist of erasing the original memory, but of mitigating a response triggered by the original memory. Exposure to novelty can turn a short-term memory into a long-term one. This process may be explained by the hypothesis of synaptic tagging. Thus, our group has demonstrated that exposure to something new can induce the extinction of aversive memory. Now, we seek to discover the molecular and cellular mechanisms to regulate this event.

Published articles:

Facilitation of fear extinction by novelty depends on dopamine acting on D1-subtype dopamine receptors in hippocampus

Hippocampal molecular mechanisms involved in the enhancement of fear extinction caused by exposure to novelty

Behavioral tagging of extinction learning


Learning the extinction of aversive memories without the need to evoke the original memory

In the same line of research, seeking to find the mechanisms involved in the process of extinction of aversive memories, our group has demonstrated that, for extinction to take place, evocation of the original memory is not necessary, i.e., the traumatic content of the fear memory does not need to be experienced for the extinction of aversive memory to occur. The group is currently seeking to find the molecular and cellular mechanisms that regulate this process.

Published article:

Extinction learning, which consists of the inhibition of retrieval, can be learned without retrieval


Influence of neurohumoral state on endogenous state-dependence in the extinction of aversive memory.

People and animals remember an anxiogenic, aversive, or stressful memory better when placed again in an anxiogenic, aversive or stressful situation similar to the one in the phase of information acquisition. This intriguing phenomenon is known as endogenous state-dependence. It was first proposed by Zornetzer (1978) and its existence was confirmed by several other studies conducted by researchers at the Memory Center. Endogenous state-dependence is extremely important for survival because it allows us to rely on a set of possible responses – including escape, fight, immobility, etc. – when faced with a dangerous situation. However, in a situation of strong emotional stress, this adaptive system can induce the unnecessary recall of traumatic memories, leading to disorders such as post-traumatic stress. The mechanisms guiding the formation, evocation and extinction of aversive memories have received considerable attention in recent years due to their potential clinical implications. In particular, a better understanding of the neurobiological mechanisms of extinction can lead to great benefits for the treatment of emotional disorders triggered by the recurrent evocation of traumatic memories.

Published article:

Fear extinction can be made state-dependent on peripheral epinephrine: role of norepinephrine in the nucleus tractus solitarius


Structures and mechanisms involved in the formation of object recognition and social recognition memory

Declarative memories are those that store information about facts, events and objects. These memories are the basis of our knowledge about the world. They define the way we interact with others and with different elements of our surrounding environment. Failure in their processing leads to devastating consequences and this can be observed, for instance, in Alzheimer patients. One of the first symptoms of this disease is inability to form and recall declarative memories, especially recognition memories, which allow us to differentiate familiar and new features, elements, situations and/or artifacts, a capacity which is obviously significant for survival. This research aims to better understand the brain structures and the biochemical and molecular mechanisms involved in the formation and maintenance of object recognition and social recognition memories. This is a subject of unquestionable scientific relevance, as a better understanding of this type of memory may contribute to the finding of potential therapeutic targets to the treatment of diseases affecting declarative memory.

Published articles:

D1 and D5 dopamine receptors participate on the consolidation of two different memories

Beta-adrenergic receptors link NO/sGC/PKG signaling to BDNF expression during the consolidation of object recognition long-term memory

On the participation of mTOR in recognition memory