Plenaries

Wednesday 7

11:30 - 12:30

“De Robertis” Lecture:

What mechanisms underlie Parkinson's disease symptoms?

Gustavo Murer

Grupo de Neurociencia de Sistemas, Instituto de Fisiología y Biofísica Bernardo Houssay, Facultad de Medicina, Universidad de Buenos Aires

Parkinson’s disease is caused by the loss of nigrostriatal dopaminergic neurons. Chronic dopamine deficiency raises functional and structural changes in the striatum that lead to the appearance of its main symptom: scarcity and slowness of voluntary movement. Given its unsettled etiology, current antiparkinsonian strategies aim at restoring stimulation of striatal dopamine receptors. The gold standard therapy is the administration of L-dopa, a dopamine precursor that alleviates motor symptoms in early stages of the disease. However, motor fluctuations (the return of symptoms before it is time for the next dose of L-dopa) and L-dopa-induced dyskinesia are common in advanced stages of the disease. During the talk I will overview our work with animal models of the disease on the mechanisms underlying Parkinsonism and L-dopa-induced dyskinesia.

16:00 - 17:00

Plenary Lecture:

Neural Representations of Social Homeostasis

Kay Tye

Salk Institute for Biological Studies

Most social species organize into social dominance hierarchies. These hierarchies decrease aggression, save energy, & maximize survival for the entire group. Individuals must consider their social rank in any social encounter and adjust their behavior accordingly. Despite social and dominance behaviors being critical for successful interactions with other group members and ultimately, our survival, it is not completely clear how the brain encodes social rank. The medial prefrontal cortex (mPFC) has been implicated in social dominance expression in rodents, and in social rank learning in humans. However, exactly how the mPFC encodes social rank and which circuits mediate this computation is not known. We developed a trial-based social competition assay in which mice compete for rewards, as well as a computer vision tool to track multiple identical animals. Together, these novel task and tool facilitated social dominance behavior quantification. We found that the mPFC encodes behavior during the competition using multiple-hidden states that are rank-independent, and mPFC population dynamics encode social rank and competitive success. The population social rank representation translated into differences at the individual cell level in the responses to task-relevant events across ranks. Finally, we identified a circuit of mPFC cells that project to the lateral hypothalamus that contribute to the social rank encoding and drive dominance behavior during the reward competition.
Thursday 8

11:30 - 12:30

Plenary Lecture:

From axon regeneration to function recovery after CNS injury

Zhigang He

Boston Children's Hospital

Spinal cord injury disrupts the axonal connection between the brain and the spinal cord below the lesion, contributing to unrecoverable functional deficits. A long term interest of my lab is to develop novel repair strategies to promote axon regeneration and restore lost function. Towards this, our research are focusing on the following questions: (1). Why injured axons fail to regenerate and how to promote axon regeneration? (2). How to increase the functionality of regenerated or spared axons after injury? I will present our recent results on each of these fronts.

16:00 - 17:00

“Hector Maldonado” Lecture:

Making memories in mice

Sheena Josselyn

Hospital for Sick Children/University of Toronto

Understanding how the brain uses information is a fundamental goal of neuroscience. Several human disorders (ranging from autism spectrum disorder to PTSD to Alzheimer’s disease) may stem from disrupted information processing. Therefore, this basic knowledge is not only critical for understanding normal brain function, but also vital for the development of new treatment strategies for these disorders. Memory may be defined as the retention over time of internal representations gained through experience, and the capacity to reconstruct these representations at later times. Long-lasting physical brain changes (‘engrams’) are thought to encode these internal representations. The concept of a physical memory trace likely originated in ancient Greece, although it wasn’t until 1904 that Richard Semon first coined the term ‘engram’. Despite its long history, finding a specific engram has been challenging, likely because an engram is encoded at multiple levels (epigenetic, synaptic, cell assembly). My lab is interested in understanding how specific neurons are recruited or allocated to an engram, and how neuronal membership in an engram may change over time or with new experience.
Friday 9

11:30 - 12:30

Plenary Lecture:

50 years since Leloir’s Nobel: Maternal stress and energy signals critical to neurodevelopment

Tracy Bale

University of Maryland School of Medicine

Profound disparities exist in maternal-child health outcomes between racial and ethnic groups. Africa-American (AA) women in the United States are significantly more likely to experience preterm birth, fetal growth restriction, maternal and infant mortality than white women. For instance, infant mortality rates remain exceptionally high in the U.S., where babies born to AA women die at 2.5X the rate as babies born to white women. The mechanisms through which fetal antecedents contribute to morbidity and mortality involves dynamic interactions between the maternal and fetal environments. Maternal stress, obesity and diabetes are known risk factors for offspring, including significant impacts on neurodevelopment. In several mouse models in our lab, we have identified maternal and transplacental signals important to brain development impacted directly and indirectly by the maternal milieu. For example, we identified the X-linked, stress sensitive, nutrient sensor O-glycosyltransferase (OGT) as a placental biomarker of maternal stress. Genetic placental-specific targeting of OGT produced developmental and metabolic impairments, and lasting impacts on hypothalamic function. Similarly, in our mouse model of maternal diet high in fat and low in soluble fermentable fiber, pregnant mice on a low fiber diet produce offspring with high levels of placental hypoxia, gut and brain inflammation and higher rates of infant mortality due to the highly proinflammatory prenatal environment.

16:00 - 17:00

“Ranwel Caputto" Lecture:

Five decades of neuroscience in Latin America: following in the footsteps of Ranwel Caputto

Juana María Pasquini

Juana M. Pasquini Depto Química Biológica e IQUIFIB Facultad de Farmacia y Bioquímica UBA- CONICET Buenos Aires Argentina

Latin American neurochemistry was born in different countries between the 1950s and 1960s with different degrees of representation and participation. Right from the start, neurochemistry was very prominent in Venezuela, Argentina, Mexico, Uruguay, Chile and Brazil. As a matter of fact, due to the important development of neuroscience en Argentina ISN organized the second meeting in Buenos Aires, in 2001. After a brief introduction, we will take a look at the development of neurochemistry in Latin America. Argentina was the home of Ranwel Caputto. This Ranwel Caputto Lecture will highlight Caputto’s personality and leadership in the neurochemistry of the twentieth century. We will also seize the opportunity to outline you on a tour of the experimental work that my students have done over the years, especially in lines related to iron metabolism in the central nervous system.
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