SAN2022 Meeting

Cecilia Conde, Inst. Ferreyra (INIMEC-CONICET-UNC) & Victoria Rozés Salvador, Dep. Bioquímica Clínica, CIBICI-CONICET

Several of the cellular processes that allow nerve cells to go through the stages of development, maturation, and aging are governed by endosomal and signaling mechanisms. The endosomal pathway regulates many cells signaling events by controlling the number, functionality, and receptors access as well as molecules available on the cell surface. This pathway, by providing a set of dynamic and biochemically specialized endomembrane structures that communicate with the plasma membrane, is increasingly viewed as a highly flexible scaffold to mediate the precise spatiotemporal control and trafficking of various biological signals. The specific principles of endosome-based signaling in the nervous system as well as the molecules that compose them are a constant subject of study due to their physiological relevance in both nervous system health and disease. Thus, the focus of this symposium is to highlight several well-defined mechanisms and molecules involved that contribute to relevant aspects of neuronal survival and degeneration.

Ching-Hwa Sung. NIH Institute, USA
“Multitasking roles by endosome in retinal homeostasis and disease”.

Christian Gonzalez Billault. Universidad de Chile, Chile
“Coordinated functions of small GTPases from the Rho, Arf, and Rab families define neuronal morphology”.

Neuronal functions are heavily dependent on their morpho-structural features. During development, precursors at the proliferation niches differentiate into neurons that contain two domains that differ in their molecular composition, structure, and functions, the axon and the somatodendritic compartment. Properly comprehending the mechanism controlling the acquisition of these conspicuous morphological and functional features is essential to define therapeutic strategies to overcome brain dysfunction linked to neurodegenerative diseases. Axon determination and elongation is an initial event in the polarization of neurons. Several cellular and molecular mechanisms control it, including membrane and cytoskeleton dynamics. We recently showed that Rab8 is a critical determinant of axon specification that is functionally coupled to the activity of Cdc42, one of the master regulators for actin dynamics. In addition, Rab35 contributes to defining axonal elongation in a mechanism involving the microtubule-associated protein 1B and the atypical protein kinase PRPK.

Interestingly, the functions associated with Rab35 are tightly controlled by Arf6, a Golgi-associated protein. It has been previously suggested that Arf6 can influence Rac1, another small GTPase that controls actin dynamics. Therefore, a hierarchical organization of small GTPases provides a molecular platform that defines which neurite will become the axon and its extension by coordinating cytoskeleton and membrane-dependent elements.


Anahí Bignante. Inst. Ferreyra, Argentina
“Role of the Go/betagama signaling pathway in amyloidogenesis”.

Alzheimer ́s disease (AD) is characterized by deposition of aggregated species of amyloid beta (Aβ) in the brain, which leads to progressive cognitive deficits and dementia. Aβ is generated by the successive cleavage of the amyloid precursor protein (APP), first by β-site APP cleaving enzyme 1 (BACE1) and subsequently by the γ-secretase complex. Conditions that enhance Aβ generation or reduce its clearance predispose to Aβ aggregation and the development of AD. In vitro studies have demonstrated that Aβ assemblies spark a feedforward loop heightening Aβ production. However, the underlying mechanism remains unknown. Here, we show that oligomers and fibrils of Aβ enhance colocalization and physical interaction of APP and BACE1 in recycling endosomes of human neurons derived from induced pluripotent stem cells and other cell types, which leads to exacerbated amyloidogenic processing of APP and intracellular accumulation of Aβ42. In cells overexpressing mutant forms of APP that are unable to bind Aβ or to activate Go protein, we have found that treatment with aggregated Aβ fail to increase colocalization of APP with BACE1 indicating that Aβ-APP/Go signaling is involved in this process. Moreover, inhibition of Gβγ subunit signaling with βARKct or gallein, prevent Aβ-dependent interaction of APP and BACE1 in endosomes, β-processing of APP and intracellular accumulation of Aβ42. Collectively, our findings uncover a signaling mechanism leading to a feedforward loop of amyloidogenesis that might contribute to Aβ pathology in early stages of AD and suggest that gallein could have therapeutic potential.

Natalí Chanaday. Vanderbilt Brain Institute, USA
“Synaptic vesicles and the secretory pathway: overlap and differences”.

The vast majority of neuron studies have a synapse-centered vision. However, there is accumulating evidence that organelles as the endoplasmic reticulum, endosomes, lysosomes and secreted extracellular vesicles can modulate the synaptic vesicle cycle and thus, neurotransmission. My work aims to understand how neuronal organelles interact and influence neuron properties. Specifically, we have recently found that extracellular vesicles can increase neurotransmitter release via the exchange of the SNARE protein synaptobrevin-2. The presentation will cover some of the novel findings we made related to synaptic vesicle fusion and endocytosis, and the overlap of the synaptic vesicle molecular machinery with other organelles in the secretory pathway.

A. Belén Elgoyhen, INGEBI & Juan D. Goutman, INGEBI, goutman@dna.uba.ar

Congenital hearing loss is one of the most prevalent sensory disabilities, affecting approximately 1 to 2 in 1,000 newborns. In more than 50% of the cases there is a genetic cause, with 70-80% being non-syndromic. More than 100 genes that can produce genetic deafness have been identified so far, implying a very diverse and heterogeneous problems. Some forms of hearing loss appear in newborns, while others develop even after several decades of life, implying that a complex interaction between genes and environment can occur. In recent years, important advances have been made in gene therapy models that aim to supplement the expression of mutant genes using viral vectors with transient expression (Holt). This system has already generated interesting results reversing profound deafness in animal models carrying mutations in genes of the mechanotransduction complex in cochlear cells. On the other hand, non-genetic causes of hearing loss produce major problems in older adults as a result of the interaction of factors such as longevity and daily exposure to very noisy environments that produce “hidden deafness” (Gómez-Casati). The identification of genes products that could prevent/delay the detrimental effects of noise and aging on hearing capacities is a fundamental step towards finding a therapy for these conditions. Synaptic nicotinic receptors mediating efferent cholinergic inputs to cochlear hair cells have been proven as candidates for relieving hair cell damage (Fuchs). In summary, this symposium will provide a unique opportunity to discuss the diverse and complex causes of hearing loss, as well as its potential treatment pathways.

Jeffrey Holt Department of Otolaryngology Boston Children’s, Harvard Medical School, USA
Putting the pieces together: the hair cell transduction complex

Our research is focused on sensory transduction or the conversion of stimulus information into  electrical information, the language of the brain. Sensory organs are at the interface between  the world around us and the internal workings of the brain. To understand how the brain  processes information we first need to understand how it collects and encodes information. As a  model for sensory transduction our lab studies the inner ear. We aim to understand how the  sensory cells and neurons in the normal inner ear function. In this talk I will discuss the  identification of the molecular components required for sensory function  

Paul Fuchs Johns Hopkins School of Medicine, Baltimore, USA

M. Eugenia Gómez-Casati, Instituto de Farmacología, F. Medicina, UBA, Argentina

The main goal of our laboratory is to increase the knowledge on the consequences of different  forms of hearing loss on the normal function of hair cells in the mammalian organ of Corti and to  study the role of the medial olivocochlear system (MOC). Noise and aging are the two most  common causative factors among the defined etiologies of hearing loss. The clinical significance  presented by noise-induced (NIHL) and age-related hearing loss (ARHL) has driven efforts to  understand the underlying molecular, physiological and biochemical mechanisms of the cochlear  damage. Knowing how the physical structures are affected by noise and/or age is crucial in search  for therapeutic agents that act as otoprotectants against hearing loss. In the last 5 years, my lab  has been trying to understand the role of the MOC system in protecting the inner ear from damage  produced by overly loud sounds and this will be the focus of my talk. We have shown an inverse  correlation between the activity of the alpha9alpha10 nAChR and noise-induced cochlear  synaptopathy. Moreover, we have shown that the MOC system mediates resistance to ARHL – presbycusis, and that this occurs via the alpha9alpha10 nAChR complexes on OHCs. These  results suggest that potentiation of the MOC feedback can trigger cellular and molecular  mechanisms to protect and/or repair the inner ear sensory epithelium. These findings are  beginning to bridge the gap from bench to clinics as they provide the first proof-of-principle supporting the enhancement of the MOC system as a viable approach for prevention or treatment  of NIHL and/or ARHL.

(This symposium will take place in Spanish)

Maria Florencia Rossetti, Instituto de Salud y Ambiente del Litoral (ISAL), CONICET-UNL, Santa Fe.
Rodrigo Echeveste, Instituto de Señales, Sistemas e Inteligencia Artificial, sinc(i), CONICET-UNL, Santa Fe.

According to the information compiled by the Sociedad Argentina de Investigación en Neurociencias (SAN) in 2021, most of the researchers surveyed in the area of Neuroscience are concentrated in CABA (61%), Buenos Aires (14%), and Cordoba (15%). The remaining 11% is distributed among the provinces of Santa Fe, Entre Ríos, Rio Negro, Mendoza, Tucumán and San Luis. In this context and within the framework of the recent formation of the Federalization Commission of the SAN, this symposium aims to make visible and publicize the research work in Neuroscience in Argentina outside the usual nodes.

Rosana Chehín
: Instituto de Medicina Molecular y Celular Aplicada-IMMCA (CONICET-UNT-Siprosa) de San Miguel de Tucumán (Tucumán)

La enfermedad de Parkinson (EP) es un trastorno neurodegenerativo crónico, progresivo y complejo, caracterizado por la pérdida selectiva de neuronas dopaminérgicas en el mesencéfalo generando alteraciones motoras, sensoriales y en estados avanzados, cognitivas. Es actualmente el segundo trastorno neurodegenerativo de mayor incidencia poblacional y al ser el envejecimiento el principal factor de riesgo, el incremento de la expectativa de vida amenaza con duplicar estas cifras en la próxima década. A pesar que la EP fue descrita hace más de 200 años, a la fecha, los únicos tratamientos disponibles son paliativos y no existe fármaco capaz de detener o al menos enlentecer el proceso de muerte neuronal. 

Desde el punto de vista biofísico, la agregación amiloide de la proteína presinática α-sinucleína (aSyn) es considerada el evento central en la iniciación y la propagación de la patología. Numerosas moléculas demostraron ser eficientes inhibidores de la agregación de esta proteína in vitro, pero no han logrado proporcionar una neuroprotección efectiva in vivo. Las altas tasas de fracasos en el pasaje de los modelos in vitro a in vivo han sido asociadas a la toxicidad o incapacidad de las mismas para atravesar la barrera hematoencefálica. 

Las tetraciclinas constituyen una gran familia de compuestos con diferentes actividades biológicas, además de su conocida actividad antibiótica. Son moléculas muy utilizadas en la clínica médica por su baja toxicidad y buena biodisponibilidad. Nuestro grupo de trabajo logró demostrar en modelos biofísicos y celulares, que ciertas tetraciclinas son capaces de interferir la agregación patológica de aSyn, así como los procesos neuroinflamatorios y el estrés oxidativo característico de los procesos neurodegenerativos. Mediante modelos biocomputacionales, pudimos además proponer las interacciones específicas entre los grupos funcionales de una tetraciclina no antibiótica y los agregados amiloides de sSyn. Esto permitió sentar las bases de la modificación racional de estos compuestos obteniendo moléculas de alta actividad neuroprotectora y baja actividad antibiótica para ser administradas en tratamientos a largo plazo. Estos hallazgos posicionan a las tetraciclinas como moléculas de interés para completar los estudios preclínicos y avanzar a los ensayos clínicos.

Álvaro F. Muchiut, Instituto Superior de Neuropsicología, Departamento de investigación de Resistencia (Chaco)

La utilización de pruebas psicológicas y neuropsicológicas validadas y de confiabilidad comprobadas, aportan evidencias valiosas al profesional en una multiplicidad de actividades, que comprenden desde el diagnóstico, el plan y el seguimiento de tratamiento hasta la selección laboral, la orientación vocacional, las pericias judiciales 

e investigación; sin embargo, no siempre se disponen de instrumentos locales/regionales o de baremos adaptados a la población a la que se pretende aplicar y, en ocasiones, siquiera corresponden a datos normativos del país. 

Por ellos desde el equipo de investigación nos hemos propuesto crear instrumentos de valoración neuropsicológica (escalas) con el fin de evaluar a niños y adolescentes de nuestra zona con las particularidades propias de la población de esta región. En este sentido comenzamos con la Escala comportamental para nivel escolar inicial (Muchiut, Vaccaro, Zapata & Pietto, 2019) donde el docente valora el comportamiento del niño entre 4 y 6 años. Luego para adolescentes la Escala de funciones ejecutivas para padres de adolescentes (Muchiut, Dri, Vaccaro & Pietto, 2020) donde los padres valoran el funcionamiento de sus hijos entre 12 y 17 años; y actualmente se encuentra en etapa de publicación la Escala de Autorreporte de Funcionamiento Ejecutivo (AFE) para adolescentes (Muchiut, Pietto & Vaccaro, 2022) en la que el propio adolescente reporta su funcionamiento ejecutivo. 

Además, como equipo realizamos los baremos del WISC-IV para la ciudad de Resistencia (Muchiut, Vaccaro, Pietto & Dri, 2021), una prueba muy utilizada en nuestra región, donde se evidenciaron diferencias significativas según el baremo sea de Buenos Aires o de Resistencia y actualmente nos encontramos en proceso de Baremación del Cuestionario de Madurez Neuropsicológica Infantil – CUMANIN, prueba muy utilizada en la población infantil de 3 a 6 años. 

En este sentido, pareciera conveniente pensar en la necesidad de la regionalización de baremos, entendiendo este término como “la acción y el efecto de regionalizar”, involucrando “organizar con criterios descentralizadores un territorio, una actividad, una entidad, etc.” (Real Academia Española, s.f.). Con base en ello, se propone “descentralizar” una prueba mediante su estandarización (adaptación y tipificación) en una región diferente en la que fue normativizada originalmente, con el objetivo principal de establecer baremos locales que contemplen las características socioculturales específicas de una zona geográfica determinada.

Si bien regionalizar un instrumento sería lo ideal, coexiste con una realidad en la que no siempre se pueden emprender los procesos de adaptación debido al gran esfuerzo que conlleva, así como los recursos tanto humanos como materiales que requiere. 

Entonces, ante los impedimentos que se puedan presentar para la regionalización de una prueba, es de especial importancia que el profesional o investigador sea cauteloso en la interpretación de los resultados si ha decidido aplicar una prueba con baremos no regionalizados. 

Victoria Peterson, Instituto de Matemática Aplicada del Litoral de Santa Fe (Santa Fe)

Las vibraciones inducidas por señales acústicas pueden colarse en el sistema de adquisición de señales de electroencefalografía intracraneales (iEEG), apareciendo como un artefacto de vibración. En experimentos de habla pronunciada, este artefacto de vibración rastrea la frecuencia fundamental (F0) de la voz del participante, abarcando la banda de alta frecuencia gamma; banda que es bien conocida por estar involucrada en la producción y percepción del habla. Por lo tanto, para el desarrollo de modelos confiables de (de)codificación de voz, es necesario contar con señales de iEEG libres de cualquier ruido inducido por las señales acústicas de interés. En este trabajo, presentamos un método de eliminación de ruido para artefactos de vibraciones acústicas. El método se basa en enfoques de filtrado espacial que buscan encontrar aquellos componentes estadísticos altamente acoplados en fase con el audio producido. Mostramos cómo los métodos tradicionales pueden poner en peligro la calidad de la señal y que nuestro método es capaz de limpiar los datos preservando las oscilaciones neuronales subyacentes.

Alejandro Wainselboim, Instituto De Ciencias Humanas, Sociales y Ambientales de Mendoza (Mendoza)

Desde la segmentación de palabras en el flujo del habla hasta la adquisición de las reglas combinatorias que rigen el orden de las mismas en unidades oracionales cargadas de contenido semántico, el cerebro humano adquiere las regularidades relevantes de su entorno que permiten al individuo comprender y producir el lenguaje natural. Nuestro propósito es el de aportar un mayor entendimiento en cuanto a los mecanismos neurocomputacionales de los cuales, junto a los datos recibidos por los mismos, emerge el lenguaje humano. En el presente trabajo nos proponemos por tanto construir un modelo cuyas hipótesis neurocomputacionales se inspiren en rasgos específicos hallados en la corteza cerebral de los mamíferos. Desarrollamos el proyecto atendiendo a distintos niveles del procesamiento del lenguaje, desde la fonética hasta la gramática emergente por la propia dinámica cortical. 

Nuestro modelo muestra resultados preliminares que aportarían un mayor entendimiento de la mecánica que subyace al lenguaje y permitirían impulsar nuevos desarrollos para el aprendizaje de máquinas con mayor inspiración en la arquitectura de la corteza de los mamíferos para la resolución de problemas relacionados al procesamiento del lenguaje natural. Consideramos este nuevo enfoque como relevante a la hora de fomentar futuras líneas de investigación con una mayor atención a la biología del cerebro humano. 

Irene Taravini, Instituto de Ciencia y Tecnología de los Alimentos de Entre Ríos (ICTAER-UNER-CONICET)

La enfermedad de Parkinson (EP) es la segunda enfermedad neurodegenerativa más prevalente a nivel mundial, afectando al 1-2 % de la población mayor de 60 años. Su incidencia es cada vez mayor debido al aumento de la expectativa de vida y, al ser crónica y progresiva, representa un costo muy alto para el sistema

de salud y las familias de quienes la padecen. Los signos clínicos son consecuencia de la degeneración de las neuronas dopaminérgicas de la substantia nigra. Dado que las causas precisas que desencadenan esta muerte neuronal no se han esclarecido surge el desafío de hallar agentes con acción protectora con el fin último de reducir los síntomas, retrasar o incluso prevenir la expresión de esta enfermedad. Hace varios años se encontró una asociación inversa entre la ingesta de café o el consumo de tabaco y la aparición de la EP. De manera similar, estudios epidemiológicos recientes, realizados en Argentina, Uruguay y Brasil, revelaron que el consumo de yerba mate (YM) presenta también una asociación inversa con el riesgo de desarrollar la EP. El consumo de mate proporciona numerosos beneficios para la salud, los que se relacionan fuertemente con la gran variedad de fitoquímicos bioactivos que componen la YM y con su capacidad antioxidante y antinflamatoria. Recientemente, en experimentos in vitro se demostró que la YM protege a las neuronas dopaminérgicas de la muerte espontánea y progresiva. En nuestro laboratorio hemos observado que la administración a largo plazo de YM en ratones hemiparkinsonianos tiene un efecto neuroprotector de las neuronas dopaminérgicas. A partir de esta evidencia poblacional y de los resultados obtenidos a partir de la experimentación in vitro e in vivo, nos hemos planteado profundizar en el análisis e identificación de modificaciones bioquímico-moleculares relacionadas al efecto neuroprotector de la yerba mate sobre las neuronas dopaminérgicas en un modelo en ratón de la EP. Los estudios actuales de nuestro grupo permitirán elucidar si las propiedades antioxidantes y antiinflamatorias que posee la YM se relacionan con su efecto neuroprotector. Dada la importancia del consumo de YM en nuestra población, esperamos que los resultados de este trabajo contribuyan a reforzar la visión emergente de la YM como un alimento funcional, permitan revalorizar su consumo y redefinir su utilización resaltando sus propiedades benéficas para la salud, utilizándose para prevenir o retrasar la expresión de la EP o tal vez como una aproximación alternativa para el tratamiento de la misma en asociación con los fármacos antiparkinsonianos frecuentemente utilizados y tener así un impacto directo en la calidad de vida de los enfermos.

Guillermina Canesini, Instituto de Salud y Ambiente del Litoral (ISAL) CONICET-UNL. Departamento de Bioquímica Clínica y Cuantitativa, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral. Santa Fe, Argentina.

The alarming increase of overfeeding and the associated metabolic and immunological disorders, make the etiology and the consequences of obesity a widely studied topic today and receives increased attention from the scientific community. It is known that, if there is an inadequate nutritional experience during the first stages of life, metabolic missprogramming of vital regulatory pathways can occur permanently affecting appetite, growth dynamics, and cognitive functions. But not only alterations during the neonatal period determine conditions in adulthood. Moreover, the overfeeding associated to the exposure to a high-fat diet can produce an altered inflammatory response, triggering changes in memory functions. On the other hand, overfeeding can be the consequence of other brain functions, as those related to sleep disorders.
The goal of the symposium is to engage the audience in an active discussion about recently published and unpublished findings on behavioral research associated with food intake, memory impairment and sleep restriction in rodent and zebrafish models. In this context, we will explore morphological, genomic and behavioral alterations to elucidate possible new mechanisms involved on these functions and to identify potential therapeutic targets for neurodevelopmental disorders.

María Florencia Rossetti, Instituto de Salud y Ambiente del Litoral, CONICET-UNL. Departamento de Bioquímica Clínica y Cuantitativa, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral. Santa Fe, Argentina
“Neonatal overfeeding: Implications for hippocampal dysfunction and environmental intervention as a mitigating factor”

The objective was to explore the long-term effects of neonatal overfeeding on  cognition and neurosteroidogenesis and to analyze enriched environmental as a mitigating  factor. Male rats were raised in small litters (4 pups/mother; SL), in which pups ingest larger  amounts of milk and gain more body weight than rats raised in normal litters (10 pups/mother;  NL). On post-natal day (PND) 21, half of the male rats were sacrificed and the rest of males  were maintained under standard condition (4 rats/cage) or environmental enrichment (EE; 8  rats/cage). For EE, cages were provided with daily changed objects and toys. At PND75,  animals were tested in locomotion activity and episodic like-memory (ELM) test. At PND90,  animals were sacrificed and brains were microdissected. Using micropunch techniques,  dentate girus (DG), CA1 and CA3 regions were isolated for mRNA quantification and  methylation studies (results under analysis). At PND21, SL animals had higher body and fat  patches weights and greater levels of cholesterol, glucose and triglycerides, than NL rats. At  PND90, these metabolic differences were not observed. However, SL rats reported an  increased in anxiety like-behavior and a poor performance in ELM test compared to NL. In  addition, mRNA expression of aromatase (estradiol synthesis) and 5α-reductase 1 decreased  in DG of SL compared to NL rats. EE was enough to attenuate anxiety like-behavior and  rescue spatial memory deficit in SL animals. In addition, EE reversed aromatase and 5α reductase 1 expression decline associated to litter reduction. These results showed that  neonatal obesity negatively impacts on cognitive functions and neurosteroidogenic pathways in  adulthood, suggesting a long-lasting effect of nutritional experience during critical periods of  early postnatal development. Importantly, environmental intervention could mitigate these  effects and restore brain and behavior functions. 

Gisela Paola Lazzarino, Center for Social and Affective Neuroscience (CSAN), Department of Biomedical and Clinical Sciences (BKV), Linköping University, Linköping, Sweden
“ The effect of high-fat diet on microglia activation and cognitive function”

High-fat diet (HFD) consumption is linked to metabolic disorders, including obesity,  diabetes, and cardiovascular disease. Additionally, it is a risk factor for the development of  memory impairment and cognitive decline, as it has a direct impact on brain function. Microglia  has an essential role in neuronal remodeling. The ingestion of HFD leads to a systemic  inflammatory response, resulting in increased stimulation of pro-inflammatory microglia which  can lead to neuronal damage. Therefore, we hypothesized that microglia could play a  fundamental role in HFD-induced cognitive decline. Thus, we aimed to investigate the role of  microglia in triggering the hippocampal dysfunction related to HFD intake in mice. For this,  C57BL/6J mice were fed HFD (45 kcal% fat) or standard chow (10 kcal% fat) for 3, or 10 days.  In addition, transgenic mice expressing an inhibitory designer receptor exclusively activated by  designer drugs (DREADD) on microglia (Cx3cr1creERT2-hM4Di) were fed for 7 days with HFD  or standard chow. In all animals, cognitive tests such as novel object recognition and object  relocation test were performed. Hippocampal microglia morphology was assessed using  immunohistochemistry. After 10 days of HFD, there was a significant reduction in the time that  the animals explored the novel and the relocated object, suggesting impaired memory.  Besides, these animals showed a lower number of endpoints and shorter branch length of their  hippocampal microglia, indicative of a more reactive phenotype. DREADD+ HFD-fed animals  performed better in the cognitive tests than WT HFD-fed mice. Preliminary data obtained  indicate that WT mice fed HFD presented higher microglial cell density than WT standard  chow-fed mice, while HFD DREADD+ animals showed a tendency to have lower microglial cell  density than WT HFD-fed animals. These results indicate that a short-term intake of HFD  affects cognitive functioning and microglia morphology, suggesting that microglia are involved  in HFD-induced cognitive impairment. In order to draw firm conclusions about the ability of  microglia inhibition to rescue HFD-induced cognitive dysfunction, further research is required. 

Ana Paula García, Instituto de Salud y Ambiente del Litoral, CONICET-UNL. Departamento de Bioquímica Clínica y Cuantitativa, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral. Santa Fe, Argentina:
“Stablishing zebrafish (Danio rerio) as a model to study the effects of sleep deprivation on food intake behavior.”

Sleep deprivation has shown to affect the lives of millions of people every day and  has a profound impact on the biology of the brain. Notably, it has been reported that in  mammals, poor or short sleep produce overfeeding, promotes higher calorie intake from fat  and carbohydrate sources, which increases the risk to overweight and obesity development.  However, the effects of sleep disturbances in the brain centers that control the food intake  behavior are largely unexplored. Zebrafish has been shown to be a suitable model for sleep  and food intake research as the brain regulation of these behaviors are highly conserved in  vertebrates. According to these, our aim is to stablish the zebrafish as a model to study the  effects of sleep deprivation on food intake behavior and in the neural circuits involved in both behaviors, sleep and food intake. In order to reduce the time of sleep, adult zebrafish were  submitted to repeated vibrations during the night. The levels of activity of the individuals were  monitored during 24 hours in order to evidence the reduction of sleep duration. We observed  that the male individuals exposed to the vibrations increased food intake as it was evidenced  that the number of pellets ingested per day was significantly increased. The effects on the  expression levels of neurotransmitters/ neuropeptides participating in control of food intake  behavior and/or sleep will be analyzed, as well as the neural activation of its producing  neurons.

Nadia Justel, Lab. Interdisciplinario de Neurociencia Cognitiva (LINC), Centro de Investigación en Neurociencias y Neuropsicología (CINN), Universidad de Palermo, CONICET

Music generates unique demands on our nervous system; therefore, the neural mechanisms involved in musical activities, such as perception, production, and creation, generate a great amount of research questions for cognitive neuroscience. For the last years, music and each of its components have been used as a tool in the research of human cognition and its underlying brain mechanisms since music has great cortical and subcortical involvement. In this symposium 5 talks will be given that show how music is able to modulate our behavior, cognition, physiology, how music modifies our brain, appreciating the close relationship between music and neuroscience.

Robert J Zatorre, Montreal Neurological Institute, McGill University
“From Perception to Pleasure: The Neuroscience of Music and why we Love it”

Music has existed in human societies since prehistory, perhaps in part because it allows  expression and regulation of emotion, and evokes pleasure. In this lecture I will present  findings from cognitive neuroscience that bear on the question of how we get from  perception of sound patterns to pleasurable responses. I will first discuss evidence that  corticocortical loops from and to the auditory cortex are responsible not only for  perceptual processes but also for working memory, sensory-motor, and predictive  functions that are essential to produce and perceive music. Then, I will discuss  neuroimaging and brain modulation studies from our lab focusing on the dopaminergic  reward system, its involvement in musical pleasure, and what happens when that system  is disrupted. I propose that pleasure in music arises from interactions between cortical  loops that enable expectancies to emerge from perceived sound patterns, and  subcortical systems responsible for reward and valuation. This model integrates  knowledge derived from basic neuroscience of reward mechanisms with independently  derived concepts, such as tension and anticipation, from music theory. It may also serve  as a way of thinking more broadly about aesthetic rewards.

Ernest Mas Herrero, Institute of Neuroscience of the University of Barcelona:
“Now you like it, now you don’t: exploring the brain generators of music-induced pleasure”

The ability to experience pleasure with music is one of the most impressive skills we  possess as humans. Prior neuroimaging studies have shown that, despite its  abstractness, music may mimic innate biologically rewarding stimuli (e.g., food) in its  ability to engage the brain’s reward circuitry. However, neuroimaging methods are  correlational and thus, do not distinguish between brain regions directly involved in  generating the hedonic experience from those that are only modulated by that  experience. To establish such a causal relationship, it is crucial to actively manipulate  brain function. Starting with a review of neuroimaging studies investigating music induced pleasure and ending with a set of studies using non-invasive brain stimulation  techniques and pharmacological interventions, in this talk, I will dig into the role of  dopaminergic and opioidergic circuits in music reward. 

Verónika Diaz Abrahan, Laboratorio Interdisciplinario de Neurociencia Cognitiva (LINC) CEMSC3 ECyT ICIFI UNSAM-CONICET
“Music‑based interventions. Experimental studies about memory modulation”

Music is a complex activity with great cognitive potential. However, its cognitive impact  depends on whether people are playing or creating music, regardless of their musical  training. A specific type of research involves implementing music-based interventions on  a single session (before, during, or after a task) to improve cognitive performance. For  the past ten years, in LINC lab we have employed music perception (listening to musical  pieces) or production (music improvisation and rhythmic reproduction) as interventions  to explore their effects as memory modulators. The aim of this presentation is to show  the results of several studies that examined the effect of music-based interventions on  memory consolidation for preschool children, young adults, old adults without cognitive  impairment and adults with Alzheimer’s disease. In general, after the acquisition of verbal  or visual emotional information, the different groups were exposed to music improvisation  (experimental condition), music imitation (active control intervention) or silence (passive  control condition) for 3 min. We then evaluated memory through two tasks (free recall  and recognition), by means of immediate and deferred measures (after a week). Across  these studies, we found the following pattern of results: participants involved in music  interventions showed a significant improvement in memory. They remembered more  verbal and visual information than the control-condition groups, especially in the deferred  measures. The emotional induction generated by the musical activities is the strongest  idea that supports the results. Our findings suggest that a focal musical activity can be a  useful intervention in different populations to promote memory enhancement. 

María Angélica Benítez, Universidad Favaloro
“Cognitive benefits of music training”

The issue of how music experiences affect development is a matter of interest that has  increased over the last two decades, motivated by the idea that music training is a useful  framework for the investigation of plasticity in the human brain. Several studies have  shown that musicians differ from non-musicians in certain aspects of brain structures  and functions. However, recent researchers in this field have reached inconsistent  conclusions. The goal of this talk is to present two recent studies about the relationship  between music training and different cognitive functions in Argentinian children (study  1), and adolescents (study 2). We compared the scores of memory, language, and  visuospatial ability evaluated through neuropsychological tests in children and  adolescents with and without music training. To evaluate their memory, we developed a  task with the International Affective Picture System. To evaluate language and  visuospatial ability, we used the Child Neuropsychological Assessment. The musicians  received almost two years of previous music training from conservatories of music in  Argentina. The main results show that musicians obtained higher scores in tests for  memory and language than subjects with no music training. There were no other  significant results. These studies are an important step forward in music neuroscience in  Argentina. We believe that new music training research in this country that controls and  manipulates imaging techniques, genetic predispositions, and levels of engagement in  training could provide new information about the relationship between music and  cognition in Latin America. This research is important not only because of its contribution  to the area of brain plasticity as a product of musical stimulation, but also because of its  relevance in the clinical area, for the rehabilitation of motor functions and the music  therapy field.