10-11 Archives

Vallent Lee Awarded a Pre-Doctoral Fellowship from the Epilepsy Foundation

Vallent Lee, a Sackler Neuroscience MD-PhD student in the Maguire lab, was awarded a pre-doctoral fellowship from the Epilepsy Foundation. The project is entitled "Role of tonic inhibition in hippocampal function and epileptogenesis" and uses a novel mouse model to investigate how specific subtypes of GABA receptors contribute to a healthy balance of excitation and inhibition, which is disrupted in the development of epilepsy. The proposed experiments will shed light upon the therapeutic potential of these receptors.

Chris Dulla Awarded Epilepsy Foundation Grant

Chris Dulla, Assistant Professor of Neuroscience, received a New Therapy Grant from the Epilepsy Foundation and Epilepsy Therapy Project for a project entitled “Disrupted glutamatergic maturation in a model of polymicrogyria”.

Brain development is an exquisitely complex process. When development is disrupted there can be serious consequences on brain function and quality of life. Polymicrogyria (PMG) is a disorder caused by improper developmental formation of the brain. People who suffer from PMG have a high (80%) incidence of epilepsy and are generally not well treated by anti-epileptic drugs nor by brain surgery. The release and removal of the neurotransmitter glutamate may be disrupted in PMG which may lead to seizure activity. Brain cells known as astrocytes remove glutamate. Changes in how astrocytes function in PMG will be studied and novel drugs will be tested which increase the brain's ability to remove glutamate and which could decrease seizure activity.

Novel Mechanism Regulating Stress Identified by Tufts Researchers

Neuroscience researchers from Tufts have demonstrated, for the first time, that the physiological response to stress depends on neurosteroids acting on specific receptors in the brain, and they have been able to block that response in mice. This breakthrough suggests that these critical receptors may be drug therapy targets for control of the stress-response pathway. This finding may pave the way for new approaches to manage a wide range of neurological disorders involving stress.

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Tufts Neuroscience Collaboration with Parthys Reverse Informatics

Tufts Neuroscience collaborates with Parthys Reverse Informatics to integrate various neuroscience genomics resources to provide a unified resource for neuroscience data mining.

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Steve Moss Awarded a Simons Foundation Autism Research Initiative (SFARI) Grant

Steve Moss, Professor of Neuroscience, was recently awarded a Simons Foundation Autism Research Initiative (SFARI) grant. This project, titled, "Defects in Tonic Inhibition and the Pathology of Autism Spectrum Disorders", will use a unique model to determine the role of the GABA(A) receptor beta 3 subunit in autism spectrum disorders and to ascertain whether neurosteroids that preferentially act to increase tonic inhibition are able to reverse the behavioral deficits seen in these disorders. The study is planned to provide novel insights into the pathology of autism spectrum disorders and ultimately to lead to the development of new therapies.

Tamara Blutstein Awarded NRSA from National Institute of Mental Health

Tamara Blutstein, a postdoctoral fellow in the Haydon Lab, was awarded a NRSA from the National Institute of Mental Health. The project entitled "The role of gliotransmission in sleep homeostasis" will examine the relationship between nitric oxide and gliotransmission, more specifically glial-derived adenosine, in the accumulation of sleep pressure after sleep deprivation and the observed cognitive deficits. These studies will provide insights into the homeostatic mechanisms that underlie sleep and wakefulness and identify potential new regulatory targets, such as glial cells.

Maribel Rios Awarded a Klarman Family Foundation Research Award

Maribel Rios, Associate Professor of Neuroscience, received a research grant from the Klarman Family Foundation for Eating Disorders Research. The project titled "Investigations of cellular and molecular mechanisms underlying the effects of BDNF and restricted food intake on binge eating" will test the hypothesis that deficient BDNF signaling cooperates with food restriction to induce synaptic maladaptations that impair function of the mesolimbic dopamine system. This neural pathway regulates reward-seeking behaviors, including consumption of palatable food and has been linked with the etiology of binge eating. These studies will provide a mechanistic understanding of cellular and molecular processes driving disordered eating to help create novel therapeutic avenues.

Neuroscience Faculty to join Cell Death in Neurodegeneration Study Section

Dr Giuseppina Tesco will serve as a member of the Cell Death in Neurodegeneration Study Section, Center for Scientific Review for the term beginning July 1st, 2011. Members are selected on the basis of their demonstrated competence and achievement in their scientific discipline as evidenced by the quality of research accomplishments, publications in scientific journals and other significant scientific activities, achievements and honors.

Sackler School Neuroscience Program Research Spotlight: Hearing for the Young and Old

Studies by Neuroscience graduate student Elizabeth Storer and her adviser, Michele Jacob, are identifying molecular interactions that are required for synapse assembly and normal sound processing.

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Glial cells of the adult brain can physiologically regulate circadian clock neurons and behavior

The Jackson lab group recently published a paper in Current Biology showing for the first time that glial cells of the adult brain can physiologically regulate circadian clock neurons and behavior. The work of Drs Fanny S Ng, Michelle M Tangredi and FR Jackson indicates that glial cells of the Drosophila brain regulate release of the circadian neurotransmitter PDF from clock neurons; this transmitter is known to be essential for daily rhythms in locomotor activity rhythms. The study also demonstrates a role for glial internal calcium stores in glia-to-neuron communication that is critical for normal circadian behavior. Finally, this research identifies astrocytes of the fly brain as a key cell type in the regulation of circadian behavior. It will be of interest to determine if there is a similar astrocytic modulation of the mammalian circadian neural circuitry.

Ng FS, Tangredi MM, Jackson FR 2011. Glial cells physiologically modulate clock neurons and circadian behavior in a calcium-dependent manner. Curr Biol. 21: 625-634. Abstract in PubMed

Tufts Neuroscience Faculty organizes Symposium at Third World Congress of Chronobiology

Rob Jackson recently organized a symposium entitled “Roles for Glial Cells in the Circadian Neural Circuitry” for the Third World Congress of Chronobiology in Puebla, Mexico (May 5-9, 2011). The symposium featured results from investigators using mammalian and Drosophila models that demonstrate important functions of glial cells, including astrocytes, in the circadian circuitry. Rob presented lab studies showing that Drosophila glial cells physiologically regulate circadian clock neurons and behavior in the adult brain.

KCC2 as a potential target for treatment of epilepsy

The Stephen Moss group recently published a manuscript in the journal Nature Neuroscience. This work focused on KCC2, a neuron-specific ion pump that maintains a low level of intracellular chloride that is essential for inhibitory neurotransmission mediated by GABAA receptors. Using a combination of techniques the group for the first time described a cellular mechanism by which pathophysiological levels of glutamate rapidly decrease KCC2 function and abolish hyperpolarizing signaling mediated by GABAA receptors. The loss of KCC2 function could explain the resistance to drugs used to treat specific forms of epilepsy. This research highlights KCC2 as a potential target for the development of novel therapeutic agents for the treatment of epilepsy and other neurological disorders.

Lee HH, Deeb TZ, Walker JA, Davies PA, Moss SJ. 2011. NMDA receptor activity downregulates KCC2 resulting in depolarizing GABA(A) receptor-mediated currents. Nat Neurosci. 14: 736-743. Abstract in PubMed