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Turrigiano Receives HFSP 2012 Nakasone Award

August 26, 2011 By

The Human Frontier Science Program Organization (HFSPO) has announced that the 2012 HFSP Nakasone Award has been conferred upon Professor of Biology Gina Turrigiano for introducing the concept of “synaptic scaling”.

Gina is the third recipient of the HFSP Nakasone Award. This award, first given in 2010, honours the vision of former Prime Minister of Japan Yasuhiro Nakasone for his efforts to launch a program of support for international collaboration and to foster early career scientists in a global context. The HFSP Nakasone Award is designed to honour scientists who have undertaken frontier-moving research in biology, encompassing conceptual, experimental or technological breakthroughs. Awardees receive an unrestricted research grant of USD 10,000, a medal and a personalised certificate. The award ceremony will be held at the annual meeting of HFSP awardees to be held in the Republic of Korea in July 2012, where Gina will give the HFSP Nakasone Lecture at the annual meeting of HFSP awardees to be held in the Republic of Korea in July 2012.

From the press release:

The concept of “synaptic scaling” was introduced to resolve an apparent paradox: how can neurons and neural circuits maintain both stability and flexibility? The number and strength of synapses shows major changes during development and in learning and memory. Such changes could potentially lead to massive changes in neuronal output that could have deleterious effects on the stability of neuronal networks and memory storage. Homeostatic mechanisms are therefore required to control neuronal output within certain limits while still maintaining the relative weights of synaptic inputs that underlie information storage. The work of Gina Turrigiano’s laboratory has shown that neurons can “tune” themselves by responding to an increase in firing rate by scaling down all excitatory synaptic strengths and vice versa. Such global changes in synaptic input limits the rate of firing (output) while maintaining changes in the relative strengths of individual synapses (input). She continues to explore the mechanisms that underlie such scaling phenomena and their function in vivo using a variety of molecular, electrophysiological, imaging and computational approaches.

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PSD-95 contributes to synaptic homeostasis

May 9, 2011 By

Most people probably take it for granted that our brains rarely experience extreme activity conditions such as epilepsy (hyperactivity) or catatonia (hypoactivity). But to neuroscientists this stability is quite puzzling, because our brain activity is constantly perturbed by both changes in the external world and by internal changes that result from learning and development. Over the past two decades, research pioneered by Brandeis neuroscientists has suggested that our brains solve this stability problem by using a set of “homeostatic” plasticity mechanisms that stabilize neural excitability. One of the best documented such mechanisms is known as homeostatic synaptic scaling, in which synaptic strengths are up- or down-regulated to compensate for external fluctuations in drive. This form of plasticity acts like a “synaptic thermostat” to maintain neural excitability within an optimal operational range. However, the molecular mechanisms by which changes in activity lead to bidirectional adjustments in synaptic strength are not fully understood. Now a recent paper published in the Journal of Neuroscience by Brandeis graduate student Qian Sun (PhD ’11) and Professor Gina Turrigiano shows that two abundant and well-studied synaptic proteins, PSD-95 and PSD-93 (or Postsynaptic Density-95 and 93), are critical for the expression of synaptic scaling.

PSD-95/PSD-93 are rock stars of the synaptic world. They are important synaptic proteins that act as “scaffolds” to organize other synaptic proteins, and are known to contribute to several non-homeostatic forms of synaptic plasticity such as long term potentiation and long term depression. This new study adds an additional critical function to the already complex role that the PSD-95 protein family plays in synaptic plasticity, by showing that PSD-95 mediates both scaling up and scaling down, but that these two directions of plasticity are mediated by distinct aspects of PSD-95 function. Taken together with other work, this study suggests that PSD-95/PSD-93 serve as critical synaptic organizers ~ synaptic conductors, if you will ~ that can mediate many forms of synaptic plasticity through distinct protein-protein interactions within the synapse. This study provides a glimpse into the complexity of the synaptic machinery, and sheds important new light into the mechanisms of homeostatic synaptic scaling.

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Visually driven intrinsic plasticity

November 19, 2010 By

In mammals including humans, proper development of the cortex is heavily dependent on sensory experience. Neurons in sensory cortex are subject to a “use it or lose it” rule, whereby if they are deprived of sensory input during a critical period of development, they lose the ability to respond altogether. This loss of responsiveness could occur through synaptic changes (synaptic plasticity), or through changes in the intrinsic ability of neurons to fire action potentials (intrinsic plasticity).

Up until now experience-dependent development has largely been ascribed to  synaptic plasticity mechanisms.  In the cover article in this week’s issue of Neuron, (Nataraj et al., Neuron 68, 750–762, November 18, 2010), Brandeis postdocs Kiran Nataraj, Nicolas Le Roux, Marc Nahmani and Sandrine Lefort from the lab of Professor Gina Turrigiano show that a form of intrinsic plasticity termed “long-term potentiation of intrinsic excitability”, or LTP-IE, plays an important role in experience-dependent refinements of cortical circuits. This study shows that sensory drive normally keeps cortical output neurons active by triggering LTP-IE, and sensory deprivation reduces the ability of these neurons to fire by preventing the activation of this form of plasticity. This suggests that LTP-IE serves a “use it or lose it” function in cortical output neurons, gating cortical output by keeping active neurons responsive, while suppressing the output of  inactive neurons.

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TNFα Signaling Maintains the Ability of Cortical Synapses to Express Synaptic Scaling

November 9, 2010 By

The brain has billions of neurons that receive, analyze, and store information about internal and external conditions, and are highly interconnected. To prevent either hyperexcitability (epilepsy) or hyopexcitability (catatonia) of brain circuits, neurons possess an array of “homeostatic” plasticity mechanisms that serve to stabilize average neuronal firing.

Synaptic scaling is one such form of homeostatic plasticity that acts like a synaptic thermostat, and allows neurons to turn up or down the gain of synaptic transmission to stabilize average activity. The signaling pathways that allow neurons to perform this neat trick are incompletely understood, and it has been controversial whether neurons do this in a cell-autonomous manner, or whether synaptic scaling is induced in response to release of soluble factors such as the pro-inflammatory cytokine TNFα.

A study published this week in Journal of Neuroscience by Brandeis postdoctoral fellow Celine Steinmetz and Professor Gina Turrigiano helps to resolve this controversy by showing that TNFα is not instructive for synaptic scaling, but instead is critical for maintaining  synapses in a plastic state in which they are able to express synaptic scaling. This study suggests that glial cells serve a permissive role in maintaining synaptic plasticity through release of soluble factors such as TNFα, while neurons actively adjust their synaptic thermostat in response to cell-autonomous changes in their own activity.

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Recent Grant Awards

January 14, 2009 By

Neuroscience Ph.D. candidate Melanie Gainey received an NRSA Fellowship from NINDS. Working in the Turrigiano lab, Melanie plans to study the role of the AMPA receptor subunit GluR2 in synaptic scaling in cultural neurons and in vivo using a conditional GluR2 knockout mouse.

Assistant Professor Suzanne Paradis received a Smith Family New Investigator Award from the Richard & Susan Smith Family Foundation. $300,000 in support over three years will support the lab’s efforts to study synapse development and specifically the role of the Sema4B protein in controlling synapse formation.

Professor Leslie Griffith received $1.1 million over 5 years from NIMH to study why sleep is required for effective memory formation. To understand this linkage at a cellular and molecular level, the Griffith lab is defining the circuits that regulate sleep in Drosophila and how these circuits affect memory formation.

Professor Larry Wangh received $1.38 million over the next year from Smiths Detection to continue research and invention of LATE-PCR et al., platform technologies for highly informative detection and diagnosis of nucleic acids in a single tube.  There are ongoing projects looking at applications to cancer, prenatal genetics, and several infectious diseases in people and animals.

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The Self-Tuning Neuron

November 7, 2008 By

Gina Turrigiano discusses “The Self-Tuning Neuron” in a new review in Cell.

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