Salk Institute
Nicola J. Allen
Assistant Professor
Molecular Neurobiology Laboratory
Nicola J. Allen

Assistant Professor
Molecular Neurobiology Laboratory


Research

Allen's lab investigates the molecular pathways that lead to connections between neurons, known as synapses, in the developing brain. Her group focuses on signaling interactions between neurons and astrocytes, a class of star-shaped glial cell. Astrocytes constitute half of the cells in the brain, and astrocyte processes, the "arms" that project outward from the cells, surround the majority of neuronal synapses in the brain. This places them in an ideal location to be actively involved in synapse formation and maintenance and in the modulation of communication between neurons. In fact, in the absence of astrocytes, few functional connections form between developing neurons, while their presence profoundly increases the number of functional synapses.

Previous studies began to identify the molecular signals between neurons and astrocytes and showed that thrombospondins and glypicans, two protein families that are secreted from developing astrocytes, affect synapse formation. The hypothesis is that astrocytes play a crucial role in dictating synapse formation and function via the release of specific proteins that determine the type of synapse that will form, and the strength of that synapse.

The current goal of the lab is to further investigate how these two protein families promote synapse formation, by identifying the neuronal receptors and cellular signaling pathways involved, and to understand how they interact to determine what type of synapse is formed. In addition, they will continue to use biochemical and molecular techniques to identify other ways that astrocytes influence distinct aspects of synapse formation and maturation and how they control the types of synapses that develop.

The pathways they identify will be investigated for roles in neurodevelopmental disorders, such as autism, that are caused by defects in synapse formation and function. In future studies, they will explore whether these developmental findings can be used to address diseases such as stroke, by promoting the repair of synaptic connections following injury.

"Neurons in the brain are connected by billions of synapses, the points of communication between nerve cells. I want to know what controls when and where these synapses are formed, and how synaptic connections are modified to allow memories to be stored."

Allen's lab investigates the molecular pathways that lead to connections between neurons, known as synapses, in the developing brain. Her group focuses on signaling interactions between neurons and astrocytes, a class of star-shaped glial cells. Astrocytes constitute half of the cells in the brain, and astrocyte processes, the "arms" that project outward from the cells, surround the majority of neuronal synapses. This places them in an ideal location to be actively involved in synapse formation and maintenance and in the modulation of communication between neurons. In fact, in the absence of astrocytes, few functional connections form between developing neurons, while their presence profoundly increases the number of functional synapses.

Previous studies began to identify the molecular signals between neurons and astrocytes and showed that thrombospondins and glypicans, two protein families that are secreted from developing astrocytes, affect synapse formation. The hypothesis is that astrocytes play a crucial role in dictating synapse formation and function via the release of specific proteins that determine the type of synapse that will form, and the strength of that connection.

The current goal of the lab is to further investigate how these two protein families promote synapse formation, by identifying the neuronal receptors and cellular signaling pathways involved, and to understand how they interact to determine what type of synapse is formed. In addition, they will continue to use biochemical and molecular techniques to identify other ways that astrocytes influence distinct aspects of synapse formation and maturation and how they control the types of connections that develop.

The pathways they identify will be investigated for roles in neurodevelopmental disorders, such as autism, that are caused by defects in synapse formation and function. In future studies, they will explore whether these developmental findings can be used to address diseases such as stroke by promoting the repair of neural connections following injury.

Lab Photo

Cari Dowling, Nicola Allen

Selected Publications

Allen NJ, Bennett ML, Foo LC, Wang GX, Chakraborty C, Smith SJ, Barres BA (2012) Astrocyte glypican 4 & 6 promote formation of excitatory synapses via GluA1 AMPA receptors. Nature, 486, p410-414.

Allen NJ (2012) Glial Control of synaptogenesis. Neuroglia (H Kettenmann & B Ransom editors), 3rd Edition, Elsevier.

Foo LC, Allen NJ, Bushong EA, Ventura PB, Chung WS, Zhou L, Cahoy JD, Daneman R, Zong H, Ellisman MH, Barres BA (2011) Development of a method for the purification and culture of rodent astrocytes. Neuron, 71, p799-811.

Eroglu C, Allen NJ, Susman MW, O'Rourke NA, Park CY, Ozkan E, Chakraborty C, Mulinyawe SB, Annis DS, Huberman AD, Green EM, Lawler J, Dolmetsch R, Garcia KC, Smith SJ, Luo ZD, Rosenthal A, Mosher DF, Barres BA (2009) Gabapentin receptor alpha2delta-1 is a neuronal thrombospondin receptor responsible for excitatory CNS synaptogenesis. Cell, 139, p380-392.

Allen NJ, Rossi DJ and Attwell D (2004) Sequential release of GABA by exocytosis and reversed uptake leads to neuronal swelling in simulated ischaemia of hippocampal slices. Journal of Neuroscience, 24, p3837-3849.

Awards and Honors

  • Human Frontier Science Program (HFSP) Long Term Fellowship, 2005-2008
  • European Molecular Biology Organisation (EMBO) Long Term Fellowship, 2004-2005
  • Wellcome Trust PhD Fellowship, 1999-2003

Get Involved

Sign up for our email newsletter

Fill out my online form.
Contact
Salk Institute for Biological Studies
Street: 10010 N Torrey Pines Rd
City: La Jolla, CA 92037
Email: webrequest@salk.edu
Phone: 858.453.4100
Charity Navigator Rating
  • Salk Twitter
  • Salk LinkedIn
  • Salk Facebook
  • Salk Instagram
  • Salk Google+
  • Salk YouTube
  • Salk RSS Feed
© Copyright 2014 Salk Institute for Biological Studies About Scientists & Research News & Media Events Support