Welcome to Zou Lab

The Zou lab at UCSD studies development, function and repair of neural circuits. We are interested in how neurons in the nervous system form highly organized and precise connections to give rise to function. We believe studying neural circuit assembly at molecular and cellular level will reveal fundamental principles of how the complex connections of the entire nervous system are organized. We also study how neural circuits degenerate and how adult central nervous system responds to injury.

Latest News

New icon Jan 19, 2015:

Hollis et al showed that reorganization of synaptic contacts can strengthen the spared circuits and lead to functional recovery after partial spinal cord injury. And blocking repulsive Wnt signalling increases axon plasticity and synaptic connections that drive greater functional recovery.

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New icon Dec 23, 2014:

Hollis et al reported a more robust conditioning lesion model. Injection of a chemical demyelinating agent, ethidium bromide, into the sciatic nerve induces a similar set of regeneration-associated genes and promotes a 2.7-fold greater extent of sensory axon regeneration in the spinal cord than sciatic nerve crush. This study provides a new method for investigating the underlying mechanisms of the conditioning response and suggests that loss of the peripheral myelin maybe a major signal to change the intrinsic growth state of adult sensory neurons and promote regeneration.

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Dec 4, 2013:

Onishi et al published new findings on signaling mechanisms that mediates growth cone turning. Commissural axons engage planar cell polarity (PCP) signaling components to turn in a Wnt gradient. Frizzled3, a Wnt receptor, undergoes endocytosis via filopodia tips. Wnt5a increases Frizzled3 endocytosis, which correlates with filopodia elongation. He discovered an unexpected antagonism between Dishevelleds, which may function as a signal amplification mechanism in filopodia.

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Oct 7, 2013:

Anna Tury et al published their studies on changes of Wnt signaling components in an ALS mouse model. Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive paralysis due to the selective death of motor neurons of unknown causes. She focused on two non-canonical Wnt signaling components, atypical PKC (aPKC) and a Wnt receptor, Ryk. aPKC expression was increased in motor neurons of the lumbar spinal cord in SOD1 (G93A) mice at different stages and may be sequestered in SOD1 aggregates. Ryk expression was also increased in the motor neurons and the white matter in the ventral lumbar spinal cord of mutant SOD1 mice with a peak at early stage. These observations indicate that Wnt/aPKC and Wnt/Ryk signaling are altered in SOD1 (G93A) mice, suggesting that changed Wnt signaling may contribute to neurodegeneration in ALS.

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