In vivo visualization of CaMKII activity in ocular dominance plasticity

Alterations in sensory experience can persistently modify the responses of cortical neurons. Ocular dominance (OD) plasticity, a process in which alternation of visual input induces a shift in cortical responsiveness, is an extensively studied model of such experience-dependent plasticity. However, the synaptic mechanisms underlying OD plasticity are not well understood. Recent studies revealed that both Hebbian and homeostatic mechanisms play a role in OD plasticity. Therefore, we were interested in monitoring the process of rapid plasticity at individual synapses in vivo to gain insight into the interplay of these two mechanisms. Ca2+/calmodulin dependent protein kinase II (CaMKII) is a major component of the postsynaptic density. Activation of CaMKII is necessary and sufficient for LTP induction, is required for OD plasticity, and its expression pattern coincides with the site of rapid plasticity in the supragranular layers II/III of the visual cortex. Moreover, CaMKII can convert transient Ca2+ influx into a prolonged biochemical process via autophosphorylation that renders CaMKII activity Ca2+ independent. Hence, CaMKII is well suited as a reporter of synaptic activity. We previously engineered a probe, Camui, which utilizes the optical phenomenon of fluorescence resonance energy transfer (FRET), to monitor CaMKII activation. This thesis embodies the work done to improve Camui to be a better tool for in vivo reporting of CaMKII activity, as well as the use of this improved probe for in vivo detection of CaMKII activity in single spines before and after 4 hrs of monocular deprivation (MD) in the ferret visual cortex.

Department dc:contributor.department

Massachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.

Grantor dc:publisher

Massachusetts Institute of Technology

Year dc:date.issued

2009

Author dc:creator

• Kwok, Show Ming

Advisor dc:contributor.advisor

• Yasunori Hayashi.

• Brain and Cognitive Sciences.

Statement dc:rights

• M.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.

Licence dc:rights.uri

• http://dspace.mit.edu/handle/1721.1/7582

Language dc:language.iso

eng

Handle dc:identifier.uri

http://hdl.handle.net/1721.1/46817

OAI identifier oai:identifier

oai:dspace.mit.edu:1721.1/46817