Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity

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Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity

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dc.contributor.advisor Zakon, H. H.
dc.creator George, Andrew Anthony
dc.date.accessioned 2010-08-20T19:53:58Z
dc.date.accessioned 2010-08-20T19:54:09Z
dc.date.available 2010-08-20T19:53:58Z
dc.date.available 2010-08-20T19:54:09Z
dc.date.created 2009-12
dc.date.issued 2010-08-20
dc.date.submitted December 2009
dc.identifier.uri http://hdl.handle.net/2152/ETD-UT-2009-12-407
dc.description.abstract Although the processes used for temporarily storing and manipulating neural information have been extensively studied at the synaptic level far less attention has been given to the underlying cellular and molecular mechanisms that contribute to change in the intrinsic excitability of neurons. More importantly, how do these mechanisms of plasticity integrate with ongoing mechanisms of regulation of neural intrinsic excitability and, in turn, homeostasis of entire neural circuits? In this dissertation I describe the underlying mechanisms that contribute to persistent neural activity and, more globally, sensorimotor adaptation using weakly electric fish as my model system. Weakly electric fish have evolved a behavior adaptation known as the jamming avoidance response (JAR), and it is this adaptation that allows the organism to elevate its own electrical discharge in response to intraspecific interactions and subsequent distortions of the animal’s electric field. The elevation operates over a wide range and in vivo can last tens of hours upon cessation of a jamming stimulus. I demonstrate that the underlying mechanisms of the adaptation are mediated by calcium-dependent signaling in the pacemaker nucleus and that calcium-mediated phosphorylation plays an important role in the regulation of the long-term frequency elevation (LTFE). I demonstrate using an in vitro brain slice preparation from the weakly electric fish, Apteronotus leptorhynchus that the engram of memory formation depends on the cooperativity of calcium-dependent protein kinases and protein phosphatases. In addition, I show that the memory formation (in the form of LTFE) does not depend on the continued flux of calcium, but rather the phosphorylation events downstream of NMDA receptor activation. Moreover, I describe the differences in the expression of protein phosphatases and protein kinases as they relate to species-specific differences in sensorimotor adaptation. It is important to note that this is the first time that the cooperativity between different isoforms of protein kinase C (PKC) have been shown to play a role in graded long-term change in neuronal activity and, in turn, providing the neural basis of species-specific behavior. The neural adaptation of the electromotor system in weakly electric fish provides an excellent model system to study the underlying cellular and molecular events of vertebrate memory formation.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.subject Electric Fish
dc.subject Neuronal Intrinsic Excitability
dc.subject Calcium
dc.subject Homeostasis
dc.subject Neuronal Plasticity
dc.subject PKC
dc.subject Calcineurin
dc.title Calcium-mediated change in neuronal intrinsic excitability in weakly electric fish: biasing mechanisms of homeostatis for those of plasticity
dc.date.updated 2010-08-20T19:54:09Z
dc.contributor.committeeMember Aldrich, Richard W.
dc.contributor.committeeMember Atkinson, Nigel S.
dc.contributor.committeeMember Mihic, S. John
dc.contributor.committeeMember Golding, Nace L.
dc.contributor.committeeMember Dalby, Kevin N.
dc.type.genre thesis
dc.type.material text
thesis.degree.department Biological Sciences, School of
thesis.degree.discipline Neuroscience
thesis.degree.grantor The University of Texas at Austin
thesis.degree.level Doctoral
thesis.degree.name Doctor of Philosophy

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