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Mechanisms of inhibition in the avia...

University of Washington.

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Mechanisms of inhibition in the avian cochlear nucleus.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	Mechanisms of inhibition in the avian cochlear nucleus./
作者:	Howard, MacKenzie A.
面頁冊數:	119 p.
附註:	Adviser: Edwin W. Rubel.
Contained By:	Dissertation Abstracts International69-02B.
標題:	Biology, Neuroscience. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoeng/servlet/advanced?query=3303292
ISBN:	9780549496182

Mechanisms of inhibition in the avian cochlear nucleus.
Howard, MacKenzie A.

Mechanisms of inhibition in the avian cochlear nucleus. - 119 p.

Adviser: Edwin W. Rubel.

Thesis (Ph.D.)--University of Washington, 2008.

The avian cochlear nucleus magnocellularis (NM) is the first central synapse receiving low frequency sound information and the first neurons of the auditory system to project axons bilaterally. Thus, NM is well suited to contribute to temporal processing important for binaural hearing. The synapses, anatomy, and physiology of NM neurons are each specialized to enhance the temporal precision of spiking. An unusual and poorly understood specialization of these neurons is their depolarizing response to GABAergic input. The goals of this dissertation are threefold, to understand: (1) the events that lead to the emergence of functional depolarizing inhibition during development; (2) the biophysical mechanisms by which GABA reduces the excitability of mature NM neurons; (3) how integration of inhibitory and excitatory synaptic input alters the temporal fidelity of NM outputs.

ISBN: 9780549496182Subjects--Topical Terms:

1017680
Biology, Neuroscience.

Mechanisms of inhibition in the avian cochlear nucleus.
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245 1 0 $a Mechanisms of inhibition in the avian cochlear nucleus.
300 $a 119 p.
500 $a Adviser: Edwin W. Rubel.
500 $a Source: Dissertation Abstracts International, Volume: 69-02, Section: B, page: 0864.
502 $a Thesis (Ph.D.)--University of Washington, 2008.
520 $a The avian cochlear nucleus magnocellularis (NM) is the first central synapse receiving low frequency sound information and the first neurons of the auditory system to project axons bilaterally. Thus, NM is well suited to contribute to temporal processing important for binaural hearing. The synapses, anatomy, and physiology of NM neurons are each specialized to enhance the temporal precision of spiking. An unusual and poorly understood specialization of these neurons is their depolarizing response to GABAergic input. The goals of this dissertation are threefold, to understand: (1) the events that lead to the emergence of functional depolarizing inhibition during development; (2) the biophysical mechanisms by which GABA reduces the excitability of mature NM neurons; (3) how integration of inhibitory and excitatory synaptic input alters the temporal fidelity of NM outputs.
520 $a Towards these goals, in vitro electrophysiological methods were used to test the synaptic and voltage-dependent membrane properties of NM neurons over a period of embryonic development. Major changes to voltage-activated K+ currents were noted between the onset of hearing and hatching. These changes were sufficient and necessary to produce a switch depolarizing postsynaptic potentials (dIPSPs) from facilitating to inhibitory. Whole cell recording and computational modeling were used to explore the biophysical mechanisms of depolarizing inhibition. The synaptic conductance, voltage-activated K+ currents, Na+ channel inactivation, and clustering of Na+ channels away from the soma all contributed to, and were necessary for functional depolarizing inhibition in NM neurons. Modeling was also used to examine the role of dIPSPs in synaptic integration and temporal summation between excitatory inputs. These experiments revealed that NM neurons transform into obligate monaural coincidence detectors during high rates of excitatory input. GABAergic inputs improved temporal coding in NM by making coincidence detection more stringent and enhanced nonlinear summation between non-coincident inputs, minimizing spiking to poorly timed excitation. Notably, while depolarizing inhibition augmented the temporal fidelity of NM, hyperpolarizing inhibition diminished it.
520 $a These results suggest a key role for depolarizing GABAergic inhibition in the temporal coding pathway of the avian auditory system. By sharpening the temporal precision of NM outputs, these synaptic inputs may serve improve the signal-to-noise characteristics of the system, enhancing binaural tasks such as sound localization that are crucial for the survival of the organism.
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791 $a Ph.D.
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