| URN |
etd-0626101-123602 |
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| Author |
Pi-Shan Chang |
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| Author's Email Address |
No Public. |
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| Statistics |
This thesis had been viewed 5567 times. Download 2303 times. |
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| Department |
Biological Sciences |
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| Year |
2000 |
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| Semester |
2 |
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| Degree |
Master |
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| Type of Document |
|
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| Language |
zh-TW.Big5 Chinese |
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| Title |
Role of Glutamatergic Neurotransmission at the Nucleus Reticularis Ventrolateralis during Experimental Endotoxemia |
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| Date of Defense |
2001-06-06 |
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| Page Count |
68 |
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| Keyword |
Endotoxemia
Spectral analysis
NRVL
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| Abstract |
The components of SAP signals of low- frequency (LF: 0.08-0.15 Hz) and very low- frequency (VLF: 0.00-0.08 Hz) related with vasomotor tone that reflects the activity of sympathetic premotor neuron in the nucleus reticularis ventrolateralis (NRVL). The Sprague-Dawely male rats with acute endotoxemia (lipopolysaccharide, LPS; 15 mg/Kg i.v.) induced a reduction phase (phaseⅠ), followed by partial recovery (phaseⅡ) and a secondary decrease (phase Ⅲ). The rats with acute endotoxemia display three phases based on change in the power density of LF and VLF component.
Pretreatment with microinjection of NMDA receptor antagonist, MK-801, and non-NMDA receptor antagonist, CNQX into the bilaterial NRVL prolong the survival time and prolong the duration time of phaseⅡ and phaseⅢ. Pretreatment with high concentration MK-801 (200 pmol) and CNQX (10 pmol) hold the MSAP and heart rate in the steady state and decrease the slope of MSAP falling during endotoxemia.The power density of pretreatment with high concentration MK-801 (200 pmol) and CNQX (10 pmol) was deceease.
We conclude that the rat during experimental endotoxemia decrease the duration time of NMDA and non-NMDA receptor activity in NRVL. The NMDA receptor and non-NMDA receptor activity in NRVL during endotoxemia contribute the slope of MSAP falling and cause to death. |
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| Advisory Committee |
Chan, J. Y. H. - chair
Chang, A. Y. W - co-chair
Chan, S. H. H. - advisor
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| Files |
indicate access worldwide |
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| Date of Submission |
2001-06-26 |
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