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Aspartic and glutamic acids increase in the frontal cortex during prostaglandin E1 hyperthermia
1Dipartimento di Fisiologia Umana e Funzioni Biologiche Integrate Filippo Bottazzi, Seconda Università degli Studi di Napoli, Italy.
Neuroscience
|March 21, 1998
Summary
Prostaglandin E1 triggers hyperthermia by increasing aspartic acid and glutamic acid release in the frontal cortex. This study monitored neurotransmitter levels and temperature changes in rats.
Area of Science:
- Neuroscience
- Physiology
- Biochemistry
Background:
- Prostaglandin E1 (PGE1) is implicated in thermoregulation.
- The role of specific amino acids in the frontal cortex during hyperthermia is not fully understood.
Purpose of the Study:
- To investigate the involvement of aspartic acid and glutamic acid in the frontal cortex during prostaglandin E1-induced hyperthermia.
- To assess the relationship between these amino acids, sympathetic nerve activity, and temperature regulation.
Main Methods:
- Male Sprague Dawley rats were used, anaesthetized with ethyl-urethane.
- Microdialysis was employed to collect extracellular fluid from the frontal cortex.
- Concentrations of aspartic and glutamic acids were measured using high-performance liquid chromatography with a fluorescence detector.
- Sympathetic nerve firing rate and tissue temperatures (colonic and brown adipose tissue) were monitored before and after intracerebroventricular prostaglandin E1 or saline injection.
Main Results:
- Intracerebroventricular prostaglandin E1 administration led to a significant increase in frontal cortical concentrations of aspartic acid and glutamic acid.
- Prostaglandin E1 also elevated sympathetic nerve firing rate and both colonic and interscapular brown adipose tissue temperatures.
- Saline injection did not produce these effects, indicating prostaglandin E1 specificity.
Conclusions:
- Intracerebroventricular prostaglandin E1 induces hyperthermia, at least in part, through the release of aspartic acid and glutamic acid in the frontal cerebral cortex.
- These excitatory amino acids likely play a crucial role in mediating the sympathetic nervous system's response to prostaglandin E1 during hyperthermia.