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Dehydration increases sodium-dependent glutamate uptake by hypothalamic paraventricular nucleus synaptosomes
Thomas S King1, Glenn M Toney, Pei-Yu Tian
1Department of Cellular and Structural Biology, The University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229-3900, USA. kingt@uthscsa.edu
Neuro Endocrinology Letters
|January 31, 2012
Summary
Water deprivation significantly increases glutamate transporter (GLUT) activity in rat hypothalamic paraventricular nucleus (PVN) synaptosomes. This enhanced glutamate uptake may help regulate body fluid balance and cardiovascular function during dehydration.
Area of Science:
- Neuroscience
- Physiology
- Molecular Biology
Background:
- The hypothalamic paraventricular nucleus (PVN) plays a critical role in regulating body fluid homeostasis and cardiovascular function.
- Glutamate transporters (GLUT) are essential for neurotransmission and maintaining extracellular glutamate concentrations.
Purpose of the Study:
- To identify and characterize Na+-dependent, high-affinity glutamate transporter (GLUT) activity in the rat PVN.
- To compare GLUT activity in the PVN of euhydrated versus water-deprived rats.
Main Methods:
- Synaptosomes were prepared from the PVN of Sprague-Dawley rats subjected to either water ad libitum (control) or water deprivation for two days.
- Glutamate uptake was measured using [3H]-glutamate as a substrate in prepared synaptosomes.
Main Results:
- Glutamate uptake in PVN synaptosomes was saturable in both groups.
- Vmax of glutamate uptake was significantly higher (p<0.001) in water-deprived rats (808 ± 58 pmol/min-mg protein) compared to controls (541 ± 22 pmol/min-mg protein).
- The Km for glutamate uptake was not significantly different between the groups.
Conclusions:
- Water deprivation leads to a significant increase in synaptosomal glutamate uptake in the rat PVN.
- This enhanced uptake may involve increased GLUT gene transcription or cell surface expression.
- Increased glutamate uptake in the PVN may modulate dehydration-induced activation of neurohypophysial hormone release and sympathetic outflow.
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