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Decrease in glutamic acid decarboxylase level in the hypothalamus of spontaneously hypertensive rats

E M Horn1, C A Shonis, M A Holzwarth

  • 1Department of Molecular and Integrative Physiology, College of Medicine, University of Illinois, Urbana 61801, USA.

Journal of Hypertension
|October 31, 1998
PubMed
Summary
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Spontaneously hypertensive rats have fewer GABA-synthesizing neurons and less GAD67 mRNA in the caudal hypothalamus. This deficit in the GABAergic system may contribute to their essential hypertension.

Area of Science:

  • Neuroscience
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Reduced gamma-aminobutyric (GABA)-mediated inhibition in the caudal hypothalamus of spontaneously hypertensive rats (SHR) compared to Wistar-Kyoto rats (WKY) has been observed.
  • The caudal hypothalamus is a critical site for cardiovascular regulation.

Purpose of the Study:

  • To investigate if reduced GABAergic inhibition in SHR is due to fewer GABA-synthesizing neurons.
  • To determine if reduced GABAergic inhibition in SHR is due to lower levels of glutamic acid decarboxylase (GAD67) messenger RNA (mRNA).

Main Methods:

  • Immunocytochemistry using an antibody against GAD67 was employed to label GABAergic neurons in the caudal hypothalamus of SHR and WKY rats.
  • GAD67 mRNA levels in the caudal hypothalamus were quantified using Northern blotting.

Related Experiment Videos

  • Blinded cell counting and densitometric analysis of Northern blots were performed for quantitative comparisons.

    • Main Results:

    • SHR exhibited a 42% reduction in GAD67-immunoreactive neurons in the caudal hypothalamus compared to WKY rats.
    • A 33% decrease in GAD67 mRNA levels was found in the caudal hypothalamus of SHR relative to WKY rats.
    • No significant differences in GAD67 expression were observed in control brain regions (cortex, midbrain, cerebellum, brain stem).

    Conclusions:

    • SHR possess fewer GABA-synthesizing neurons and lower GAD67 mRNA in the caudal hypothalamus than WKY rats.
    • This deficiency in the GABAergic system within the caudal hypothalamus may be a contributing factor to the development of essential hypertension in SHR.
    • The findings highlight a potential molecular mechanism underlying hypertension in this animal model.