Differential Regulation of Glucose Concentrations in the Precuneus by Glutamate and γ-Aminobutyric Acid

Thursday, October 11, 2012 — Poster Session III
10:00 a.m. – Noon	Natcher Conference Center, Building 45	NIA	IMAG-31

Authors

• AA Willette
• D Reiner
• M Mattson
• D Kapogiannis

Abstract

BACKGROUND: Dysregulation of glucose metabolism, as well as changes in excitatory and inhibitory signaling, occurs in aging and neurodegenerative disorders. Cortical glutamatergic and γ-Aminobutyric Acid (GABA) signaling consume 82% and 18% respectively of the energy derived from glucose metabolism. Yet, it is not known how glutamate and GABA concentrations relate to regional glucose concentration. We investigated the association between neurotransmitter and glucose concentrations in the precuneus, an age-sensitive area with strong glutamatergic and GABAergic signaling. Neuronal density, accounted for by N-acetyl-aspartate (NAA), and age were also considered. METHODS: In 22 healthy male volunteers aged 24-75 years, two-dimensional Magnetic Resonance Spectroscopy (MRS) quantified glutamate, GABA, NAA, and glucose in precuneus. RESULTS: In a linear regression model, glucose concentrations were collectively modulated by glutamate (β=-0.499, p=.027), GABA (β=0.496, p=.021), and NAA (β=0.708, p=.002), but not age (β=.015, p=.943). Increased age was correlated with increased GABA (r=.455, p =.033). CONCLUSIONS: Increased neural density may result in more glucose being recruited to a cortical region. Glutamate and GABA modulate glucose concentrations in a roughly equal manner. We speculate that increased glutamatergic signaling results in a greater portion of recruited glucose being consumed and lowering the glucose concentration, whereas GABA exerts the opposite effect.

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