Inhibition of succinate dehydrogenase (SDH) by the mitochondrial toxin 3‐nitropropionic acid (3‐NP) has gained acceptance as an animal model of Huntington's disease. In this study ¹³C NMR spectroscopy was used to measure the tricarboxylic acid (TCA) cycle rate in the rat brain after 3‐NP treatment. The time course of both glutamate C4 and C3 ¹³C labelling was monitored in vivo during an infusion of [1‐¹³C]glucose. Data were fitted by a mathematical model to yield the TCA cycle rate (V_tca) and the exchange rate between α‐ketoglutarate and glutamate (V_x). 3‐NP treatment induced a 18% decrease in V_tca from 0.71 ± 0.02 µmol/g/min in the control group to 0.58 ± 0.02 µmol/g/min in the 3‐NP group (p < 0.001). V_x increased from 0.88 ± 0.08 µmol/g/min in the control group to 1.33 ± 0.24 µmol/g/min in the 3‐NP group (p < 0.07). Fitting the C4 glutamate time course alone under the assumption that V_x is much higher than V_tca yielded V_tca=0.43 µmol/g/min in both groups. These results suggest that both V_tca and V_x are altered during 3‐NP treatment, and that both glutamate C4 and C3 labelling time courses are necessary to obtain a reliable measurement of V_tca.