Lead acutely reduces glucose utilization in the rat brain especially in higher auditory centers

The 2-deoxyglucose autoradiographic method was used to assess the effects of acute lead exposure on regional brain glucose metabolism in the rat. Eight male Long-Evans hooded rats weighing between 317 and 364 g were cannulated for access to the femoral artery and vein, then given an iv bolus of lead acetate (27 mg Pb/kg as 50 mg PbAc/kg) or saline and observed for the six hours prior to the start of the 2-deoxyglucose experiment. Under controlled conditions of light and sound, the rats were injected with ¹⁴C-2-deoxyglucose, then sacrificed after 45 min. The brains were frozen in isopentane cooled to -40°C and 20 μm sections were made. Every third slice was dried on glass slides and apposed to Kodak SB5 X-ray film for five days. Local cerebral metabolic rates (ICMRglu) were measured by densitometry with a computerized image analyzer. Four other rats were similarly given lead (but not 2-deoxyglucose), and blood samples taken at -1, 15, 30, 60, 120, and 360 min had corresponding lead levels of 1.8±1.4, 156±14.6, 182±20.4, 155±17.4, 134±12.5 and 36±2.3 ppm. Whole brain lead was 0.45±0.22 and 1.20±0.15 ppm in the control and lead-treated groups, respectively (p < 0.025). Significant reductions in ICMRglu occurred in the following structures: medial geniculate bodies (15.6 ± 2.5%), inferior colliculus (13.8 ± 4.6%), and sensory cortex (9.8 ± 1.8%). Among those structures showing the greatest percent reductions were several auditory centers, including lateral lemniscus (13.0 ± 4.6%), auditory cortex (10.4 ± 4.1%), and superior olivary complex (8.0 ± 7.0%). The auditory centers are known to be among the most metabolically active in the mammalian brain. Brain areas with the highest glucose metabolism, highest Na, K-ATPase activity and greatest synaptic densities may be especially vulnerable to the effects of lead.