@article {Gao1200, author = {Feng Gao and Shuang Wang and Chunlei Zhao and Hongwei Zhan and Hong Zhang}, title = {Anterior thalamic nucleus stimulation modulates regional cerebral metabolism: A FDG-MicroPET study in rats}, volume = {50}, number = {supplement 2}, pages = {1200--1200}, year = {2009}, publisher = {Society of Nuclear Medicine}, abstract = {1200 Objectives The mechanism underlying the antiepileptic function of deep brain stimulation (DBS) of the anterior thalamic nucleus (ATN) remains unknown. Experimental studies revealed that DBS of the ATN has a similar anticonvulsant action with ATN lesions. We investigated the effects of the DBS or lesioning of ATN on regional cerebral metabolism (rCMR) with FDG-MicroPET. Methods A baseline scan was obtained before the animals were treated by DBS(n=8) or chemical lesioning induced by ibotenic acid (n=8). The second scan was taken when the rats were subjected to high frequency stimulation of the ATN bilaterally or one week after the lesioning surgery. A third scan was taken one week after the second scan to observe the recovery of rCMR. The PET and MRI images were co-registered using ASIPro VM. The rCMR in each region of interest was normalized by division with the global metabolic rate of glucose of the entire brain. Results Bilateral ATN stimulation reversibly increased glucose uptake in the target region (15.2 \%), the thalamus(9.1 \%) and hippocampus(16.9 \%), and decreased glucose uptake in the cingulate cortex(11.0 \% )and frontal cortex(12.0 \%). However, bilateral ATN lesioning decreased glucose uptake only in the target region(13.6 \%). Animals with bilateral ATN lesions showed no metabolic changes after ATN stimulation. Conclusions DBS of the ATN induces metabolic activation of the target area and selectively modulates energy metabolism in several structures crucial for seizure generation. This process occurs through efferent or afferent fibers from the target via a different mechanism than ATN lesioning.}, issn = {0161-5505}, URL = {https://jnm.snmjournals.org/content/50/supplement_2/1200}, eprint = {https://jnm.snmjournals.org/content}, journal = {Journal of Nuclear Medicine} }