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This important study \citep{25199956} follows up on the autopsy results from the Vaccarino lab by comparing RNA transcripts from the basal ganglia of 9 TS and 9 matched control subjects. The most strongly associated set of downregulated transcripts involved striatal interneurons, consistent with the autopsy studies. The leading set of upregulated transcripts involved immune-related genes even though none of the TS subjects met the diagnostic criteria for pediatric autoimmune streptococcal-associated neuropsychiatric disorders or pediatric acute onset neuropsychiatric syndrome. There was a lack of overlap between the results obtained in the present study using brain tissue and previous studies using blood samples. The authors conclude that their results "strongly [implicate] disrupted interneuron signaling in the pathophysiology of severe TS and suggests that metabolic alterations may be linked to their death or dysfunction."  The GAGA-A GABA-A  antagonist picrotoxin was injected into targets throughout corticostriatal regions in adult mice \cite{25597650}. Infusions into the central and dorsolateral striatum produced intermittent non-rhythmic stereotyped lifting of the front or hind paw or head jerks. Infusions into the dorsomedial striatum did not have a significant behavioral effect. Infusion into the ventral striaum produced locomotor activation with sterotypical sniffing and wall licking. Infusions into the sensorimotor cortex produced similar movements in addition to exploration of the cage. sniffing and occasional licking. When an NMDA receptor antagonist was infused into the dorsolateral striatum prior to infusing picrotoxin into the same location, tic frequency decreased significantly thus demonstrating the role of glutamateric activity in tic generation. Infusion of a GABA-A antagonist into the sensorimotor cortex 10 minutes before picrotoxin infusion into the dorsolateral striatum also resulted in significant tic suppression.EEG recordings allowed experimenters to determine whether the infusions were causing seizures or not. The interpretation of these results was that the tic-like movements were generated from enhanced striatal responsivity to afferent glutamatergic synaptic input rather than to autonomous striatal activity. The brain circuits underlying tics were studied using the first genetically engineered mouse model of TS+OCD ("Ticcy" D1CT-7) transgenic mice   \cite{26453289}. This  ### Neuroimaging and electrophysiology studies