Tuberous Sclerosis Complex (TSC) is a multisystem genetic disorder caused by 
mutation in either Tsc1 or Tsc2 genes that leads to the hyper activation of the 
mTOR pathway, a key signalling pathway for synaptic plasticity. TSC is 
characterized by benign tumors arising in different organs and severe 
neuropsychiatric symptoms, such as epilepsy, intellectual disability, autism, 
anxiety and depressive behaviour. Rapamycin is a potent inhibitor of mTOR and 
its efficacy in treating epilepsy and neurological symptoms remains elusive. In 
a mouse model in which Tsc1 has been deleted in embryonic telencephalic neural 
stem cells, we analyzed anxiety- and depression-like behaviour by elevated-plus 
maze (EPM), open-field test (OFT), forced-swim test (FST) and tail-suspension 
test (TST), after chronic administration of rapamycin. In addition, spectral 
analysis of background EEG was performed. Rapamycin-treated mutant mice 
displayed a reduction in anxiety- and depression-like phenotype, as shown by the 
EPM/OFT and FST, respectively. These results were inline with EEG power spectra 
outcomes. The same effects of rapamycin were observed in wild-type mice. 
Notably, in heterozygous animals we did not observe any EEG and/or behavioural 
variation after rapamycin treatment. Together these results suggest that both 
TSC1 deletion and chronic rapamycin treatment might have a role in modulating 
behaviour and brain activity, and point out to the potential usefulness of 
background EEG analysis in tracking brain dysfunction in parallel with 
behavioural testing.