Takeaway: In line with recent publications of others, these null results further challenge core assumptions about cTBS. They also highlight the importance of reporting negative findings, especially in NHP work.

📄 Read the full paper here: tinyurl.com/cTBSPFCNHP
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Despite some evidence of cTBS impacting neural activity, those effects didn’t translate into expected inhibition/disinhibition patterns - or behavior. We discuss possible reasons for this: task sensitivity, protocol choices, and the challenge of probing timescale network effects in PFC.

Contralateral neural spiking: we found no evidence for disinhibition in left PFC after cTBS to the right PFC. Effects were minimal and no stronger than after SHAM or M1 stimulation.

Error rates: No reliable differences after cTBS-PFC vs. cTBS-SHAM / M1
RTs: No consistent effects on general RT distribution, RT trends over time, or within session change
Peak velocity: Only small effects, but not specific to cTBS-PFC.

In 80 daily sessions, we looked for changes in behavior (saccade RT, error rates, peak velocity) as well as spiking in contralateral PFC.
TLDR: we found no clear behavioral or neural evidence that cTBS-PFC caused inhibition or disinhibition.

We tested a key assumption in TMS research: cTBS inhibits the targeted area and disinhibits its contralateral homologue. We had two 🐒 perform a pro/anti-saccade task and applied cTBS to right PFC, M1, or as a SHAM control and recorded spiking activity in the left PFC before and after.