Effective spread and timecourse of neural inactivation caused by lidocaine injection in monkey cerebral cortex.

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We studied the effective spread of lidocaine to inactivate neural tissue in the frontal cortex of the rhesus monkey. Injections of 2% lidocaine at 4 microl/min were made while units were recorded 1 or 2 mm away. To inactivate units 1 mm away from the injection site 100% of the time, 7 microl of lidocaine had to be injected. To inactivate units 2 mm away from the injection site 100% of the time, 30 microl of lidocaine were required. Units were maximally inactivated around 8 min after the start of a lidocaine injection, and they gradually recovered, regaining most of their initial activity by around 30 min after the start of an injection. The volume of lidocaine required to inactivate neurons > 90% of the time could be estimated by the spherical volume equation, V = 4/3 pi (r)3. To prolong the inactivation, a slower infusion of lidocaine subsequent to an initial bolus was effective. Saline control injections had no effect. These results allow both a prediction of the timecourse of neural inactivation and an estimate of the spread of neural inactivation following injection of lidocaine into the monkey cerebral cortex.







Marc A. Sommer

Professor of Biomedical Engineering

We study circuits for cognition. Using a combination of neurophysiology and biomedical engineering, we focus on the interaction between brain areas during visual perception, decision-making, and motor planning. Specific projects include the role of frontal cortex in metacognition, the role of cerebellar-frontal circuits in action timing, the neural basis of "good enough" decision-making (satisficing), and the neural mechanisms of transcranial magnetic stimulation (TMS).

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