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

The macaque frontal eye field (FEF) is involved in the generation of saccadic eye movements and fixations. To better understand the role of the FEF, we reversibly inactivated a portion of it while a monkey made saccades and fixations in response to visual stimuli. Lidocaine was infused into a FEF and neural inactivation was monitored with a nearby microelectrode. We used two saccadic tasks. In the delay task, a target was presented and then extinguished, but the monkey was not allowed to make a saccade to its location until a cue to move was given. In the step task, the monkey was allowed to look at a target as soon as it appeared. During FEF inactivation, monkeys were severely impaired at making saccades to locations of extinguished contralateral targets in the delay task. They were similarly impaired at making saccades to locations of contralateral targets in the step task if the target was flashed for ≤100 ms, such that it was gone before the saccade was initiated. Deficits included increases in saccadic latency, increases in saccadic error, and increases in the frequency of trials in which a saccade was not made. We varied the initial fixation location and found that the impairment specifically affected contraversive saccades rather than affecting all saccades made into head-centered contralateral space. Monkeys were impaired only slightly at making saccades to contralateral targets in the step task if the target duration was 1000 ms, such that the target was present during the saccade: latency increased, but increases in saccadic error were mild and increases in the frequency of trials in which a saccade was not made were insignificant. During FEF inactivation there usually was a direct correlation between the latency and the error of saccades made in response to contralateral targets. In the delay task, FEF inactivation increased the frequency of making premature saccades to ipsilateral targets. FEF inactivation had inconsistent and mild effects on saccadic peak velocity. FEF inactivation caused impairments in the ability to fixate lights steadily in contralateral space. FEF inactivation always caused an ipsiversive deviation of the eyes in darkness. In summary, our results suggest that the FEF plays major roles in (1) generating contraversive saccades to locations of extinguished or flashed targets, (2) maintaining contralateral fixations, and (3) suppressing inappropriate ipsiversive saccades.

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“…This has been shown to inactivate units 1.5 mm away, i.e., at the recording electrode, with nearly 100% certainty (Tehovnik and Sommer, 1997).…”

Section: Infusion Methodsmentioning

confidence: 98%

Reversible inactivation of macaque frontal eye field

1997

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“…We previously have described the infusion methods (Sommer and Tehovnik 1997) and quantified the time course and spread of cortical inactivation subsequent to lidocaine infusion (Tehovnik and Sommer 1997a). In summary, a 30-gauge needle was attached to a stainless-steel cannula that was connected to a 100-µl Hamilton syringe using PE 50 tubing.…”

Section: Infusion Methodsmentioning

confidence: 99%

“…A hydraulic microdrive held the needle assembly, loaded with lidocaine or saline, in parallel with a recording microelectrode (Pt-Ir, glass-coated, ~1.0 MΩ at 1 kHz), so that the needle and microelectrode moved in concert through the dura, into the brain, with their tips 1.5 mm apart. We infused 18 µl of lidocaine or saline at 4 µl/min; this volume and rate of lidocaine infusion causes short-term neural inactivation (usually for less than 40 min) 1.5 mm from the needle tip, i.e., at the microelectrode, nearly 100% of the time (Tehovnik and Sommer 1997a). Equivalent volumes and rates of saline infusion have no detectable neural effects (Tehovnik and Sommer 1997a).…”

Section: Infusion Methodsmentioning

confidence: 99%

“…We infused 18 µl of lidocaine or saline at 4 µl/min; this volume and rate of lidocaine infusion causes short-term neural inactivation (usually for less than 40 min) 1.5 mm from the needle tip, i.e., at the microelectrode, nearly 100% of the time (Tehovnik and Sommer 1997a). Equivalent volumes and rates of saline infusion have no detectable neural effects (Tehovnik and Sommer 1997a).…”

Section: Infusion Methodsmentioning

confidence: 99%

“…We think this possibility is remote because we studied an extensive range of the DMFC (Fig. 1A, B) and each infusion was relatively large, inactivating neurons at least 1.5 mm from the needle tip (Tehovnik and Sommer 1997a). Also, when we inactivated the same or adjacent DMFC sites during the double-step task (Fig.…”

Section: Dmfc Activity and The Generation Of Saccades And Fixationsmentioning

confidence: 97%

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Reversible inactivation of macaque dorsomedial frontal cortex: effects on saccades and fixations

Sommer

Tehovnik

1999

Experimental Brain Research

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Neural recording and electrical stimulation results suggest that the dorsomedial frontal cortex (DMFC) of macaque is involved in oculomotor behavior. We reversibly inactivated the DMFC using lidocaine and examined how saccadic eye movements and fixations were affected. The inactivation methods and monkeys were the same as those used in a previous study of the frontal eye field (FEF), another frontal oculomotor region. In the first stage of the present study, monkeys performed tasks that required the generation of single saccades and fixations. During 15 DMFC inactivations, we found only mild, infrequent deficits. This contrasts with our prior finding that FEF inactivation causes severe, reliable deficits in performance of these tasks. In the second stage of the study, we investigated whether DMFC inactivation affected behavior when a monkey was required to make more than one saccade and fixation. We used a double-step task: two targets were flashed in rapid succession and the monkey had to make two saccades to foveate the target locations. In each of five experiments, DMFC inactivation caused a moderate, significant deficit. Both ipsi-and contraversive saccades were disrupted. In two experiments, the first saccades were made to the wrong place and had increased latencies. In one experiment, first saccades were unaffected, but second saccades were made to the wrong place and had increased latencies. In the remaining two experiments, specific reasons for the deficit were not detected. Saline infusions into DMFC had no effect. Inactivation of FEF caused a larger double-step deficit than did inactivation of DMFC. The FEF inactivation impaired contraversive first or second saccades of the sequence. In conclusion, our results suggest that the DMFC makes an important contribution to generating sequential saccades and fixations but not single saccades and fixations. Compared with the FEF, the DMFC has a weaker, less directional, more task-dependent oculomotor influence. Key words Saccadic eye movements · Fixations · Dorsomedial frontal cortex · Supplementary eye field · Frontal eye field · Reversible inactivation IntroductionThe oculomotor properties of cortex near the frontal midline of macaque were first examined in detail by Schlag and Schlag-Rey (1987). They named this region the supplementary eye field. We and others (Mann et al. 1988;Bon and Lucchetti 1992;Heinen 1995) use the anatomical designation, dorsomedial frontal cortex (DMFC) (issues of nomenclature are reviewed by Tehovnik 1995 andSchall 1997). Regardless of terminology, the areas near the frontal midline that have been studied by oculomotor physiologists overlap with one another (Fig. 1A; for a more detailed comparison see Tehovnik 1995). The experiments of this report were specifically carried out on the DMFC as mapped using electrical stimulation (Tehovnik and Lee 1993; see Fig. 1A); this defines an area that includes large portions of the regions examined by other investigators.In this report, we focus on the contribution of the macaque DMFC ...

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Post‐training reversible inactivation of hippocampus reveals interference between memory systems

2002

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A post-training reversible lesion technique was used to examine the effects of neural inactivation of the dorsal hippocampus on place and response learning. Male Long-Evans rats trained in one of two versions of a water plus-maze task received post-training intra-hippocampal infusions of the local anesthetic drug bupivacaine (0.75% solution, 0.5 microl), or saline. Post-training intra-hippocampal infusions of bupivacaine attenuated acquisition of the place task and enhanced acquisition of the response task. Delayed (2-h) post-training infusions of bupivacaine did not affect retention in either task. The findings demonstrate (1) enhanced learning after reversible hippocampal lesions that is independent of treatment influences on non-mnemonic factors, and (2) inactivation of the dorsal hippocampus during the post-training memory consolidation period is sufficient to enhance response learning.

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

Cited by 151 publications

References 17 publications

Reversible inactivation of macaque frontal eye field

Reversible inactivation of macaque frontal eye field

Reversible inactivation of macaque dorsomedial frontal cortex: effects on saccades and fixations

Post‐training reversible inactivation of hippocampus reveals interference between memory systems

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