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L Escola

Publications and source records attributed to L Escola.

3 recordsLinked to original sources

Time predictability modulates pre-supplementary motor area neuronal activity.

Two monkeys were trained in a delayed sequential motor task in which the time interval between events and the delay duration were either fixed or variable. Single-unit neuronal activity was recorded in the pre-supplementary motor area (pre-SMA). During the delay, we observed a gradual increase in activity (build-up pattern) in the fixed but not in the variable condition. In the former but not in the latter, the monkey had the opportunity to estimate time duration. Consequently, the build-up pattern observed in the pre-SMA might represent the neuronal substrate of a time accumulator system proposed by previous authors on the basis of functional imaging data. Such a system could play a critical role in the working memory of temporal information.

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Disruption of information processing in the supplementary motor area of the MPTP-treated monkey: a clue to the pathophysiology of akinesia?

It has been suggested that the underactivity of mesial frontal structures induced by dopamine depletion could constitute one of the main substrates underlying akinesia in Parkinson's disease. Functional imaging and movement-related potential recordings indicate an implication of the frontal lobes in this pathological process, but the question has not yet been investigated at a cellular level using single unit recording. We therefore compared neuronal activity in both the presupplementary motor area (pre-SMA) and the supplementary motor area proper (SMAp) of the Macaca mulatta monkey during a delayed motor task, before and after MPTP treatment. In the pre-SMA, which receives strong inputs from the prefrontal cortex, the baseline firing frequency and the percentage of neurons responding to visual instruction cues decreased in lesioned monkeys. In the SMAp, which sends direct outputs to the primary motor cortex, not only was the response to visual cues impaired, but the percentage of SMAp neurons responding to intracortical microstimulation fell and the threshold of response rose. Neuronal activity after the Go signal diminished sharply in both structures in the symptomatic animal and the discharge pattern became more irregular; in the SMAp neuronal activity remained modified longer. Most of these changes could already be observed in the presymptomatic animal presenting no clinical signs of parkinsonism. These data would indicate that, at the moment when dopamine depletion has impaired the ability of cortical neurons to operate the focused selection of incoming information giving instructions for movement, pre-SMA and SMAp neurons are also in a state of severe hypoactivity. The conjunction of these phenomena could play a critical role in the genesis of akinesia.

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Neuronal activity in the monkey motor thalamus during bicuculline-induced dystonia.

Recent data suggest that a decreased basal ganglia output may occur in dystonia, resulting in an increased thalamic drive to the mesial premotor cortex. In a previous work we found that injection of the GABAA antagonist bicuculline into the rostral motor thalamus induced contralateral dystonic postures, whereas myoclonic jerks were frequent after injection into the caudal motor thalamus. In the present study, we performed electrophysiological recordings in the rostral and caudal parts of the ventrolateral thalamus of two cynomolgus monkeys before and after bicuculline injections or saline injections. Discharge frequencies of thalamic neurons were increased after bicuculline injections vs. controls. Their discharge pattern was more bursty in the caudal part in which bursts of neuronal activity were correlated with myoclonic jerks. After bicuculline injection, neurons responded more frequently and less selectively to passive limb movements in both parts of the motor thalamus. Conversely, the response to microstimulation increased after bicuculline injection, particularly in the caudal part. Our data show that acute bicuculline-induced dystonia is associated with a reversible overactivity and disorganization of neuronal activity in the motor thalamus. Such a phenomenon might induce an overspreading of cortical activity leading to dystonia. We postulate that the distinct clinical syndromes observed after bicuculline injections into the rostral and caudal motor thalamus are due to differences both in the neuronal circuitry within each thalamic nucleus and in segregated cortical projections.

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