Distance- and error-related discharge of cells in premotor cortex of rhesus monkeys

Flament, D.; Onstott, Donna; Fu, Qing Gong; Ebner, Timothy J.

doi:10.1016/0304-3940(93)90308-8

Cited by 8 publications

(2 citation statements)

References 23 publications

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“…1996; Shen & Alexander, 1997; Zhang et al . 1997), including the visuomotor errors and adaptation induced by a change in the gain of the movement/visual cursor relationship (Flament et al . 1993; Wise et al .…”

Section: Introductionmentioning

confidence: 99%

Increase in syntaxin 1B and glutamate release in mossy fibre terminals following induction of LTP in the dentate gyrus: a candidate molecular mechanism underlying transsynaptic plasticity

Helme‐Guizon¹,

Davis²,

Israël³

et al. 1998

Eur J of Neuroscience

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A growing body of evidence suggests that modulation of certain proteins of the exocytotic machinery is, in part, involved in the biochemical changes that underlie long-term synaptic plasticity. We have previously shown that the induction of long-term potentiation (LTP) at perforant path to dentate granule cell synapses in the rat hippocampus induces changes in the mRNA levels of syntaxin 1B and synapsin I, known to be involved in neurotransmitter release. Immunohistochemical staining suggested that concomitant changes in these proteins occurred at mossy fibre synapses, downstream of those synapses at which LTP was induced, leading us to postulate that such a mechanism might underlie a form of transsynaptic plasticity. Here we have used a specific mossy-fibre synaptosome preparation to quantify levels of proteins and measure, using a chemiluminescent glutamate assay, depolarization-induced glutamate release from these synaptosomes after induction of LTP in the dentate gyrus in vivo. We show that 5 h after the induction of LTP, there is an increase in the protein levels of syntaxin 1B and, although to a lesser extent, the synapsins I and II, associated with an increase in depolarization-induced release of glutamate within these terminals. Increases in both the protein levels and glutamate release were not observed when dentate gyrus LTP was blocked by an NMDA receptor antagonist. From these results we propose a molecular mechanism for the propagation of synaptic plasticity through hippocampal circuits.

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Section: Introductionmentioning

confidence: 99%

Increase in syntaxin 1B and glutamate release in mossy fibre terminals following induction of LTP in the dentate gyrus: a candidate molecular mechanism underlying transsynaptic plasticity

Helme‐Guizon¹,

Davis²,

Israël³

et al. 1998

Eur J of Neuroscience

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“…Current understanding of PMd function theorizes a fundamental role in the transformation of visual information into motor behaviour (Weinrich & Wise, 1982;Caminiti et al, 1991;Johnson et al, 1996;Wise et al, 1996). Consistent with this role, the discharge of PMd neurons is known to be strongly correlated with a spectrum of kinematic aspects of reaching movements, including movement direction, distance, target position and arm posture (Caminiti et al, 1991;Fu et al, 1993;Johnson et al, 1996;Scott et al, 1997) and is also modulated by visuospatial aspects of the task (di Pellegrino & Wise, 1993b;Johnson et al, 1996;Shen & Alexander, 1997;Zhang et al, 1997), including the visuomotor errors and adaptation induced by a change in the gain of the movement/visual cursor relationship (Flament et al, 1993;Wise et al, 1998). Since a system concerned with accuracy would be expected to be in¯uenced by visuospatial aspects of movements, it follows that the ®ring of PMd neurons may be modulated by the accuracy requirements of reaching movements.…”

Section: Introductionmentioning

confidence: 86%

Representation of accuracy in the dorsal premotor cortex

Gomez

Flament³

et al. 2000

Eur J of Neuroscience

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The endpoint accuracy of a reaching movement strongly affects kinematics, particularly during the final phases of movement. However, where and how accuracy is represented in the central nervous system remains unknown. In this study, the discharge of 150 neurons located primarily in the dorsal premotor cortex (PMd), were recorded from monkeys performing an instructed delay, centre-out reaching task in which movement direction and target size were systematically varied. Linear regression analyses were used to assess the dependence of movement kinematics and cell discharge on target direction, size and tangential velocity (i.e. speed). The speed and timing of the movement were dependent on both direction and target size. Initially direction was the dominant predictor whilst target size became more important as the hand reached the target. A temporal multiple linear regression analysis found significant correlations with target size in 99 of 150 cells. The discharge of 134 cells was directionally tuned and 83 cells modulated with mean speed. Significant correlations of discharge with target size occurred throughout the task as did correlations with direction. However, correlations with direction preferentially occurred early in the task, prior to movement onset, whilst correlations with target size tended to occur late, well after movement onset. This temporal dependency of the firing in relationship to target direction and size mirrored that observed for the kinematics. We conclude that the discharge of PMd cells is highly correlated with the accuracy requirement of the movement. The timing of the correlations suggest that accuracy information is available for the planning and for the on-line control of endpoint accuracy.

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