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Senior Investigator

Lance M. Optican, Ph.D.

Laaboratory of Sensorimotor Research
Building 49 Room 2A50
49 Convent Drive MSC4435
Bethesda MD 20892-4435
Office: (301) 496-3549

Fax: (301) 402-0511

Dr. Optican received a B.S. degree in Physics & Biosystems Analysis from the California Institute of Technology in 1972. He received his Ph.D. degree in Biomedical Engineering in 1978 from the Johns Hopkins School of Medicine, where he worked with David A. Robinson studying the cerebellar-dependent adaptive control of rapid eye movements (saccades). Dr. Optican obtained postdoctoral training with F.A. Miles at the NIMH, studying visually induced adaptive control of saccades. Since 1982, Dr. Optican has been a Research Biomedical Engineer in the NEI and in 1988 was appointed Chief of the Section on Neural Modeling within the Laboratory of Sensorimotor Research. His laboratory explores how the brain converts visual information into rapid eye movements.

Brain functions arise through the complex interactions of many neurons. During behavior, neurophysiological techniques can observe the responses of some neurons, but they cannot reveal directly the nature of their functional interactions. The Neural Modeling Section was established to provide insight into the nature of neuronal interactions underlying motor behavior through theoretical and mathematical modeling. Without good models, it is impossible to explain what signals are intrinsic to the brain, what behaviors to expect, or how to interpret the effects of brain lesions. My goal is to construct and test models of sensory and motor functions that are based on experimental observations.

The most extensive use of this approach has been to describe the neuronal properties of the saccadic system. Saccades are the rapid, voluntary movements that redirect our gaze. The movement is controlled by neurons in several areas of the neocortex (e.g., LIP, FEF), by brain stem neurons (e.g., pre-motor burst neurons and motor neurons), and by two specialized structures (the Superior Colliculus and the cerebellum). Our neuromimetic model reproduces most features of visually guided saccadic behavior, with only known cell types and with the correct time course of activity. This lets us learn a great deal about how the brain actually performs movements.

Neuromimetic Saccade Model

Schematic Diagram of the Neuromimetic Saccade Model

Schematic diagram of the neuromimetic saccade model.

Visual input is relayed from the cerebral areas of the frontal eye fields (FEF) and lateral intraparietal cortex (LIP). The desired target (in retinotopic coordinates) goes to both the superior colliculus (SC) and the cerebellum (CB). There are three outputs from the SC. One relays information about the selected target to the CB. The second provides a veto signal to the brain stem omnipause neurons (OPNs), which gate the medium lead burst neurons (MLBNs) that drive the motor neurons of the eye (MNs). The third output is a retinal coordinate drive signal (RD), that starts the eye moving in the approximate direction of the target.

The CB also provides three outputs. One is an inhibitory signal that reduces the output of the SC during the saccade. The second is a pilot drive signal (PD) that steers the eye in the appropriate movement to acquire the desired target. The third output is a choke signal that cuts off the RD and PD drives to stop the saccade. Feedback goes from the MLBNs to the CB, completing the local feedback loop.
Staff Image
  • Pierre Daye, Ph.D.
    Postdoctoral Fellow

  • Christian Quaia, Ph.D.
    Staff Scientist

  • 1) Quaia C, Optican LM, Cumming BG (2013)
  • Terminator disparity contributes to stereo matching for eye movements and perception.
  • J. Neurosci, 33(48), 18867-18879
  • 2) Daye PM, Optican LM, Blohm G, Lefevre P. (2013)
  • Hierarchical control of two-dimensional gaze saccades
  • J. Comput Neurosci Sept 6, Epub ahead of print
  • 3) Daye PM, Optican LM, Blohm G, Lefevre P (2013)
  • Hierarchical control of two-dimensional gaze saccades.
  • J. Comput Neurosci, Epub
  • 4) Shaikh AG, Palla A, Marti S, Olasagasti I, Optican LM, Zee DS, Straumann D (2013)
  • Role of Cerebellum in Motion Perception and Vestibulo-ocular Reflex-Similarities and Disparities.
  • Cerebellum, 12(1), 97-107
  • 5) Daye PM, Monosov IE, Hikosaka O, Leopold DA, Optican LM (2013)
  • pyElectrode: an open-source tool using structural MRI for electrode positioning and neuron mapping.
  • J Neurosci Methods, 213(1), 123-31
  • 6) Quaia C, Optican LM, Cumming BG (2013)
  • Terminator disparity contributes to stereo matching for eye movements and perception.
  • J. Neurosci, 33(48), 18867-18879
  • 7) Shaikh AG, Optican LM, Zee DS (2013)
  • Membrane Mechanisms of Tremor., Chapter 2 in Mechanisms and Emerging Therapies in Tremor Disorders
  • G. Grimaldi and M. Manto (eds.)
  • 8) Quaia C, Sheliga BM, Optican LM, Cumming BG. (2013)
  • Temporal evolution of pattern disparity processing in humans.
  • J Neurosci, 33(8), 3465-76
  • 9) Daye PM, Optican LM, Roze E, Gaymard B, Pouget P (2013)
  • Neuromimetic model of saccades for localizing deficits in an atypical eye-movemnt pathology.
  • Journal of Translational Medicine, 11, 125
  • 10) Quaia C, Joiner WM, FitzGibbon EJ, Optican LM, Smith MA (2010)
  • Eye Movement sequence generation in humans: motor or goal updating?
  • Journal of Vision, 10(14):23, 1-31
  • 11) Shaikh AG, Wong AL, Optican LM, Miura K, Solomon D, Zee DS (2010)
  • Sustained eye closure slows saccades
  • Vision Research, 6(50), 1665-75
  • 12) Shaikh AG, Hong S, Liao Ke, Tian J, Solomon D, Zee DS, Leigh RJ, Optican LM. (2010)
  • Oculopalatal tremor explained by a model of inferior olivary hypertrophy and cerebellar plasticity.
  • Brain, 133, 923-940
  • 13) Quaia C., Ying H.S., Optican L.M (2009)
  • The viscoelastic properties of passive eye muscle in primates. II: testing the quasi-linear theory.
  • PLoS One, 4(8), e6480
  • 15) Quaia C., Ying H.S., Nichols A.M., Optican L.M (2009)
  • The viscoelastic properties of passive eye muscle in primates. I: static forces and step responses.
  • PLoS One, 4(4), e4850
  • 17) Shaikh A.G., Ramat S., Optican L.M., Miura K., Leigh R.J., Zee D.S. (2008)
  • Saccadic burst cell membrane dysfunction is responsible for saccadic oscillations.
  • J. Neuro-Ophthalmol, 18, No.4, 3299-336
  • 18) Quaia C, Lefèvre P, Optican LM (1999)
  • Model of the control of saccades by superior colliculus and cerebellum
  • J. Neurophysiol., 82, 999-1018
  • 19) Lefèvre P, Quaia C, Optican LM (1998)
  • Distributed model of control of saccades by superior colliculus and cerebellum
  • Neural Networks, 11, 1175-1190
  • 20) Quaia C and Optican LM (1998)
  • Commutative saccadic generator is sufficient to control a 3-D ocular plant with pulleys
  • J. Neurophysiol., 79, 3197-3215
  • 21) Quaia C and Optican LM (1997)
  • Model with distributed vectorial premotor bursters accounts for the component stretching of oblique saccades
  • J. Neurophysiol. , 778, 1120-1134
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