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The effects of ion channel blockers validate the conductance‐based model of saccadic oscillations
Author(s) -
Shaikh Aasef G.,
Zee David S.,
Optican Lance M.,
Miura Kenichiro,
Ramat Stefano,
Leigh R. John
Publication year - 2011
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2011.06130.x
Subject(s) - saccadic masking , ethosuximide , oscillation (cell signaling) , amplitude , conductance , propranolol , physics , chemistry , neuroscience , medicine , eye movement , psychology , optics , biochemistry , condensed matter physics , epilepsy , phenytoin
Conductance‐based models of reciprocally inhibiting burst neurons suggest that intrinsic membrane properties and postinhibitory rebound (PIR) determine the amplitude and frequency of saccadic oscillations. Reduction of the low‐threshold calcium currents ( I T ) in the model decreased the amplitude but increased the frequency of the simulated oscillations. Combined reduction of hyperpolarization‐activated cation current ( I h ) and I T in the model abolished the simulated oscillations. We measured the effects of a selective blocker of I T (ethosuximide) in healthy subjects on the amplitude and frequency of saccadic oscillations evoked by eye closure and of a nonselective blocker of I h and I T (propronolol) in a patient with microsaccadic oscillation and limb tremor syndrome (mSOLT). Ethosuximide significantly reduced the amplitude but increased the frequency of the saccadic oscillations during eye closure in healthy subjects. Propranolol abolished saccadic oscillations in the mSOLT patient. These results support the hypothetical role of postinhibitory rebound, I h , and I T , in generation of saccadic oscillations and determining their kinematic properties.