Membrane channel properties of premotor excitatory burst neurons may underlie saccade slowing after lesions of omnipause neurons

Journal of Computational Neuroscience

Volumn 20, Issue 1, 2006, Pages 25-41

  Miura, Kenichiro ^a   Optican, Lance M ^b  

^a KYOTO UNIVERSITY GRADUATE SCHOOL OF MEDICINE   (Japan)

^b NATIONAL EYE INSTITUTE   (United States)

Author keywords

Eye movements; Glutamate; Glycine; Hodgkin Huxley; Model; NMDA receptors; Raphe interpositus nucleus; RIP; Saccades

Indexed keywords

BRAIN; EYE MOVEMENTS; NEURONS;

'CURRENT; BRAIN STEM; CHANNEL PROPERTY; GLUTAMATE; HODGKIN-HUXLEY; MEMBRANE CHANNELS; NMDA RECEPTOR; RAPHE INTERPOSITUS NUCLEUS; RIP; SIMULATION STUDIES;

AMINO ACIDS;

CALCIUM CHANNEL T TYPE; GLYCINE; GLYCINE RECEPTOR; N METHYL DEXTRO ASPARTIC ACID;

ARTICLE; CELL ACTIVITY; CONTROLLED STUDY; LATENT PERIOD; MATHEMATICAL MODEL; MEMBRANE CHANNEL; MEMBRANE CURRENT; NERVE CELL; NERVE CELL MEMBRANE; NERVE CONDUCTION; NERVE LESION; NEUROTRANSMISSION; PATHOPHYSIOLOGY; PRIORITY JOURNAL; SACCADIC EYE MOVEMENT; SIMULATION;

EID: 33646114749     PISSN: 09295313     EISSN: None     Source Type: Journal    
DOI: 10.1007/s10827-006-4258-y     Document Type: Article

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