Synaptic transmission depressed by colchicine blockade of axoplasmic flow.
Colchicine, which inhibits axoplasmic transport and induces organelle alterations in nerve terminals, was injected intraocularly in pigeons. Electrical stimulation of the optic nerve yielded normal evoked potentials in retinotectal fibers, whereas postsynaptic responses recorded in the tectum were reduced. Postsynaptic depression suggests a deficit of synaptic transmission, presumably dependent on colchicine interference with migrating material.
D000818:Animals; D001369:Axons / Q000187:drug effects*; D001693:Biological Transport, Active / Q000187:drug effects; D003078:Colchicine / Q000494:pharmacology*; D010856:Columbidae; D003593:Cytoplasm / Q000187:drug effects*; D004558:Electric Stimulation; D004594:Electrophysiology; D005071:Evoked Potentials; D008636:Mesencephalon / Q000502:physiology; D008722:Methods; D009411:Nerve Endings / Q000187:drug effects; D009900:Optic Nerve; D012160:Retina / Q000502:physiology; D013569:Synapses / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects*; D013572:Synaptic Vesicles / Q000187:drug effects
D003078:Colchicine