Kainate-induced lesion in the optic tectum: dependency upon optic nerve afferents or glutamate.
Kainic acid is known to induce characteristic lesions in neurons receiving an intact input with presumed glutamate-mediated neurotransmission. There are indications for glutamate as a transmitter of retinal afferent terminals in the pigeon optic tectum. After tectal injection of kainic acid (0.5-2.0 microgram in 0.5 microliter) the optic tectum was studied by light and electron microscopy and the following changes were observed: (a) within 1-48 h important neuropil vacuolization predominantly in lower part of layer 5. Such vacuoles were sometimes postsynaptic to identified retinal afferent terminals: (b) within 1 h to 21 days progressive neuronal cell loss throughout the tectal layers. These toxic effects were not observed 2-12 weeks after contralateral retinal ablation but could partially be restored by combined glutamate (0.2 mg) and kainate injection. Thus in the pigeon tectum, kainic acid neurotoxicity is dependent upon an intact retinal input, a finding consistent with a special role for glutamate - possibly as a transmitter - in retinal terminals.
D000818:Animals; D010856:Columbidae; D005971:Glutamates / Q000494:pharmacology / Q000502:physiology*; D007608:Kainic Acid / Q000633:toxicity*; D009410:Nerve Degeneration / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000648:ultrastructure; D009900:Optic Nerve / Q000502:physiology*; D011759:Pyrrolidines / Q000633:toxicity*; D012160:Retina / Q000502:physiology; D014793:Visual Cortex / Q000033:anatomy & histology / Q000187:drug effects*; D014795:Visual Pathways / Q000502:physiology
D005971:Glutamates; D011759:Pyrrolidines; D007608:Kainic Acid