Glutamic acid binding in goldfish brain and denervated optic tectum.
The binding of L-glutamic acid to goldfish brain membranes and changes in tectal binding following optic nerve denervation and regeneration were investigated. Saturable, reversible, and specific binding occurred to sodium-free washed membranes from goldfish brain at a single population of sites having an apparent Kd of 3.4 microM and a capacity of 10 pM/mg original tissue. Binding was enriched in crude synaptosomal (P2) subcellular fractions. There was a 10-fold regional variation in the concentration of binding sites. In pharmacological studies protection constants (Kp) (the concentration which resulted in a 50% inhibition of binding) ranged from 4 microM for glutamate to greater than 10 mM for GABA. Following eye removal, the total number of tectal glutamic acid binding sites was stable for 4 days, followed by a rapid loss in binding, reaching 40% of control at 24 days. After optic nerve crush and optic nerve regeneration, the number and concentration of binding sites was not different from control. The relationship between glutamate, nicotinic, and muscarinic receptor sites in the retinotectal pathway is discussed.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D003714:Denervation; D005971:Glutamates / Q000378:metabolism*; D006054:Goldfish; D009409:Nerve Crush; D009416:Nerve Regeneration; D009900:Optic Nerve / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000378:metabolism*; D017470:Receptors, Glutamate; D013116:Spinal Cord / Q000378:metabolism; D013477:Superior Colliculi / Q000378:metabolism*; D013570:Synaptic Membranes / Q000378:metabolism; D009435:Synaptic Transmission; D014795:Visual Pathways / Q000378:metabolism
D005971:Glutamates; D011956:Receptors, Cell Surface; D017470:Receptors, Glutamate