Glutamate-containing dipeptides enhance specific binding at glutamate receptors and inhibit specific binding at kainate receptors in rat brain

Agonists, antagonists and modulators of excitatory amino acid receptors in the guinea‐pig myenteric plexus

“…However, after 3 h of superfusion of the preparation at a rate of The experiments shown in the figure were performed in preparations first exposed for at least 3h to a Mg2+-free Ringer solution and subsequently, for 30min, to the following Mg2 + concentrations. (0) (Zaczek et al, 1983;Ferkany et al, 1984), did not affect the spontaneous motility or the L-Glu (3 x 10-5M)-induced ileal contraction. On the other hand, the dipeptide aspartyl-glutamate was among the most active compounds tested (see Table 1).…”

Induction of glutamate binding sites in hippocampal membranes by transient exposure to high concentrations of glutamate or glutamate analogs

“…Experimentation with TG is subject to a possible error not encountered with glutamate induction: Whereas incomplete removal of glutamate during the wash procedure would lead to an apparent reduction of binding in the binding assay, residual TG might stimulate glutamate binding directly through its presence in the incubation. However, the amount of 1.1 f 0.7 nmol/mg protein (n = 6) of residual TG determined in washed membranes via separation on HPLC could give a concentration of about 0.22 KM free TG in the binding assay incubation, which is too far below the EC,, of 11 PM (Ferkany et al, 1984) to cause a significant binding increase. Moreover, the percentage increase in binding in TG-preincubated membranes was the same at protein concentrations ranging from 6.5 to 260 &ml; at the lowest protein concentration, free TG, as determined by HPLC, could maximally be 8 nM.…”

“…6, No. 2, Feb. 1986 Ferkany et al (1983Ferkany et al ( , 1984 have reported that several glutamyldipeptides increase [3H]glutamate binding when present in the binding incubation; they suggested that these peptides may control the number of available glutamate binding sites through a second, modulatory binding site. The use of a Cl--free buffer for their incubations suggested that TG regulated one of the Cl--independent glutamate binding sites, but we have found that binding increase in the presence of Cl-is much more pronounced than in its absence, and also that the pharmacological profile of [3H]glutamate binding in the presence of TG and Cl-strongly resembles that for Cl--dependent binding (not shown).…”