J. Biol. Chem., Vol. 259, Issue 20, 12763-12768, 10, 1984
Agonists and cations regulate the glutamic acid receptors on intact neuroblastoma hybrid cells
AT Malouf, JT Coyle and RL Schnaar
Glutamate is thought to be a major excitatory neurotransmitter in the
vertebrate brain. In the preceding paper (Malouf, A. T., Schnaar, R. L.,
and Coyle, J. T. (1984) J. Biol. Chem. 259, 12756-12762), we demonstrated
specific binding of [3H]glutamate to membranes from a neuroblastoma hybrid
cell line, N18-RE-105. These sites are pharmacologically and kinetically
similar to those seen on rat brain membranes and are regulated by ions
added to the isolated membranes. In the current paper, we describe an
additional level of regulation for the glutamate receptor in this cell
line. Long-term incubation (72 h) of intact N18-RE-105 cells with glutamate
(10 mM) results in a 2- to 3- fold increase in [3H]glutamate binding.
Scatchard analysis reveals that the increase in binding is due to an
increase in the number of glutamate receptors without significant change in
their affinity. The ability of glutamate analogs to induce such
up-regulation mirrors their ability to compete for [3H]glutamate binding to
isolated membranes, suggesting that up-regulation is receptor-mediated.
Binding of [3H]glutamate to membranes isolated from cells grown in the
presence of glutamate can be further up-regulated by brief exposure (10
min) of the isolated membranes to calcium ions. This suggests that
agonist-induced and calcium-induced up-regulation occur via independent
mechanisms. The short-term ion-induced up-regulation and the long-term
agonist-induced up-regulation described in this paper may model two levels
of synaptic potentiation reported to occur in the vertebrate hippocampus.
The N18- RE-105 cell line may offer a homogeneous cell type in which to
study the molecular mechanisms underlying these phenomena.
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