Open AccessInducible expression of neuronal glutamate receptor channels in the NT2 human cell line.
Author(s) -
Donald P. Younkin,
ChaMin Tang,
Marcia Hardy,
Usha R. Reddy,
Qing Shi,
Samuel J. Pleasure,
Virginia M.Y. Lee,
David Pleasure
Publication year - 1993
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.90.6.2174
Subject(s) - glutamate receptor , nmda receptor , neuroscience , biology , neurotransmission , microbiology and biotechnology , patch clamp , nervous system , excitatory postsynaptic potential , neuroblast , synaptic plasticity , neuron , neurotoxicity , metabotropic glutamate receptor , central nervous system , neurotoxin , receptor , chemistry , electrophysiology , biochemistry , neurogenesis , inhibitory postsynaptic potential , organic chemistry , toxicity
Glutamate receptor (GluR) channels are responsible for a number of fundamental properties of the mammalian central nervous system, including nearly all excitatory synaptic transmission, synaptic plasticity, and excitotoxin-mediated neuronal death. Although many human and rodent neuroblast cell lines are available, none has been directly shown to express GluR channels. We report here that cells from the human teratocarcinoma line NT2 are induced by retinoic acid to express neuronal N-methyl-D-aspartate (NMDA) and non-NMDA GluR channels concomitant with their terminal differentiation into neuron-like cells. The molecular and physiologic characteristics of these human GluR channels are nearly identical to those in central nervous system neurons, as demonstrated by PCR and patch clamp recordings, and the cells demonstrate glutamate-induced neurotoxicity.