The ion channels activated by glutamate that are sensitive to N-methyl-Daspartate (NMDA) are designated NMDA Receptors (NMDAR). The NMDAR plays an essential role in memory, neuronal development and it has also been implicated in several disorders of the central nervous system including Alzheimers, epilepsy and ischemic neuronal cell death (Grosshans et al., 2002, Wenthold et al., 2003, Carroll and Zukin, 2002). There are a number of different splice variants of the NR1-Subunit (Foldes et al., 1994, Zukin and Bennett, 1995). Differential splicing of three exons in the NR1-Subunit generates up to eight NR1-Subunit splice variants and 7 of these have been identified in cDNA libraries. These exons encode a 21 amino acid N-terminal domain (N1) and adjacent sequences in the C-terminus (C1 and C2). Splicing out the C2 cassette eliminates the first stop codon and produces a new reading frame that generates a new sequence of 22 amino acids (C2). Considerable attention has been focused on the distribution and expression of these splice variants that may affect the functional properties and regulation of the NMDAR.
The ion channels activated by glutamate that are sensitive to N-methyl-Daspartate (NMDA) are designated NMDA Receptors (NMDAR). The NMDAR plays an essential role in memory, neuronal development and it has also been implicated in several disorders of the c
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