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J Physiol Volume 563, Number 3, 777-793, March 15, 2005 DOI: 10.1113/jphysiol.2004.080655
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Reduced glycine transporter type 1 expression leads to major changes in glutamatergic neurotransmission of CA1 hippocampal neurones in mice

Marzia Martina1,2, Marie-Eve B.-Turcotte1,2, Samantha Halman1,2, Guochuan Tsai3, Mario Tiberi1,2, Joseph T Coyle3 and Richard Bergeron1,2

1 Departments of Cellular and Molecular Medicine, and Psychiatry, University of Ottawa, Ottawa, ON, Canada
2 Ottawa Health Research Institute, 725 Parkdale Avenue, Ottawa, ON, K1Y 4E9, Canada
3 Harvard Medical School, McLean Hospital, 115 Mills Street, Belmont, MA 02478, USA

To investigate the effects of persistent elevation of synaptic glycine at Schaffer collateral–CA1 synapses of the hippocampus, we studied the glutamatergic synaptic transmission in acute brain slices from mice with reduced expression of glycine transporter type 1 (GlyT1+/–) as compared to wild type (WT) littermates using whole-cell patch-clamp recordings of CA1 pyramidal cells. We observed faster decay kinetics, reduced ifenprodil sensitivity and increased zinc-induced antagonism in N-methyl-D-aspartate receptor (NMDAR) currents of GlyT1+/– mice. Moreover, the ratio {alpha}-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor (AMPAR)/NMDAR was decreased in mutants compared to WT. Surprisingly, this change was associated with a reduction in the number of AMPARs expressed at the CA1 synapses in the mutants compared to WT. Overall, these findings highlight the importance of GlyT1 in regulating glutamatergic neurotransmission.

(Received 6 December 2004; accepted after revision 17 January 2005; first published online 20 January 2005)
Corresponding author M. Martina: Ottawa Health Research Institute, 725 Parkdale Avenue, Ottawa, Ontario, Canada K1Y 4E9. Email:mmartina{at}ohri.ca




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