N-methyl D-aspartate receptors (NMDARs) are ionotropic glutamate receptors highly abundant in the brain and present in the lung, kidneys, red blood cells and in the heart of a variety of species including humans. Upon stimulation with glutamate and glycine these non-selective ion channels mediate calcium uptake and depolarize the membrane, both processes having crucial impact on heart function. Channels are hetero-tetramers consisting of glutamate-binding (NR2A,B,C or D) and glycine-binding (NR1, 3A and 3B) subunits. Subunit composition defines the agonist-, antagonist and ion permeability preferences, amplitude and deactivation time of the receptors. In rat heart NR2D and NR3A expression was recently shown to dominate. In human heart only NR1 was reported to be expressed so far. In this study we have explored the expression pattern of all known NMDAR subunits in four chambers of human heart and performed co-variance analysis of the transcript levels relating them to the loss of cardiac rhythmicity and hypertrophic remodeling.
N-methyl D-aspartate receptor in human heart function
Kosenkov, Dmitry;TESSARI, Maddalena;FAGGIAN, Giuseppe
2014-01-01
Abstract
N-methyl D-aspartate receptors (NMDARs) are ionotropic glutamate receptors highly abundant in the brain and present in the lung, kidneys, red blood cells and in the heart of a variety of species including humans. Upon stimulation with glutamate and glycine these non-selective ion channels mediate calcium uptake and depolarize the membrane, both processes having crucial impact on heart function. Channels are hetero-tetramers consisting of glutamate-binding (NR2A,B,C or D) and glycine-binding (NR1, 3A and 3B) subunits. Subunit composition defines the agonist-, antagonist and ion permeability preferences, amplitude and deactivation time of the receptors. In rat heart NR2D and NR3A expression was recently shown to dominate. In human heart only NR1 was reported to be expressed so far. In this study we have explored the expression pattern of all known NMDAR subunits in four chambers of human heart and performed co-variance analysis of the transcript levels relating them to the loss of cardiac rhythmicity and hypertrophic remodeling.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.