Abstract
N-Methyl-D-aspartate (NMDA) subtype of glutamate receptors is expressed in the human lungs and central nervous system. NMDA receptor potentiation could increase calcium ion influx and promote downstream signaling mechanisms associated with cellular contractions that are disrupted in severe acute respiratory syndrome. Pharmacological effects generated by triggering glutamate receptor function in the brain, coupled with concurrent stimulation of the respiratory tract, may produce a synergetic effect, improving the airway smooth muscle function. A novel multipronged intervention to simultaneously potentiate NMDA receptors expressed both in the central nervous system and airway muscles would be helpful for the treatment of severe acute respiratory syndrome that deteriorates peripheral and central nervous system function before causing death in humans.
Highlights
N-Methyl-D-aspartate (NMDA) subtype of glutamate receptors is expressed in the human lungs and central nervous system
The N-methyl-D-aspartate (NMDA) receptor is a major subtype of glutamate receptors, which are predominantly expressed throughout the nervous system and in all vital organs in the human body.[1]
These findings indicate that NMDA receptors could control the respiratory tract function in vertebrate animals.[23]
Summary
An increasing body of evidence suggests the expression of functional NMDA receptors in the lungs and their critical role in glutamate induced acute lung injury and acute respiratory distress syndrome.[4,13,14,17,18,19,20] Despite its direct role in lung injury, little effort has been taken to develop NMDA receptor based therapeutic strategies for the treatment of lung diseases.
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