The learning chemical, glutamate, is released at neuronal synapses, where it activates neurons by binding to ion channel receptors. Glutamate is also abundant in the blood—particularly in clot-forming platelets—but its function outside the brain was unknown.
Morrell et al. now find that glutamate increases platelet activation and clumping. Glutamate treatment increased the expression of clot-inducing adhesion molecules on platelets that were activated with thrombin—a blood enzyme that becomes activated during infection or injury. The platelets carried glutamate receptors, which flood the cell with sodium ions when stimulated. Sodium triggers a structural change in thrombin receptors, which might enhance their affinity for thrombin. Mice lacking glutamate receptors and those treated with drugs that block them were slow to form clots.
The authors speculate that, like neurons, activated platelets form synapses with neighboring platelets into which they spew glutamate. The high glutamate concentration within these spaces might keep the cells stuck together and further enlarge the clot by snaring more platelets, which then add to the glutamate pool. Drugs that block glutamate receptors might be potentially useful in preventing stroke, heart attacks, and other diseases that can be triggered by clots.