Fig. 2
From: Role of spinal astrocytes through the perisynaptic astrocytic process in pathological pain
PAPs as physical barrier keeping glutamates and K+ in synaptic cleft at pathological state of pain. A, In the basal state, glutamate aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1), which are specifically expressed in astrocytes, clear the excessive glutamates remained in the synaptic cleft. After being transported into astrocytes, glutamates are converted into glutamines by glutamine synthetase (GS). In addition, astrocytes maintain the homeostasis of K+ concentration in extracellular space through a specific K+ channel, Kir4.1. The glial coverage and the regulated mechanism make synaptic transmission accurate. B, In the pathological pain states, the expression of GLAST, GLT-1, and Kir4.1 is decreased, while the PAP’s encapsulation remains stable. These changes lead to the accumulation of glutamates and K+ ions in the synaptic cleft. Consequently, postsynaptic membranes become more excitable and transfer the pain signal abnormally