Tranexamic acid impairs hippocampal synaptic transmission mediated by gamma aminobutyric acid receptor type A

Escape From Oblivion: Neural Mechanisms of Emergence From General Anesthesia

“…Further, pharmacological research focused on antagonizing GABA A Rs in ex vivo brain slice preparations may identify novel strategies for hastening emergence from general anesthesia. 146,147 Because the majority of anesthetics delivered in industrialized nations use GABAergic drugs, changes in electroencephalographic patterns (or increases in processed electroencephalographic measures of hypnosis) can be used to evaluate pharmacological mechanisms of emergence. Although many options exist for pharmacological antagonization of GABA A Rs, concern for seizure generation has understandably hindered research in this area.…”

G‐alpha interacting protein interacting protein, C terminus 1 regulates epileptogenesis by increasing the expression of metabotropic glutamate receptor 7

“…Numerous studies have shown that abnormal synaptic transmission is an important pathogenetic mechanism. [8][9][10] As a scaffolding protein, GIPC1 is relatively highly expressed in various normal tissues including brain tissue. 12 Since GIPC1 regulates the cell surface expression and endocytic trafficking of numerous transmembrane receptors and signaling complexes, 39 it plays an important role in synaptic transmission.…”

“…4 However, among these mechanisms, an imbalance between excitatory and inhibitory synaptic transmission is known as the common epileptogenic mechanism. [8][9][10] Therefore, further studies on the role of synaptic transmission in epileptogenesis are important to develop more effective epilepsy treatments.…”

The emerging role of tranexamic acid and its principal target, plasminogen, in skeletal health

“…Studies indicate that TXA acts as a competitive antagonist of Gly receptors 135 , 138 and NMDA receptors 115 in the CNS, which may contribute to the proconvulsant effects of TXA. The γ -aminobutyric acid type A (GABA A ) receptors 139 , another major inhibitory compound in the CNS, can also be blocked by TXA in seizure-prone CNS structures like the amygdala and the hippocampus 135 , 140 , 141 . Besides, α -amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors and kainate (KA) receptors, both belonging to the ionotropic glutamate receptor family along with NMDA receptors, have been reported to be inhibited by TXA as well.…”