Recent advances, comparative performance, and data requirements of artificial intelligence-assisted technologies for the diagnosis of gastric cancer.
Authors: Zhang Z, Liu Z, Zhang X, Lv K, Huang Y, Zheng C, He T
Journal: Frontiers in gastroenterology (Lausanne, Switzerland)
depression treatment
mental health
open access
Abstract
Ketamine (CHClNO) is a phencyclidine-derived
dissociative anesthetic composed of two enantiomers, -ketamine (KS) and -ketamine (KR). These molecules
differ markedly in their pharmacodynamic properties, with KS exhibiting
greater affinity as a noncompetitive antagonist of -methyl--aspartate (NMDA) receptorsparticularly
those presynaptically located on glutamatergic neuronsresulting
in higher anesthetic potency compared with KR. Clinically, KS is widely
employed in human surgical and critical care settings, whereas the
racemic formulation (KSR) remains the most commonly used preparation
in medical and veterinary procedures requiring anesthesia, analgesia,
or rapid dissociation. Beyond its anesthetic properties, ketamine
modulates multiple neural
systems, notably by increasing dopaminergic transmission in the mesolimbic
pathway through NMDA receptor blockade. This inhibition can disinhibit
glutamatergic circuits and enhance activation of non-NMDA receptors
such as AMPA and kainate, consequently amplifying dopamine release
in regions such as the nucleus accumbens. At higher doses,
however, widespread glutamatergic inhibition may paradoxically reduce
dopaminergic output, producing a state of functional hypoactivity. Ketamine’s neuropharmacological complexity extends to its
effects on cortical dynamics. Studies have shown that ketamine disrupts
NMDA- and AMPA-mediated connectivity in frontoparietal networks, alters high-frequency EEG patterns in humans, and contributes to neurobiological mechanisms
relevant to rapid-acting antidepressant responses. These actions may vary substantially between enantiomers,
as suggested by evidence of differential neuroprotective outcomes and distinct behavioral or neurochemical responses
associated with each compound.
dissociative anesthetic composed of two enantiomers, -ketamine (KS) and -ketamine (KR). These molecules
differ markedly in their pharmacodynamic properties, with KS exhibiting
greater affinity as a noncompetitive antagonist of -methyl--aspartate (NMDA) receptorsparticularly
those presynaptically located on glutamatergic neuronsresulting
in higher anesthetic potency compared with KR. Clinically, KS is widely
employed in human surgical and critical care settings, whereas the
racemic formulation (KSR) remains the most commonly used preparation
in medical and veterinary procedures requiring anesthesia, analgesia,
or rapid dissociation. Beyond its anesthetic properties, ketamine
modulates multiple neural
systems, notably by increasing dopaminergic transmission in the mesolimbic
pathway through NMDA receptor blockade. This inhibition can disinhibit
glutamatergic circuits and enhance activation of non-NMDA receptors
such as AMPA and kainate, consequently amplifying dopamine release
in regions such as the nucleus accumbens. At higher doses,
however, widespread glutamatergic inhibition may paradoxically reduce
dopaminergic output, producing a state of functional hypoactivity. Ketamine’s neuropharmacological complexity extends to its
effects on cortical dynamics. Studies have shown that ketamine disrupts
NMDA- and AMPA-mediated connectivity in frontoparietal networks, alters high-frequency EEG patterns in humans, and contributes to neurobiological mechanisms
relevant to rapid-acting antidepressant responses. These actions may vary substantially between enantiomers,
as suggested by evidence of differential neuroprotective outcomes and distinct behavioral or neurochemical responses
associated with each compound.