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This suggests that DCS treatment facilitated fear memory recall at test.
Similarly, we demonstrated facilitated fear conditioning in Y1 receptor KO mice, suggesting that NPY inhibits fear conditioning by acting on postsynaptic Y1 receptors.
Furthermore, central oxytocin administration in rats 10 minutes prior to fear conditioning did not affect fear conditioning, but did subsequently decrease fear expression and facilitated fear extinction [ 54].
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Some studies suggest that DCS may not only augment extinction learning but could also facilitate fear memory reconsolidation.
These data suggest that dexamethasone may serve as a pharmacological agent with which to facilitate fear extinction and discrimination in individuals with PTSD.
Translational research suggests that D-cycloserine (DCS), a partial N-methyl-D-aspartate (NMDA) receptor agonist, might facilitate fear extinction and exposure therapy by either enhancing NMDA receptor function during extinction or by reducing NMDA receptor function during fear memory consolidation.
Conditioned fear responses can be depressed by two approaches: facilitating fear extinction [6] or inhibiting fear reconsolidation [7], [8], [9].
Thus, any intervention facilitating fear extinction or disrupting fear memory may have a therapeutic value on PTSD.
Enhanced emotional memory may be stimulated through elevated noradrenaline levels, and data suggest that yohimbine hydrochloride, a noradrenaline agonist, can facilitate fear extinction.
The neurotransmitter dopamine is an important modulator of LA activity and facilitates fear memory formation, but whether dopamine neurons aid in the establishment of discriminative fear coding by the LA is unknown.
Given that impairment of fear extinction has been implicated in the pathogenesis of posttraumatic stress disorder (PTSD), effective pharmacological interventions that facilitate fear extinction may provide alternative strategies to conventional treatment.
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