It is suggested that the mechanism involved in physostigmine management of early alcohol withdrawal may lie in physostigmine induced beta-endorphin release.
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http://dx.doi.org/10.1016/0306-9877(89)90067-4 | DOI Listing |
ACS Omega
September 2024
Department of Pharmaceutical Engineering & Technology, Indian Institute of Technology (B.H.U.), Varanasi 221005, Uttar Pradesh, India.
Despite the advent of new treatment strategies, cholinesterase inhibitors (ChEIs) are still the go-to treatment for dementia disorders. ChEIs act by inhibiting the main acetylcholine-degrading enzyme, acetylcholinesterase (AChE). Nonetheless, accumulating evidence indicates that the impact of inhibition of the sister enzyme, butyrylcholinesterase (BChE), could be even broader in older adults due to the multifaceted role of BChE in several biological functional pathways.
View Article and Find Full Text PDFClin Toxicol (Phila)
July 2024
MN Regional Poison Center, Minneapolis, Minnesota, USA.
Introduction: Physostigmine is an effective antidote for antimuscarinic delirium. There is little evidence for its use to reverse delirium following second generation antipsychotic exposure. The purpose of this study is to describe the safety and effectiveness of physostigmine in reversing delirium from second generation antipsychotic exposure.
View Article and Find Full Text PDFAm J Ther
July 2024
Division of Medical Toxicology, Emergency Departement, Virginia Commonwealth University, Richmond, VA.
Background: Flumazenil is a competitive benzodiazepine (BZD) antagonist most used for treating delirium in BZD overdoses. Since its introduction, many have expressed concerns about its safety secondary to the risk of inducing BZD withdrawal and refractory seizures.
Study Question: What is the incidence of adverse drug events after the administration of flumazenil in patients with suspected iatrogenic BZD delirium?
Study Design: This is a retrospective cross-sectional study of patients from a single center from 2010 to 2013.
Neuropsychopharmacology
November 2024
Department of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN, 37240, USA.
Prevailing hypotheses on the mechanisms of antidepressant action posit that antidepressants directly counteract deficiencies in major neurotransmitter signaling systems that underlie depression. The rapidly acting antidepressant ketamine has been postulated to correct excess glutamatergic signaling via glutamatergic antagonism leading to the rescue of neuronal structural deficits and reversal of behavioral symptoms. We studied this premise using systemic administration of the acetylcholinesterase inhibitor physostigmine, which has been shown to rapidly elicit a shorter-term period of depressed mood in humans via cholinergic mechanisms.
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