Pax's Biomarker Technology Suggests a Different Site of Action for "Rapid Acting Antidepressant" Ketamine

		 Mark Mitchell Rasenick
title: 	  	Distinguished University Professor
department: 	  	Physiology and Biophysics, Department of
address: 	  	2095 COMRB, MC 901
phone: 	  	312-996-6641
fax: 	  	312-996-1414
netid: 	  	raz

Ketamine acts within hours to ameliorate depression for some. This common drug of abuse is generally thought to work by blocking a receptor for the excitatory neurotransmitter, glutamate.

A recent study by Rasenick and colleagues, using Pax Biomarker technology, was published in the Nature journal, "Molecular Psychiatry." The paper reveals that one mechanism of ketamine action is independent of the NMDA receptor.

Curiously, ketamine elicits the same actions as any other antidepressant observed with MoodMark™ R&D, but rather than 3 days of incubation, the "rapid acting" ketamine required only 15 minutes.

Breakthrough study finds new mechanism explaining ketamine's antidepressant effects.

A team at the University of Illinois at Chicago has uncovered a new mechanism that helps explain the remarkably rapid, and long-lasting, antidepressant effects of the controversial drug ketamine. The exciting research reveals the drug operates in a similar way to conventional SSRI antidepressants, except is it significantly more effective.


For decades, there has been a growing body of anecdotal evidence suggesting ketamine has extraordinarily rapid antidepressant effects. Originally developed as an anesthetic, before moving into recreational circles due to its psychedelic and dissociative qualities, the drug is now being seriously investigated for its uniquely novel effects on the brain.


Mark Rasenick and his team at the University of Illinois at Chicago College of Medicine initially started their research by investigating the neurological mechanisms behind SSRI drugs, the most common antidepressant medication. The research revealed that patients with depression have larger volumes of G proteins held inactive in "lipid rafts" on cell membranes in the brain. These G proteins are vital in helping nerve cells signal effectively and suppressing their activity could lead to many hallmark symptoms of depression


Read the original article at New Atlas, and the new research published in the journal Molecular Psychiatry.

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