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Melissa officinalis (Lemon balm) mechanism of action


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#1 rautavaara

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Posted 01 March 2010 - 07:47 PM


I recently stumbled over this article that identifies the mechanism of action of Melissa officinalis (Lemon balm). It turns out that it is an inhibitor of GABA transaminase, an enzyme that breaks down GABA. This means that it has a mechanism of action that is generally comparable to what MAOIs are doing for monoamines and acetylcholinesterase inhibitors are doing for acetylcholine. I thought that this might be of interest to this community.

Bioassay-guided fractionation of lemon balm (Melissa officinalis L.) using an in vitro measure of GABA transaminase activity.

Awad R, Muhammad A, Durst T, Trudeau VL, Arnason JT.

A novel pharmacological mechanism of action for the anxiolytic botanical Melissa officinalis L. (lemon balm) is reported. The methanol extract was identified as a potent in vitro inhibitor of rat brain GABA transaminase (GABA-T), an enzyme target in the therapy of anxiety, epilepsy and related neurological disorders. Bioassay-guided fractionation led to the identification and isolation of rosmarinic acid (RA) and the triterpenoids, ursolic acid (UA) and oleanolic acid (OA) as active principles. Phytochemical characterization of the crude extract determined RA as the major compound responsible for activity (40% inhibition at 100 microg/mL) since it represented approximately 1.5% of the dry mass of the leaves. Synergistic effects may also play a role.


http://www.ncbi.nlm....pubmed/19165747
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#2 Johann

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Posted 02 March 2010 - 06:34 PM

Thank you. That is of interest to me. Do you use Lemon balm? If so, what type
of prepartation? Tea, capsule, etc?

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#3 KimberCT

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Posted 02 March 2010 - 07:05 PM

Definitely interesting. I suspected that valerian extracts were GABA-T inhibitors, but I never even looked at Lemon Balm.

#4 rautavaara

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Posted 02 March 2010 - 07:53 PM

Thank you. That is of interest to me. Do you use Lemon balm? If so, what type
of prepartation? Tea, capsule, etc?


I occasionally use tea in the evening. A tea made from two tea bags can have quite noticable calming effects. ever tried any other form or higher doses so far. I might try a higher dose for the sake of experimentation, it seems to be quite safe.

#5 pinnacle

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Posted 24 April 2010 - 03:00 AM

Would a pure Rosmarinic Acid extract such as the one from LEF have a more pronounced effect on inhibition of GABA-T, rather than a general Lemon Balm extract?

Edited by pinnacle, 24 April 2010 - 03:00 AM.


#6 nito

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Posted 24 April 2010 - 03:37 AM

i have these tablets called kalms sothing lozenges with Lemon Balm. I have tried a few of them and i think it kinda make me feel a bit more mellow initially. But over time it has been harder to get those effects again.

#7 pinnacle

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Posted 24 April 2010 - 04:12 AM

Great cheers for your reply! Based on that study showing Rosmarinic Acid (RA) being the major compound in Lemon Balm responsible for inhibiting GABA-T, I think I'll try a pure RA extract and report back if there's any worthwhile therapeutic effects.

#8 Animal

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Posted 24 April 2010 - 11:44 AM

GABA Transaminase isn't the only enzyme involved in the breakdown of GABA, that is why Lemon Balm is only a mild anxiolytic.

#9 KimberCT

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Posted 24 April 2010 - 04:08 PM

GABA Transaminase isn't the only enzyme involved in the breakdown of GABA, that is why Lemon Balm is only a mild anxiolytic.


What are the others?

#10 LabRat84

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Posted 24 April 2010 - 04:17 PM

GABA Transaminase isn't the only enzyme involved in the breakdown of GABA, that is why Lemon Balm is only a mild anxiolytic.


What are the others?

Yes, I'd like to know as well. If you're right, my chart will need updating. I couldn't find any other enzymes.

If by "involved in" you mean the entire catabolic pathway, I guess you're right - the enzymes that break down glutamate are also "involved in" the breakdown of GABA. This Wikipedia illustration is pretty good.

#11 chrono

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Posted 24 April 2010 - 08:54 PM

Inhibition of TBPS binding probably also plays a role in its anxiolysis:

Pharmacological profile of an essential oil derived from Melissa officinalis with anti-agitation properties: focus on ligand-gated channels.

A dual radioligand binding and electrophysiological study, focusing on a range of ligand-gated ion channels, was performed with a chemically-validated essential oil derived from Melissa officinalis (MO), which has shown clinical benefit in treating agitation. MO inhibited binding of [35S] t-butylbicyclophosphorothionate (TBPS) to the rat forebrain gamma-aminobutyric acid (GABA)(A) receptor channel (apparent IC50 0.040+/-0.001 mg mL(-1)), but had no effect on N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropianate (AMPA) or nicotinic acetylcholine receptors. Electrophysiological analyses with primary cultures of rat cortical neurons demonstrated that MO reversibly inhibited GABA-induced currents in a concentration-dependent manner (0.01-1 mg mL(-1)), whereas no inhibition of NMDA- or AMPA-induced currents was noted. Interestingly, MO elicited a significant dose-dependent reduction in both inhibitory and excitatory transmission, with a net depressant effect on neurotransmission (in contrast to the classical GABA(A) antagonist picrotoxinin which evoked profound epileptiform burst firing in these cells). The anti-agitation effects in patients and the depressant effects of MO in in-vitro we report in neural membranes are unlikely to reflect a sedative interaction with any of the ionotropic receptors examined here.


On the importance of TBPS:

"35S-TBPS binding is a sensitive index of the function of the GABAergic synapses. Since TBPS inhibits the GABAergic neurotransmission by a direct blockage of the GABA-gated chloride channels, the inhibition of 35S-TBPS binding to the chloride channel by these anxiolytic drugs implies an increased ability to generate chloride current, resulting in enhanced function of the GABAergic synapses." [Anxiety: psychobiological and clinical perspectives]

I'm a little confused by the results (italicized) concerning inhibition of GABA-induced currents at certain doses. From what I can tell, most anxiolytics enhance the Cl current. Does this imply that part of MO's MOA is having an effect detrimental to GABA enhancement (though the net effect is still depressant)? And might this be the reason it's only a "weak" anxiolytic?

Also of note is that MO exhibits radical-scavenging properties (19760174).

Edited by chrono, 25 September 2010 - 10:32 AM.
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#12 KimberCT

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Posted 26 April 2010 - 12:13 PM

Sounds right... very interesting. I wonder if this means that Lemon Balm has the potential for long term anxiolytic use without the development of tolerance... or possibly may improve GABA-a sensitivity in the long run?

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#13 psych0therapist

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Posted 29 July 2021 - 12:39 AM

Old thread, but I’ve been on regular BZD sleeping medication (various, both commonly known and esoteric, such as Clomethiazole for instance) and always take a strong Lemon-Balm tablet with my pam’s/lam’s.

It’s been several years, but my meds still help me sleep, and with proper supplementation, my sleep quality’s actually pretty good. Long-term use is discouraged but YOLO as the kids say these days; all to say that something as benign as Lemon Balm’s seemed to help me for 4+ years of nightly use.




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