Two Endocannabinoids Enhance Memory

“Both anandamide (AEA) and 2AG play roles in enhancing memory consolidation in the hippocampus. AEA via both CB1 and CB2R while 2AG activates CB2R signaling only.”

- Dr. David Hepburn

Abstract:

The endocannabinoid system is a key modulator of memory consolidation for aversive experiences.
The fatty acid amide hydrolase (FAAH) inhibitor URB597, which increases anandamide levels by inhibiting its hydrolysis, facilitates memory consolidation through a concurrent activation of both cannabinoid receptor type 1 (CB1) and 2 (CB2).

Read the full article here:

https://www.ncbi.nlm.nih.gov/pubmed/29842858

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Dr. Dave Hepburn website: https://doctordavidhepburn.com

Early Life Stress and the ECS

“Levels of eCBs (AEA and 2AG) and the entire ECS, in fact, change in the hippocampus (memory) amygdala (fear) and PFC (executive) after early life stress. These continue in some of these regions into adulthood. Collectively, these data demonstrate that early life stress can alter the normative development (ontogeny) of the eCB system, resulting in a sustained deficit in function, particularly within the hippocampus, in adulthood.”

- Dr. David Hepburn 

Abstract:

Early-life stress modulates the development of cortico-limbic circuits and increases vulnerability to adult psychopathology. Given the important stress-buffering role of endocannabinoid (eCB) signaling, this is a comprehensive investigation of the developmental trajectory of the eCB system and the impact of exposure to early life stress induced by repeated maternal separation (MS; 3 h/day) from postnatal day 2 (PND2) to PND12.

Read full article here:

https://www.ncbi.nlm.nih.gov/pubmed/30496752

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Dr. David Hepburn website: https://doctordavidhepburn.com

Cannabis helps Spasticity in Lou Gehrig’s (ALS) disease

“Add ALS spasticity to MS spasticity as targets for cannabis therapy. A recent Italian study showed those on low dose cannabis spraynotonly improved, but nobody discontinued due to side effects.”

-   Dr. David Hepburn

Abstract:

Spasticity is a major determinant of disability and decline in quality of life in patients with motor neuron disease. Cannabinoids have been approved for symptomatic treatment of spasticity in multiple sclerosis. It was investigated whether cannabinoids might also reduce spasticity in patients with motor neuron disease.

Researchers found in this proof-of-concept trial, nabiximols had a positive effect on spasticity symptoms in patients with motor neuron disease and had an acceptable safety and tolerability profile. These findings should be investigated further in larger clinical trials.

Read the full article here:

https://www.ncbi.nlm.nih.gov/pubmed/30554828

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Dr. Dave Hepburn website: https://doctordavidhepburn.com

Singing or Running Elevate Endocannabinoids and Boosts Mood - Dr. David Hepburn

Article Recommended by Dr. David Hepburn:

An Analysis of Endocannabinoid Concentrations and Mood Following Singing and Exercise in Healthy Volunteers

The euphoric feeling described after running is, at least in part, due to increased circulating endocannabinoids (eCBs). eCBs are lipid signaling molecules involved in reward, appetite, mood, memory and neuroprotection. 

The aim of this study was to investigate whether activities other than running can increase circulating eCBs. Nine healthy female volunteers (mean 61 years) were recruited from a local choir. Circulating eCBs, haemodynamics, mood and hunger ratings were measured before and immediately after 30 min of dance, reading, singing or cycling in a fasted state. 

Singing increased plasma levels of anandamide (AEA) by 42% (P < 0.05), palmitoylethanolamine (PEA) by 53% (P < 0.01) and oleoylethanolamine (OEA) by 34% (P < 0.05) and improved positive mood and emotions (P < 0.01), without affecting hunger scores. 

Dancing did not affect eCB levels or hunger ratings, but decreased negative mood and emotions (P < 0.01). 

Cycling increased OEA levels by 26% (P < 0.05) and tended to decrease how hungry volunteers felt, without affecting mood. 

"The “runners high” which was thought years ago to be courtesy of our endorphins is now known to be caused by our endogenous cannabinoid, anandamide (AEA). While dancing and cycling did not elevate AEA, singing actually did. No comments on if you sound like a hound being dragged through a keyhole. Anybody interested in starting a jogging choir to get high?  
Increases in AEA underlies the rewarding and pleasurable effects of singing and exercise and ultimately some of the long-term beneficial effects on mental health, cognition and memory."

-Dr. Dave Hepburn

To read the full article please visit:

https://www.frontiersin.org/articles/10.3389/fnbeh.2018.00269/full

Dr. Dave Hepburn website:https://doctordavidhepburn.com

Cannabinoid Receptor Protects Against Hearing Loss Caused by Chemotherapy - Dr. David Hepburn

Article recommend by Dr. David Hepburn:

The Endocannabinoid/Cannabinoid Receptor 2 System Protects Against Cisplatin-Induced Hearing Loss

Abstract

Previous studies have demonstrated the presence of cannabinoid 2 receptor (CB2R) in the rat cochlea which was induced by cisplatin. In an organ of Corti-derived cell culture model, it was also shown that an agonist of the CB2R protected these cells against cisplatin-induced apoptosis. In the current study, we determined the distribution of CB2R in the mouse and rat cochleae and examined whether these receptors provide protection against cisplatin-induced hearing loss. In a knock-in mouse model expressing the CB2R tagged with green fluorescent protein, we show distribution of CB2R in the organ of Corti, stria vascularis, spiral ligament and spiral ganglion cells. A similar distribution of CB2R was observed in the rat cochlea using a polyclonal antibody against CB2R. Trans-tympanic administration of (2-methyl-1-propyl-1H-indol-3-yl)-1-naphthalenylmethanone (JWH015), a selective agonist of the CB2R, protected against cisplatin-induced hearing loss which was reversed by blockade of this receptor with 6-iodo-2-methyl-1-[2-(4-morpholinyl)ethyl]-1H-indol-3-yl](4-methoxyphenyl)methanone (AM630), an antagonist of CB2R. JWH015 also reduced the loss of outer hair cells (OHCs) in the organ of Corti, loss of inner hair cell (IHC) ribbon synapses and loss of Na+/K+-ATPase immunoreactivity in the stria vascularis. Administration of AM630 alone produced significant hearing loss (measured by auditory brainstem responses) which was not associated with loss of OHCs, but led to reductions in the levels of IHC ribbon synapses and strial Na+/K+-ATPase immunoreactivity. Furthermore, knock-down of CB2R by trans-tympanic administration of siRNA sensitized the cochlea to cisplatin-induced hearing loss at the low and middle frequencies. Hearing loss induced by cisplatin and AM630 in the rat was associated with increased expression of genes for oxidative stress and inflammatory proteins in the rat cochlea. In vitro studies indicate that JWH015 did not alter cisplatin-induced killing of cancer cells suggesting this agent could be safely used during cisplatin chemotherapy. These data unmask a protective role of the cochlear endocannabinoid/CB2R system which appears tonically active under normal conditions to preserve normal hearing. However, an exogenous agonist is needed to boost the activity of endocannabinoid/CB2R system for protection against a more traumatic cochlear insult, as observed with cisplatin administration.

“One of the several possible nasty side effects of a common anticancer medication, is hearing loss. Activation of CB2R appears to prevent this, indicating an important role of the ECS (endocannabinoid system) in neuroprotection."

Dr. David Hepburn

To read the full article please visit:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6110918/

Dr. David Hepburn website:
doctordavidhepburn.com