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Homeostasis: Publius’ Alcohol Political Cannabinoid Science

8/30/2014

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PictureThe Cannabis Papers by Publius (2011)







The Cannabis Papers: A citizen’s guide to cannabinoids (2011)

By Publius

 
Today’s science roundup looks at four articles on how the cannabinoid system (CS) modulates our health through homeostasis ~ including one on the de-homeostatic (harmful) effects caused by chronic alcohol use on one’s CS. The line-up links to 2014 PubMed articles discussing: heteromerization, chronic alcohol harms, sensory information salience and stress response attenuation.

 
I. Heteromerization (GPR55 and CB2) and the CS
“In HEK293 cells expressing GPR55 and cannabinoid CB2 R receptors, heteromers that are unique signaling units are formed. The signaling by agonists of either receptor is governed i) by the presence or absence of the partner receptors (with the consequent formation of heteromers) and ii) by the activation state of the partner receptor.”
Heteromerization of GPR55 and cannabinoid CB2 receptors modulates signaling.
Balenga NA, Martínez-Pinilla E, Kargl J, Schröder R, Peinhaupt M, Platzer W, Bálint Z, Zamarbide M, Dopeso-Reyes I, Ricobaraza A, Pérez-Ortiz JM, Kostenis E, Waldhoer M, Heinemann A, Franco R.
Br J Pharmacol. 2014 Jul 22. doi: 10.1111/bph.12850. [Epub ahead of print]
PMID: 25048571 [PubMed - as supplied by publisher]
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II. De-Homeostasis (Chronic Alcohol Use) and the CS
“Chronic use of alcohol is associated with structural and functional alterations in brain areas that subserve cognitive processes. Of particular importance is the prefrontal cortex (PFC) that is involved in higher order behaviors such as decision making, risk assessment and judgment. … Overall, these results suggest that ethanol's down-regulation of cannabinoid signaling results in altered network activity in the prefrontal cortex.”
Chronic ethanol alters network activity and endocannabinoid signaling in the prefrontal cortex.
Pava MJ, Woodward JJ.
Front Integr Neurosci. 2014 Jul 18;8:58. doi: 10.3389/fnint.2014.00058. eCollection 2014.
PMID: 25100953 [PubMed] Free Article
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III. Homeostasis (Sensory Information) and the CS
“Emerging evidence from both basic and clinical research demonstrates an important role for endocannabinoid (ECB) signaling in the processing of emotionally salient information, learning, and memory. Cannabinoid transmission within neural circuits involved in emotional processing has been shown to modulate the acquisition, recall, and extinction of emotionally salient memories and importantly, can strongly modulate the emotional salience of incoming sensory information.”
The role of cannabinoid transmission in emotional memory formation: implications for addiction and schizophrenia.
Tan H, Ahmad T, Loureiro M, Zunder J, Laviolette SR.
Front Psychiatry. 2014 Jun 30;5:73. doi: 10.3389/fpsyt.2014.00073. eCollection 2014. Review.
PMID: 25071606 [PubMed] Free PMC Article
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IV. Homeostasis (Stress Response) and the CS
“Endocannabinoids are produced on demand and function to attenuate many of the physiological effects of the stress response. The endocannabinoid system is made up of cannabinoid receptors, the fatty acid signaling molecules that bind to and activate these receptors, and the enzymes that synthesize and catabolize these endocannabinoid signaling molecules.”
The endocannabinoid system modulates stress, emotionality, and inflammation.
Crowe MS, Nass SR, Gabella KM, Kinsey SG.
Brain Behav Immun. 2014 Jun 19. pii: S0889-1591(14)00172-X. doi: 10.1016/j.bbi.2014.06.007. [Epub ahead of print] Review.
PMID: 24953427 [PubMed - as supplied by publisher]
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Brain Video:
Why Do Some People Become Alcoholics?

Posted by Bryan W. Brickner


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Alzheimer’s, Cancer and Homeostatic Cannabinoid Science

6/29/2014

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PictureThe Cannabis Papers by Publius (2011)








The Cannabis Papers: A citizen’s guide to cannabinoids (2011)
By Publius

The CS World Cup: Goaltender Edition

Today, tending to the goals of mediating Alzheimer’s and preventing carcinogenesis, Publius spotlights two June abstracts from PubMed on the homeostatic cannabinoid system (CS). For Alzheimer’s disease it is CS
modulation of cognitive decline; for preventing carcinogenesis the findings unveil a previously unknown CS signaling platform: CB2-GPR55 receptor heteromers.



I. CS Mediates Cognitive Decline In Alzheimer's Disease

Set: “It has been widely reported that β-amyloid peptide (Aβ) blocks long-term potentiation (LTP) of hippocampal synapses. Here, we show evidence that Aβ more potently blocks the potentiation of excitatory postsynaptic potential (EPSP)-spike coupling (E-S potentiation). This occurs, not by direct effect on excitatory synapses or postsynaptic neurons, but rather through an indirect mechanism: reduction of endocannabinoid-mediated peritetanic disinhibition.”

Setting: “During high-frequency (tetanic) stimulation, somatic synaptic inhibition is suppressed by endocannabinoids. We find that Aβ prevents this endocannabinoid-mediated disinhibition, thus leaving synaptic inhibition more intact during tetanic stimulation.”

Science: “This intact inhibition opposes the normal depolarization of hippocampal pyramidal neurons that occurs during tetanus, thus opposing the induction of synaptic plasticity. Thus, a pathway through which Aβ can act to modulate neural activity is identified, relevant to learning and memory and how it may mediate aspects of the cognitive decline seen in Alzheimer's disease.”
β-Amyloid Inhibits E-S Potentiation through Suppression of Cannabinoid Receptor 1-Dependent Synaptic Disinhibition.
Orr AL, Hanson JE, Li D, Klotz A, Wright S, Schenk D, Seubert P, Madison DV.
Neuron. 2014 Jun 18;82(6):1334-45. doi: 10.1016/j.neuron.2014.04.039.
PMID: 24945775 [PubMed - in process]
Related citations


II. CS Oncology Signaling Unveiled: Evidence of Previously Unknown Platforms

Set: “The G protein-coupled receptors CB2 (CB2R) and GPR55 are overexpressed in cancer cells and human tumors. As a modulation of GPR55 activity by cannabinoids has been suggested, we analyzed whether this receptor participates in cannabinoid effects on cancer cells.”

Setting: “Here, we show that CB2R and GPR55 form heteromers in cancer cells, that these structures possess unique signaling properties, and that modulation of these heteromers can modify the antitumoral activity of cannabinoids in vivo.”

Science: “These findings unveil the existence of previously unknown signaling platforms that help explain the complex behavior of cannabinoids and may constitute new targets for therapeutic intervention in oncology.”
Targeting CB2-GPR55 Receptor Heteromers Modulates Cancer Cell Signaling.
Moreno E, Andradas C, Medrano M, Caffarel MM, Pérez-Gómez E, Blasco-Benito S, Gómez-Cañas M, Pazos MR, Irving AJ, Lluís C, Canela EI, Fernández-Ruiz J, Guzmán M, McCormick PJ, Sánchez C.
J Biol Chem. 2014 Jun 18. pii: jbc.M114.561761. [Epub ahead of print]
PMID: 24942731 [PubMed - as supplied by publisher] Free Article
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Video: Homeostasis 1, Physiological Principles ~ Dr. John Campbell

Posted by Bryan W. Brickner

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Homeostatic Cannabinoid Science ~ Publius’ May Roundup

5/30/2014

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Picture
Astrocyte / Blood-Brain Barrier by Ben Brahim Mohammed

The Cannabis Papers: A citizen’s guide to cannabinoids (2011)
By Publius

Here are seven new 2014 findings on how the cannabinoid system (CS) modulates homeostasis and other systems in our bodies: the roundup links to recent PubMed articles on the urinary, neuroendocrine, digestive, central nervous and serotonin systems.

I. Urinary System (Kidney / Diabetes) and CS
“A functionally active endocannabinoid system is present within the kidney. The cannabinoid receptor type 2 (CB2) is expressed by both inflammatory cells and podocytes, and its activation has beneficial effects in experimental diabetic nephropathy. … Thus, CB2 deletion worsens diabetic nephropathy, independent of bone marrow-derived cells.”
Deficiency of cannabinoid receptor of type 2 worsens renal functional and structural abnormalities in streptozotocin-induced diabetic mice.
Barutta F, Grimaldi S, Franco I, Bellini S, Gambino R, Pinach S, Corbelli A, Bruno G, Rastaldi MP, Aveta T, Hirsch E, Di Marzo V, Gruden G.
Kidney Int. 2014 May 14. doi: 10.1038/ki.2014.165. [Epub ahead of print]
PMID: 24827776 [PubMed - as supplied by publisher]
Related citations

II. Neuroendocrine System (Skin) and CS
“Recent evidence has shown that the neuroendocrine regulation of human skin biology also extends to keratins, the major structural components of epithelial cells. For example, thyrotropin-releasing hormone, thyrotropin, opioids, prolactin, and cannabinoid receptor 1-ligands profoundly modulate human keratin gene and protein expression in human epidermis and/or hair follicle epithelium in situ.”
Harnessing neuroendocrine controls of keratin expression: A new therapeutic strategy for skin diseases?
Ramot Y, Paus R.
Bioessays. 2014 May 13. doi: 10.1002/bies.201400006. [Epub ahead of print]
PMID: 24823963 [PubMed - as supplied by publisher]
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III. Digestive System and CS
“Palmitoylethanolamide (PEA), a naturally-occurring acylethanolamide chemically related to the endocannabinoid anandamide, interacts with targets that have been identified in peripheral nerves controlling gastrointestinal motility, i.e. cannabinoid (CB1 and CB2 ) receptors, transient receptor potential vanilloid type-1 (TRPV1), and peroxisomal proliferator activated receptor α (PPARα).”
Ultramicronized palmitoylethanolamide normalizes intestinal motility in a murine model of post-inflammatory accelerated transit: involvement of CB1 receptors and TRPV1.
Capasso R, Orlando P, Pagano E, Aveta T, Buono L, Borrelli F, Di Marzo V, Izzo AA.
Br J Pharmacol. 2014 May 12. doi: 10.1111/bph.12759. [Epub ahead of print]
PMID: 24818658 [PubMed - as supplied by publisher]
Related citations

IV. Central Nervous System and CS
“G-protein-coupled receptors (GPCRs) constitute an example of proteins that are the key factors in the framework needed to sustain brain and nerve structure and function. The versatility underlying nervous system anatomy takes advantage of a recently discovered feature of GPCRs, the possibility to form heteromers that, placed at specific neuronal subsets and at specific locations (pre-, post-, or peri-synaptic), contribute to attain unique neural functions.”
G-Protein-Coupled Receptor Heteromers as Key Players in the Molecular Architecture of the Central Nervous System.
Brugarolas M, Navarro G, Martínez-Pinilla E, Angelats E, Casadó V, Lanciego JL, Franco R.
CNS Neurosci Ther. 2014 May 9. doi: 10.1111/cns.12277. [Epub ahead of print]
PMID: 24809909 [PubMed - as supplied by publisher]
Related citations

V. Serotonin System and the CS
“Serotonin (5-HT) plays pivotal roles in the pathogenesis of post-infectious irritable bowel syndrome (PI-IBS), and luminal 5-HT time-dependently modulates visceral nociception. We found that duodenal biopsies from PI-IBS patients exhibited increased 5-HT and decreased anandamide levels and that decreased anandamide was associated with abdominal pain severity, indicating a link between 5- HT and endocannabinoid signaling pathways in PI-IBS.”
Vagal anandamide signaling via cannabinoid receptor 1 contributes to luminal 5-HT modulation of visceral nociception in rats.
Feng CC, Yan XJ, Chen X, Wang EM, Liu Q, Zhang LY, Chen J, Fang JY, Chen SL.
Pain. 2014 May 8. pii: S0304-3959(14)00225-5. doi: 10.1016/j.pain.2014.05.005. [Epub ahead of print]
PMID: 24813296 [PubMed - as supplied by publisher]
Related citations

VI. Central Nervous System (Blood-Brain Barrier) and CS
“Early brain injury (EBI), following subarachnoid hemorrhage (SAH), comprises blood-brain barrier (BBB) disruption and consequent edema formation. … We suggest that CB2R stimulation attenuates neurological outcome and brain edema, by suppressing leukocyte infiltration into the brain through TGF-β1 up-regulation and E-selectin reduction, resulting in protection of the BBB after SAH.”
Cannabinoid type 2 receptor stimulation attenuates brain edema by reducing cerebral leukocyte infiltration following subarachnoid hemorrhage in rats.
Fujii M, Sherchan P, Krafft PR, Rolland WB, Soejima Y, Zhang JH.
J Neurol Sci. 2014 Apr 30. pii: S0022-510X(14)00270-6. doi: 10.1016/j.jns.2014.04.034. [Epub ahead of print]
PMID: 24819918 [PubMed - as supplied by publisher]
Related citations

VII. Central Nervous System (Memory) and CS
“The reactivation of a memory can result in its destabilization, necessitating a process of memory reconsolidation to maintain its persistence. Here we show that the destabilization of a contextual fear memory is potentiated by the cannabinoid CB1 receptor agonist Arachidonyl-2-chloroethylamide (ACEA). … These results indicate that memory expression and destabilization, while being independent from one another, are both dependent upon memory reactivation. Moreover, memory destabilization can be enhanced pharmacologically, which may be of therapeutic potential.”
Inhibition and enhancement of contextual fear memory destabilization.
Lee JL, Flavell CR.
Front Behav Neurosci. 2014 Apr 28;8:144. doi: 10.3389/fnbeh.2014.00144. eCollection 2014.
PMID: 24808841 [PubMed] Free PMC Article
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Bonus Video:

Posted by Bryan W. Brickner

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Indiscernible Cannabinoid System Science ~ Publius’ February 2014 Roundup

2/27/2014

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Picture
The Cannabis Papers: A citizen’s guide to cannabinoids (2011)
By Publius 


This roundup links to seven 2014 PubMed articles on cannabinoids modulating other systems in our bodies, such as: the olfactory, endocrine, vanilloid, serotonin, opioid, dopamine, and nervous systems. There’s also a bit of systemic science ~ getting a good night’s sleep.


I. Olfactory System and CS
“Thus, CB1 receptor-dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior.”

The endocannabinoid system controls food intake via olfactory processes.
  Soria-Gómez E, Bellocchio L, Reguero L, Lepousez G, Martin C, Bendahmane M, Ruehle S, Remmers F, Desprez T, Matias I,
  Wiesner T, Cannich A, Nissant A, Wadleigh A, Pape HC, Chiarlone AP, Quarta C, Verrier D, Vincent P, Massa F, Lutz B,
  Guzmán M, Gurden H, Ferreira G, Lledo PM, Grandes P, Marsicano G.
  Nat Neurosci. 2014 Mar;17(3):407-15. doi: 10.1038/nn.3647. Epub 2014 Feb 9.
  PMID: 24509429 [PubMed - in process]

II. Endocrine System (Hypothalamus-pituitary axis) and CS
“Whereas the effect on 3β-HSD was counteracted by SR141716A (Rimonabant) - a selective antagonist of CB1, thus indicating a CB1 dependent modulation - the effect on cyp17 was not, suggesting a possible involvement of receptors other than CB1, probably the type-1 vanilloid receptor (TRPV1), since AEA works as an endocannabinoid and an endovanilloid as well.”

Hypothalamus-pituitary axis: an obligatory target for endocannabinoids to inhibit steroidogenesis in frog testis.
  Chianese R, Ciaramella V, Fasano S, Pierantoni R, Meccariello R.
  Gen Comp Endocrinol. 2014 Feb 21. pii: S0016-6480(14)00053-7. doi: 10.1016/j.ygcen.2014.02.010. [Epub ahead of print]
  PMID: 24566122 [PubMed - as supplied by publisher]

III. Vanilloid System (Schizophrenia) and CS
“Our results indicate that the schizophrenia-like behaviors displayed by SHR [Spontaneously Hypertensive Rats]  are differently altered by cannabinoid and vanilloid drugs when compared to control animals and suggest the endocannabinoid and the vanilloid systems as a potential target for the treatment of schizophrenia.”

Effects of cannabinoid and vanilloid drugs on positive and negative-like symptoms on an animal model of schizophrenia: The SHR strain.
  Almeida V, Peres FF, Levin R, Suiama MA, Calzavara MB, Zuardi AW, Hallak JE, Crippa JA, Abílio VC.
  Schizophr Res. 2014 Feb 17. pii: S0920-9964(14)00062-0. doi: 10.1016/j.schres.2014.01.039. [Epub ahead of print]
  PMID: 24556469 [PubMed - as supplied by publisher]

IV. Serotonin, Opioid, and Dopamine Systems and CS
“In this review we highlight the evidence for the physiological role of such constitutive GPCR [G protein-coupled receptor]   activity (in particular for cannabinoid 1, serotonin 2C and mu-opioid receptors) in the ventral tegmental area and in its output regions like the nucleus accumbens. We also address the behavioral relevance of constitutive GPCR signaling and discuss the repercussions of its abolition in dopamine-related psychiatric diseases.”

The vital role of constitutive GPCR activity in the mesolimbic dopamine system.
  Meye FJ, Ramakers GM, Adan RA.
  Transl Psychiatry. 2014 Feb 11;4:e361. doi: 10.1038/tp.2013.130.
  PMID: 24518399 [PubMed - in process]

V. Sleep, Systems and CS
“Overall, these findings demonstrate that the EC [Endo-Cannabinoid] system actively regulates cortical up-states and important features of NREM sleep such as its duration and low frequency cortical oscillations.”

Endocannabinoid Modulation of Cortical Up-States and NREM Sleep.
  Pava MJ, den Hartog CR, Blanco-Centurion C, Shiromani PJ, Woodward JJ.
  PLoS One. 2014 Feb 10;9(2):e88672. doi: 10.1371/journal.pone.0088672. eCollection 2014.
  PMID: 24520411 [PubMed - in process] Free PMC Article

VI. Central Nervous System and CS
“In the present study, we discovered that 2-AG significantly protects CN neurons in culture against lipopolysaccharide (LPS)-induced inflammatory response.”

Endocannabinoid 2-Arachidonylglycerol Protects Primary Cultured Neurons Against LPS-Induced Impairments in Rat Caudate Nucleus.
  Lu Y, Peng F, Dong M, Yang H.
  J Mol Neurosci. 2014 Feb 9. [Epub ahead of print]
  PMID: 24510751 [PubMed - as supplied by publisher]

VII. Nervous System (Alzheimer’s/Dementia) and CS
“The altered CB1 levels appear, rather, to be age-and/or pathology-dependent, indicating an involvement of the endocannabinoid system in AD pathology and supporting the ECS as a potential novel therapeutic target for treatment of AD.”

Altered Expression of the CB1 Cannabinoid Receptor in the Triple Transgenic Mouse Model of Alzheimer's Disease.
  Bedse G, Romano A, Cianci S, Lavecchia AM, Lorenzo P, Elphick MR, Laferla FM, Vendemiale G, Grillo C, Altieri F, Cassano
  T, Gaetani S.
  J Alzheimers Dis. 2014 Feb 4. [Epub ahead of print]
  PMID: 24496074 [PubMed - as supplied by publisher]

~.~
February's Video
What if Cannabinoids in Cannabis Cured Cancer & Other Diseases?

  Posted by bwb.

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Cannabinoid System Stops Cancer ~ Publius’ February 2014 Prevention Awareness

2/26/2014

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Picture
The Cannabis Papers: A citizen’s guide to cannabinoids (2011)
By Publius

Cancer prevention awareness and the cannabinoid system are the focus of February’s health update from Publius and The Cannabis Papers: A citizen’s guide to cannabinoids (2011). This month: PubMed science on inflammation, a unique receptor, GPR55, and the ability of one’s cannabinoid system to induce apoptosis, programmed cancer cell death.

2014 ~ Inflammation (HIV-1) and CS/GPR55
“Receptors for THC, CB1, CB2, and GPR55, are differentially expressed on multiple cell types including monocytes and macrophages, which are important modulators of inflammation in vivo and target cells for HIV-1 infection.”

Δ9-Tetrahydrocannabinol Treatment During Human Monocyte Differentiation Reduces Macrophage Susceptibility to HIV-1 Infection.
Williams JC, Appelberg S, Goldberger BA, Klein TW, Sleasman JW, Goodenow MM.
J Neuroimmune Pharmacol. 2014 Feb 23. [Epub ahead of print]
PMID: 24562630 [PubMed - as supplied by publisher]


2013 ~ Alcohol, Dentric Cells and CS/GPR55
"Our results provide insights into alcohol mechanisms of DC [dentric cell] regulation and show, for the first time, that alcohol is inducing CNR2 [CB2] and GPR55 in human DCs."

Differential expression and functional role of cannabinoid genes in alcohol users.
Agudelo M, Yndart A, Morrison M, Figueroa G, Muñoz K, Samikkannu T, Nair MP.
Drug Alcohol Depend. 2013 Dec 1;133(2):789-93. doi: 10.1016/j.drugalcdep.2013.08.023. Epub 2013 Sep 5.
PMID: 24060590 [PubMed - in process]


2013 ~ Inflammation (Cancer) and CS/GPR55
“GPR55 has been shown to have a role in cancer and gastrointestinal inflammation, as well as in obesity and type 2 diabetes mellitus (T2DM).”

A potential role for GPR55 in the regulation of energy homeostasis.
Simcocks AC, O'Keefe L, Jenkin KA, Mathai ML, Hryciw DH, McAinch AJ.
Drug Discov Today. 2013 Dec 24. pii: S1359-6446(13)00423-6. doi: 10.1016/j.drudis.2013.12.005. [Epub ahead of print] Review.
PMID: 24370891 [PubMed - as supplied by publisher]


2013 ~ CS Synergistic Against Cancer
“The observed synergistic effect with cannabinoid agonists implicates an involvement of the cannabinoid system.”

Cytotoxic effect of efavirenz is selective against cancer cells and associated with the cannabinoid system.
Hecht M, Harrer T, Büttner M, Schwegler M, Erber S, Fietkau R, Distel LV.
AIDS. 2013 Aug 24;27(13):2031-40. doi: 10.1097/QAD.0b013e3283625444.
PMID: 23612009 [PubMed - in process]


2011 ~ GPR55 Driving Cancer Cell Migration
“It has now been revealed that LPI [L-α-lysophosphatidylinositol] activates GPR55, a G protein-coupled receptor that couples to G(12/13) and G(q) proteins, which direct oncogenic signalling. New evidence indicates that LPI and GPR55 are key partners in driving cancer cell proliferation and migration.”

L-α-lysophosphatidylinositol meets GPR55: a deadly relationship.
Ross RA.
Trends Pharmacol Sci. 2011 May;32(5):265-9. doi: 10.1016/j.tips.2011.01.005. Epub 2011 Mar 1.
PMID: 21367464 [PubMed - indexed for MEDLINE]


2010 ~ Breast Cancer and CS/GPR55
“LPI and GPR55 play a role in the modulation of migration, orientation and polarization of breast cancer cells in response to the tumour microenvironment.”

A role for L-alpha-lysophosphatidylinositol and GPR55 in the modulation of migration, orientation and polarization of human breast cancer cells.
Ford LA, Roelofs AJ, Anavi-Goffer S, Mowat L, Simpson DG, Irving AJ, Rogers MJ, Rajnicek AM, Ross RA.
Br J Pharmacol. 2010 Jun;160(3):762-71. doi: 10.1111/j.1476-5381.2010.00743.x.
PMID: 20590578 [PubMed - indexed for MEDLINE] Free PMC Article


2006 ~ Evolution and CS/GPR55
“Within this limited number of twelve organisms, the endocannabinoid genes exhibited heterogeneous evolutionary trajectories, with functional orthologs limited to mammals (TRPV1 and GPR55), or vertebrates (CB2 and DAGLbeta), or chordates (MAGL and COX2), or animals (DAGLalpha and CB1-like receptors), or opisthokonta (animals and fungi, NAPE-PLD), or eukaryotes (FAAH).”

Evolutionary origins of the endocannabinoid system.
McPartland JM, Matias I, Di Marzo V, Glass M.
Gene. 2006 Mar 29;370:64-74. Epub 2006 Jan 23.
PMID: 16434153 [PubMed - indexed for MEDLINE]

~ posted by bwb

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Indiscernible Cannabinoid Science ~ A 2013 Publius Roundup

12/29/2013

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Picture
The Cannabis Papers: A citizen’s guide to cannabinoids (2011)
by Publius

~ Here are a few recent 2013 findings on cannabinoids modulating other systems in our bodies: the roundup links to recent PubMed articles on the central nervous, circulatory, dopamine, integumentary (skin), lymphatic, and urinary systems.

I. Urinary System and CS
“Cannabinoids are reported to reduce sensory activity of isolated tissues, cause antihyperalgesia in animal studies of bladder inflammation, affect urodynamic parameters reflecting sensory functions in animal models, and appear to have effects on storage symptoms in humans.”

Cannabinoids and the endocannabinoid system in lower urinary tract function and dysfunction.
Hedlund P.
Neurourol Urodyn. 2013 Sep 23. doi: 10.1002/nau.22442. [Epub ahead of print]
PMID: 24285567 [PubMed - as supplied by publisher]

II. Integumentary System / Skin and CS
“Overall, these findings demonstrate that AEA [anandamide] induces cytotoxicity against human melanoma cells in the micromolar range of concentrations through a complex mechanism, which involves COX-2 and LOX-derived product synthesis and CB1 activation.”

Anticancer activity of anandamide in human cutaneous melanoma cells.
Adinolfi B, Romanini A, Vanni A, Martinotti E, Chicca A, Fogli S, Nieri P.
Eur J Pharmacol. 2013 Oct 15;718(1-3):154-9. doi: 10.1016/j.ejphar.2013.08.039. Epub 2013 Sep 13.
PMID: 24041928 [PubMed - in process]

III. Nervous System and CS
“This review will provide the reader with the foundational basic and clinical science linking the endocannabinoid system and the phytocannabinoids with their potentially therapeutic role in the management of chronic pain.”

The endocannabinoid system, cannabinoids and pain.
Fine PG, Rosenfeld MJ.
Rambam Maimonides Med J. 2013 Oct 29;4(4):e0022. doi: 10.5041/RMMJ.10129.
PMID: 24228165 [PubMed] Free PMC Article

IV. Central Nervous System / Autism and CS
“Our data indicate CB2 receptor as potential therapeutic target for the pharmacological management of the autism care.”

Cannabinoid receptor type 2, but not type 1, is up-regulated in peripheral blood mononuclear cells of children affected by autistic disorders.
Siniscalco D, Sapone A, Giordano C, Cirillo A, de Magistris L, Rossi F, Fasano A, Bradstreet JJ, Maione S, Antonucci N.
J Autism Dev Disord. 2013 Nov;43(11):2686-95. doi: 10.1007/s10803-013-1824-9.
PMID: 23585028 [PubMed - in process]

V. Circulatory and Lymphatic Systems / Bone Marrow and CS
“CBD may therefore recruit MSCs [mesenchymal stem cells] to sites of calcifying tissue regeneration and subsequently support bone regeneration via an osteoanabolic action on MSCs.”

Increase of mesenchymal stem cell migration by Cannabidiol via activation of p42/44 MAPK.
Schmuhl E, Ramer R, Salamon A, Peters K, Hinz B.
Biochem Pharmacol. 2013 Dec 1. pii: S0006-2952(13)00747-8. doi: 10.1016/j.bcp.2013.11.016. [Epub ahead of print]
PMID: 24304686 [PubMed - as supplied by publisher]

VI. Circulatory System and CS
“Cannabinoids also modulate the actions of vasoactive compounds including acetylcholine [nicotinic], methoxamine, angiotensin II and U46619 (thromboxane mimetic).”

Vascular targets for cannabinoids: animal and human studies.
Stanley C, O'Sullivan SE.
Br J Pharmacol. 2013 Dec 16. doi: 10.1111/bph.12560. [Epub ahead of print]
PMID: 24329566 [PubMed - as supplied by publisher]

VII. Dopamine System and CS
“Cannabinoids also increase dopamine release within the mesolimbic system, a neural pathway generally implicated in timing behavior.”

Cannabinoid receptor activation shifts temporally engendered patterns of dopamine release.
Oleson EB, Cachope R, Fitoussi A, Tsutsui K, Wu S, Gallegos JA, Cheer JF.
Neuropsychopharmacology. 2013 Dec 18. doi: 10.1038/npp.2013.340. [Epub ahead of print]
PMID: 24345819 [PubMed - as supplied by publisher]

~bwb~

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    Author

    Brickner has a 1997 political science doctorate from Purdue University, cofounded Illinois NORML in 2001, and was a 2007 National NORML Cannabis Advocate Awardee. He is also publisher and coauthor of the 2011 book banned by the Illinois Department of Corrections – The Cannabis Papers: A Citizen’s Guide to Cannabinoids.

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