Sandbox 420: Difference between revisions

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==Abstract==
==Abstract==
K2 and other newly popularized drugs laced with synthetic cannabinoids, which mimic those found in marijuana, bind similarly to G-coupled receptors found throughout the body and nervous system. CBR1, in particular, is comprised of 472, mostly nonpolar amino acids that fold into a secondary structure consisting of ten α-helices and one β-pleated sheet forming a transmembrane domain. Binding to endogenous and exogenous ligands alike, CBR1 acts as an activator in a signal transduction pathway to aid in regulating many major bodily systems.  
K2 and other newly popularized drugs laced with synthetic cannabinoids, which mimic those found in marijuana, bind similarly to g-coupled receptors found throughout the body and nervous system. CBR1, in particular, is comprised of 472, mostly nonpolar amino acids that fold into a secondary structure consisting of ten alpha helices and one beta pleated sheet forming a transmembrane domain. Binding to endogenous and exogenous ligands alike, CBR1 acts as an activator in a signal transduction pathway to aid in regulating many major bodily systems.  
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.
You may include any references to papers as in: the use of JSmol in Proteopedia <ref>DOI 10.1002/ijch.201300024</ref> or to the article describing Jmol <ref>PMID:21638687</ref> to the rescue.


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First emergent in Europe in 2004, an herbal incense product known as Spice or K2 was quickly utilized all over the world as a synthetic form of marijuana. Although sold legally in many areas as a “natural incense” that is “not for human consumption”, K2 is a plant-based material with traces of astoundingly potent synthetic cannabinoids, a fact that many users and retailers alike do not fail to recognize.  
First emergent in Europe in 2004, an herbal incense product known as Spice or K2 was quickly utilized all over the world as a synthetic form of marijuana. Although sold legally in many areas as a “natural incense” that is “not for human consumption”, K2 is a plant-based material with traces of astoundingly potent synthetic cannabinoids, a fact that many users and retailers alike do not fail to recognize.  
Synthetic cannabinoids (SCBs) are chemically derived forms of the naturally-occurring psychotropic cannabinoid, tetrahydrocannabinol (THC), found in marijuana (1,2). Cannabinoids bind and activate cannabinoid receptors, CB1R and CB2R, which are found throughout the body (1).  CB1R is primarily found in the cerebellum as well as the hippocampus, hypothalamus, cerebral cortex, striatum and brainstem; all vital areas of the central nervous system (1).  
Synthetic cannabinoids (SCBs) are chemically derived forms of the naturally-occurring psychotropic cannabinoid, tetrahydrocannabinol (THC), found in marijuana (1,2). Cannabinoids bind and activate cannabinoid receptors, CB1R and CB2R, which are found throughout the body (1).  CB1R is primarily found in the cerebellum as well as the hippocampus, hypothalamus, cerebral cortex, striatum and brainstem; all vital areas of the central nervous system (1).  
Although SCBs are chemically similar to THCs, which exhibit relatively mild side effects when used recreationally, the use of K2 has been linked to many serious health conditions. Due to the delocalization of CB1R receptors throughout the body and in crucial parts of the CNS that regulate bodily functions, K2 can affect many systems of the body simultaneously. Cardiovascularly, K2 can cause tachycardia, tachyarrhythmia,  hypertension and, in rare cases, myocardial infarction (2,3,4). Neurologically, K2 can cause extreme paranoia, psychosis, hallucinations, memory and learning disruptions, dependence and even seizures (1).  
Although SCBs are chemically similar to THCs, which exhibit relatively mild side effects when used recreationally, the use of K2 has been linked to many serious health conditions. Due to the delocalization of CB1R receptors throughout the body and in crucial parts of the CNS that regulates bodily functions, K2 can affect many systems of the body simultaneously. Cardiovascularly, K2 can cause tachycardia, tachyarrhythmia,  hypertension and, in rare cases, myocardial infarction (2,3,4). Neurologically, K2 can cause extreme paranoia, psychosis, hallucinations, memory and learning disruptions, dependence and even seizures (1).  


==Structure==
==Structure==
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<references/>


<ref> 1) Brents, Lisa K., and Paul L. Prather. “The K2/Spice Phenomenon: Emergence, Identification,  
<ref>Brents, Lisa K., and Paul L. Prather. “The K2/Spice Phenomenon: Emergence, Identification,  
Legislation and Metabolic Characterization of Synthetic Cannabinoids in Herbal Incense  
Legislation and Metabolic Characterization of Synthetic Cannabinoids in Herbal Incense  
Products.” Drug metabolism reviews 46.1 (2014): 72–85. PMC. Web. 16 Nov. 2015. </ref>
Products.” Drug metabolism reviews 46.1 (2014): 72–85. PMC. Web. 16 Nov. 2015. </ref>


  <ref> 2) "The History of Synthetic Drugs (Spice, K2 and Bath Salts)." Narconon International. Web.
  <ref>"The History of Synthetic Drugs (Spice, K2 and Bath Salts)." Narconon International. Web.
17 Nov. 2015. </ref>
17 Nov. 2015. </ref>


<ref> 3) Mir MD, Arshid, Adebsi Obafemi MD, Amy Young MD, and Colin Kane MD.
<ref>Mir MD, Arshid, Adebsi Obafemi MD, Amy Young MD, and Colin Kane MD.
"Myocardial Infarction Associated With Use of the Synthetic Cannabinoid K@."Pediatrics. Print.</ref>
"Myocardial Infarction Associated With Use of the Synthetic Cannabinoid K@."Pediatrics. Print.</ref>


<ref>4) Lapoint, J. et al. “Severe Toxicity Following Synthetic Cannabinoid Ingestion.” Clinical
<ref>Lapoint, J. et al. “Severe Toxicity Following Synthetic Cannabinoid Ingestion.” Clinical
toxicology (Philadelphia, Pa.) 49.8 (2011): 760–764. PMC. Web. 17 Nov. 2015.</ref>
toxicology (Philadelphia, Pa.) 49.8 (2011): 760–764. PMC. Web. 17 Nov. 2015.</ref>


<ref>5) Svizenska, Ivana, Petr Dubovy, and Alexandra Sulcova. "Cannabinoid Receptors 1 and 2
<ref>Svizenska, Ivana, Petr Dubovy, and Alexandra Sulcova. "Cannabinoid Receptors 1 and 2
(CB1 and CB2), Their Distribution, Ligands and Functional Involvement in Nervous System Structures — A Short Review." Elsevier B.V. Web. 17 Nov. 2015. <http://www.sciencedirect.com/science/article/pii/S0091305708001743>. </ref>
(CB1 and CB2), Their Distribution, Ligands and Functional Involvement in Nervous System Structures — A Short Review." Elsevier B.V. Web. 17 Nov. 2015. <http://www.sciencedirect.com/science/article/pii/S0091305708001743>. </ref>


<ref>6) Domenici, Maria R., Shahnaz C. Azad, Giovanni Marsicano, Anja Schierloh, Carsten T.
<ref>Domenici, Maria R., Shahnaz C. Azad, Giovanni Marsicano, Anja Schierloh, Carsten T.
Wotjak, Hans-Ulrich Dodt, Walter Zieglgansberger, Beat Lutz, and Gerhard Rammes."Cannabinoid Recepter Type 1 Located on Presynaptic Terminals of Principal Neurons in the Forebrain Controls Glutamatergic Synaptic Transmission." The Journal of Neuroscience (2006). Print. </ref>
Wotjak, Hans-Ulrich Dodt, Walter Zieglgansberger, Beat Lutz, and Gerhard Rammes."Cannabinoid Recepter Type 1 Located on Presynaptic Terminals of Principal Neurons in the Forebrain Controls Glutamatergic Synaptic Transmission." The Journal of Neuroscience (2006). Print. </ref>


<ref>7) Albayram, Onder et al. “Role of CB1 Cannabinoid Receptors on GABAergic Neurons in
<ref>Albayram, Onder et al. “Role of CB1 Cannabinoid Receptors on GABAergic Neurons in
Brain Aging.” Proceedings of the National Academy of Sciences of the United States of America 108.27 (2011): 11256–11261. PMC. Web. 17 Nov. 2015.</ref>
Brain Aging.” Proceedings of the National Academy of Sciences of the United States of America 108.27 (2011): 11256–11261. PMC. Web. 17 Nov. 2015.</ref>


<ref>8) Han, Jing, Philip Kesner, Mathilde Metna-Laurent, Tingting Duan, Lin Xu, Francois Georges,
<ref>Han, Jing, Philip Kesner, Mathilde Metna-Laurent, Tingting Duan, Lin Xu, Francois Georges,
Muriel Koehl, Djoher Nora Abrous, Juan Mendizabal-Zubiaga, Pedro Grandes, Qingsong Liu, Guang Bai, Wei Wang, Lize Xiong, Wei Ren, Giovanni Marsicano, and Xia Zhang. "Acute Cannabinoids Impair Working Memory through Astroglial CB1 Receptor Modulation of Hippocampal LTD." Cell: 1039-050. Print. </ref>
Muriel Koehl, Djoher Nora Abrous, Juan Mendizabal-Zubiaga, Pedro Grandes, Qingsong Liu, Guang Bai, Wei Wang, Lize Xiong, Wei Ren, Giovanni Marsicano, and Xia Zhang. "Acute Cannabinoids Impair Working Memory through Astroglial CB1 Receptor Modulation of Hippocampal LTD." Cell: 1039-050. Print. </ref>


<ref>9) Jager, Gerry, and Renger F. Witkamp. "The Endocannabinoid System and Appetite: Relevance
<ref>Jager, Gerry, and Renger F. Witkamp. "The Endocannabinoid System and Appetite: Relevance
for Food Reward." Nutr. Res. Rev. Nutrition Research Reviews: 172-85. Print. </ref>
for Food Reward." Nutr. Res. Rev. Nutrition Research Reviews: 172-85. Print. </ref>


<ref>10) Fantegrossi, William E. et al. “Distinct Pharmacology and Metabolism of K2 Synthetic
<ref>Fantegrossi, William E. et al. “Distinct Pharmacology and Metabolism of K2 Synthetic
Cannabinoids Compared to Δ9-THC: Mechanism Underlying Greater Toxicity?” Life sciences 97.1 (2014): 45–54. PMC. Web. 16 Nov. 2015</ref>
Cannabinoids Compared to Δ9-THC: Mechanism Underlying Greater Toxicity?” Life sciences 97.1 (2014): 45–54. PMC. Web. 16 Nov. 2015</ref>
<references/>
<references/>

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