Yeah true but the longer you let your bud go the sleepier the effects tend to get the more medicated things start to get. I guess is my point lol.. Again it's all in the strain when you harvest and how you play headband 707
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Yeah true but the longer you let your bud go the sleepier the effects tend to get the more medicated things start to get. I guess is my point lol.. Again it's all in the strain when you harvest and how you play headband 707
Sleepy effect from going longer is from more CBN. More amber trichomes will have the same effect.Yeah true but the longer you let your bud go the sleepier the effects tend to get the more medicated things start to get. I guess is my point lol.. Again it's all in the strain when you harvest and how you play headband 707
CBD is ALL in the strain. Not anything else.
Yeah true but the longer you let your bud go the sleepier the effects tend to get the more medicated things start to get. I guess is my point lol.. Again it's all in the strain when you harvest and how you play headband 707
Indeed. Got a cool link here that shows more Compounds. Or Chemo Types. Now notice this quote.
"1The total given in the 1980 review was 421. The 2 glycoproteins of unknown structures, however, make the total 423.2The simple acids and fatty acids in the 1995 review are given as 21 and 22, respectively. They should, however, be 20 and 23, respectively, which leaves the total unchanged.3The CBC-and miscellaneous-type cannabinoids in the 1995 review are given as 5 and 11, respectively. They should, however, be 4 and 12, respectively, which leaves the total unchanged. "
http://www.sciencedirect.com/science/article/pii/S002432050500891X
History Of Cannabanoid Studies going back to 1840
Cannabis use for medicinal purposes dates back at least 3,000 years.[1-5] It was introduced into Western medicine in the 1840s by W.B. O’Shaughnessy, a surgeon who learned of its medicinal properties while working in India for the British East Indies Company. Its use was promoted for reported analgesic, sedative, anti-inflammatory, antispasmodic, and anticonvulsant effects.
In 1937, the U.S. Treasury Department introduced the Marihuana Tax Act. This Act imposed a levy of one dollar an ounce for medicinal use of Cannabis and one hundred dollars an ounce for recreational use. Physicians in the United States were the principal opponents of the Act. The American Medical Association (AMA) opposed the Act because physicians were required to pay a special tax for prescribing Cannabis, use special order forms to procure it, and keep special records concerning its professional use. In addition, the AMA believed that objective evidence that Cannabis was addictive was lacking and that passage of the Act would impede further research into its medicinal worth.[6] In 1942, Cannabis was removed from the U.S. Pharmacopoeia because of persistent concerns about its potential to cause harm.[2,3]
In 1951, Congress passed the Boggs Act, which for the first time, included Cannabis with narcotic drugs. In 1970, with the passage of the Controlled Substances Act, marijuana was classified as a Schedule I drug. Drugs in this category are distinguished as having no accepted medicinal use. Other Schedule I substances include heroin, LSD, mescaline, methaqualone, and gamma-hydroxybutyrate.
Despite its designation as having no medicinal use, Cannabis was distributed to patients by the U.S. government on a case-by-case basis under the Compassionate Use Investigational New Drug program established in 1978. Distribution of Cannabis through this program was discontinued in 1992.[1-4] In 2010, the U.S. Department of Veteran Affairs approved marijuana use for patients in states where its medicinal use is legal.
The main psychoactive constituent of Cannabis was identified as delta-9-tetrahydrocannabinol (THC). In 1986, synthetic delta-9-THC in sesame oil was licensed and approved for the treatment of chemotherapy -associated nausea and vomiting under the generic name dronabinol. Clinical trials determined that dronabinol was as effective as or better than other antiemetic agents.[7] Dronabinol was also studied for its ability to stimulate weight gain in patients with AIDS in the late 1980s. Clinical trial results showed no significant weight gain, although patients reported an improvement in appetite. [8,9]
Within the past 20 years, the neurobiology of cannabinoids has been analyzed.[10-13] The first cannabinoid receptor, CB1, was pharmacologically identified in the brain in 1988. A second cannabinoid receptor, CB2, was identified in 1993. The highest concentration of CB2 receptors is located on B lymphocytes and natural killer cells, suggesting a possible role in immunity. Endogenous cannabinoids (endocannabinoids) have been identified and appear to have a role in pain modulation, control of movement, feeding behavior, and memory.[11]
References
Abel EL: Marihuana, The First Twelve Thousand Years. New York: Plenum Press, 1980. Also available online. Last accessed March 17, 2011.
Joy JE, Watson SJ, Benson JA, eds.: Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999. Also available online. Last accessed March 17, 2011.
Mack A, Joy J: Marijuana As Medicine? The Science Beyond the Controversy. Washington, DC: National Academy Press, 2001. Also available online. Last accessed March 17, 2011.
Booth M: Cannabis: A History. New York, NY: St Martin's Press, 2003.
Russo EB, Jiang HE, Li X, et al.: Phytochemical and genetic analyses of ancient cannabis from Central Asia. J Exp Bot 59 (15): 4171-82, 2008. [PUBMED Abstract]
Schaffer Library of Drug Policy.: The Marihuana Tax Act of 1937: Taxation of Marihuana. Washington, DC: House of Representatives, Committee on Ways and Means, 1937. Available online. Last accessed March 17, 2011.
Sallan SE, Zinberg NE, Frei E 3rd: Antiemetic effect of delta-9-tetrahydrocannabinol in patients receiving cancer chemotherapy. N Engl J Med 293 (16): 795-7, 1975. [PUBMED Abstract]
Gorter R, Seefried M, Volberding P: Dronabinol effects on weight in patients with HIV infection. AIDS 6 (1): 127, 1992. [PUBMED Abstract]
Beal JE, Olson R, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 10 (2): 89-97, 1995. [PUBMED Abstract]
Devane WA, Dysarz FA 3rd, Johnson MR, et al.: Determination and characterization of a cannabinoid receptor in rat brain. Mol Pharmacol 34 (5): 605-13, 1988. [PUBMED Abstract]
Devane WA, Hanus L, Breuer A, et al.: Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 258 (5090): 1946-9, 1992. [PUBMED Abstract]
Pertwee RG: Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacol Ther 74 (2): 129-80, 1997. [PUBMED Abstract]
Felder CC, Glass M: Cannabinoid receptors and their endogenous agonists. Annu Rev Pharmacol Toxicol 38: 179-200, 1998. [PUBMED Abstract]
http://wacanga.com/nationalcancerinstitute.html
Cannabis use for medicinal purposes dates back at least 3,000 years.[1-5] It was introduced into Western medicine in the 1840s by W.B. O’Shaughnessy, a surgeon who learned of its medicinal properties while working in India for the British East Indies Company. Its use was promoted for reported analgesic, sedative, anti-inflammatory, antispasmodic, and anticonvulsant effects.
In 1937, the U.S. Treasury Department introduced the Marihuana Tax Act. This Act imposed a levy of one dollar an ounce for medicinal use of Cannabis and one hundred dollars an ounce for recreational use. Physicians in the United States were the principal opponents of the Act. The American Medical Association (AMA) opposed the Act because physicians were required to pay a special tax for prescribing Cannabis, use special order forms to procure it, and keep special records concerning its professional use. In addition, the AMA believed that objective evidence that Cannabis was addictive was lacking and that passage of the Act would impede further research into its medicinal worth.[6] In 1942, Cannabis was removed from the U.S. Pharmacopoeia because of persistent concerns about its potential to cause harm.[2,3]
In 1951, Congress passed the Boggs Act, which for the first time, included Cannabis with narcotic drugs. In 1970, with the passage of the Controlled Substances Act, marijuana was classified as a Schedule I drug. Drugs in this category are distinguished as having no accepted medicinal use. Other Schedule I substances include heroin, LSD, mescaline, methaqualone, and gamma-hydroxybutyrate.
Despite its designation as having no medicinal use, Cannabis was distributed to patients by the U.S. government on a case-by-case basis under the Compassionate Use Investigational New Drug program established in 1978. Distribution of Cannabis through this program was discontinued in 1992.[1-4] In 2010, the U.S. Department of Veteran Affairs approved marijuana use for patients in states where its medicinal use is legal.
The main psychoactive constituent of Cannabis was identified as delta-9-tetrahydrocannabinol (THC). In 1986, synthetic delta-9-THC in sesame oil was licensed and approved for the treatment of chemotherapy -associated nausea and vomiting under the generic name dronabinol. Clinical trials determined that dronabinol was as effective as or better than other antiemetic agents.[7] Dronabinol was also studied for its ability to stimulate weight gain in patients with AIDS in the late 1980s. Clinical trial results showed no significant weight gain, although patients reported an improvement in appetite. [8,9]
Within the past 20 years, the neurobiology of cannabinoids has been analyzed.[10-13] The first cannabinoid receptor, CB1, was pharmacologically identified in the brain in 1988. A second cannabinoid receptor, CB2, was identified in 1993. The highest concentration of CB2 receptors is located on B lymphocytes and natural killer cells, suggesting a possible role in immunity. Endogenous cannabinoids (endocannabinoids) have been identified and appear to have a role in pain modulation, control of movement, feeding behavior, and memory.[11]
References
Abel EL: Marihuana, The First Twelve Thousand Years. New York: Plenum Press, 1980. Also available online. Last accessed March 17, 2011.
Joy JE, Watson SJ, Benson JA, eds.: Marijuana and Medicine: Assessing the Science Base. Washington, DC: National Academy Press, 1999. Also available online. Last accessed March 17, 2011.
Mack A, Joy J: Marijuana As Medicine? The Science Beyond the Controversy. Washington, DC: National Academy Press, 2001. Also available online. Last accessed March 17, 2011.
Booth M: Cannabis: A History. New York, NY: St Martin's Press, 2003.
Russo EB, Jiang HE, Li X, et al.: Phytochemical and genetic analyses of ancient cannabis from Central Asia. J Exp Bot 59 (15): 4171-82, 2008. [PUBMED Abstract]
Schaffer Library of Drug Policy.: The Marihuana Tax Act of 1937: Taxation of Marihuana. Washington, DC: House of Representatives, Committee on Ways and Means, 1937. Available online. Last accessed March 17, 2011.
Sallan SE, Zinberg NE, Frei E 3rd: Antiemetic effect of delta-9-tetrahydrocannabinol in patients receiving cancer chemotherapy. N Engl J Med 293 (16): 795-7, 1975. [PUBMED Abstract]
Gorter R, Seefried M, Volberding P: Dronabinol effects on weight in patients with HIV infection. AIDS 6 (1): 127, 1992. [PUBMED Abstract]
Beal JE, Olson R, Laubenstein L, et al.: Dronabinol as a treatment for anorexia associated with weight loss in patients with AIDS. J Pain Symptom Manage 10 (2): 89-97, 1995. [PUBMED Abstract]
Devane WA, Dysarz FA 3rd, Johnson MR, et al.: Determination and characterization of a cannabinoid receptor in rat brain. Mol Pharmacol 34 (5): 605-13, 1988. [PUBMED Abstract]
Devane WA, Hanus L, Breuer A, et al.: Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 258 (5090): 1946-9, 1992. [PUBMED Abstract]
Pertwee RG: Pharmacology of cannabinoid CB1 and CB2 receptors. Pharmacol Ther 74 (2): 129-80, 1997. [PUBMED Abstract]
Felder CC, Glass M: Cannabinoid receptors and their endogenous agonists. Annu Rev Pharmacol Toxicol 38: 179-200, 1998. [PUBMED Abstract]
http://wacanga.com/nationalcancerinstitute.html
You honestly have to wonder "who" had this much power to hold this plant down since 1840? WOW what bullshit this has been and who told them they could tell me what to do in this respect? I'm so sick and tired of this agrument with this obvious uninformed communist type Gov.that thinks they know what is good for me and they are going to put me inline! I don't remember ever voting these type of ppl in and I don't know how they got where they are today! That being said I'm sure you could play all day with the endless combinations of cannabis and it's amazing properties headband 707
This is the theory, whatever is going on, when take it PREVENTS receptors from binding, in many forms, not just limited to Cb2, i believe my Anti Depressants stop working the next day after a edible untill i take my next dose. Also IF cant bind this is why the cancer cant spread, cuts off its food source, and makes the other cells go back to normal.
Delta2 has been found in a person, considered a DNA GENETIC CODE MISHAP, to have a H.I.V. Genetic code to prevent it. And its called Delta 2. Very close, if not the same as Delta 9? So now we may have found a way to slow or stop the progression of desiese by not allowing it to continue to do damage. and fix what has been damage.
INSTEAD of 30 different Vaccinations that coast a TON of money, paid for by your insurance company.
So instead of giving people 30 different disease with Preventive measures, the actually anti Venom, you can actually fight off these LIFE THREATENING disease with a "beta blocker" or Receptor Blocker" Reason why it works with Seizures, Pain (cb2 receptors in spine) and other Neurological issues like cerapalsy.
The delta 2 DNA found in this modern man, was though to be created from the plague, which could of been a mutation to adapt to what was killing everyone.
Just my thoughts, ideas, and Prognosis, of or findings.
Delta2 has been found in a person, considered a DNA GENETIC CODE MISHAP, to have a H.I.V. Genetic code to prevent it. And its called Delta 2. Very close, if not the same as Delta 9? So now we may have found a way to slow or stop the progression of desiese by not allowing it to continue to do damage. and fix what has been damage.
INSTEAD of 30 different Vaccinations that coast a TON of money, paid for by your insurance company.
So instead of giving people 30 different disease with Preventive measures, the actually anti Venom, you can actually fight off these LIFE THREATENING disease with a "beta blocker" or Receptor Blocker" Reason why it works with Seizures, Pain (cb2 receptors in spine) and other Neurological issues like cerapalsy.
The delta 2 DNA found in this modern man, was though to be created from the plague, which could of been a mutation to adapt to what was killing everyone.
Just my thoughts, ideas, and Prognosis, of or findings.
Delta 2, Th2 cells prove to be genetic disposition as a resistance to HIV-1
Delta 2, Th2 cells prove to be genetic disposition as a resistance to HIV-1
http://www.ncbi.nlm.nih.gov/pubmed/15965616
Virus Genes. 2005 Aug;31(1):113-9.
The molecular mechanism of human resistance to HIV-1 infection in persistently infected individuals--a review, hypothesis and implications.
Becker Y.
Source
Department of Molecular Virology, Faculty of Medicine, The Hebrew University of Jerusalem, Israel. becker@md.huji.ac.il
Abstract
Resistance to HIV-1 infection in Europeans is associated with a mutation in the gene that codes for the CCR5 protein that is present in Th2 cells and serves as a coreceptor for HIV-1 R5 strain. A deletion of 32 amino acids from the cytokine receptor prevents infection. This mutation prevails in Europeans and is absent in Africans. However, duplication of a gene that codes for a chemokine that binds to the CCR5 was discovered in Africans (mean gene copy 6 while in non-Africans the mean gene copy is 3). Higher expression of these genes protects T cells against HIV-1 infection in vitro. It should be noted that resistance to HIV-1 R5 variant does not protect against HIV-1 R4 variant. It was reported that a minority of highly HIV-1 exposed African professional sex workers (APSW) were resistant to the virus infection during a 10 years period. Recently, the analysis of the cytokines in the serum of the persistently infected seronegative women revealed that the latter hypo-expresses the cytokine IL-4. Since the molecular events during HIV-1 infection are associated with a marked increase in the levels of IL-4 and IgE in the sera of the infected individuals, it suggests that AIDS is an allergy. Thus, a very low level of IL-4 production may abrogate the virus infection. Studies on the human IL-4 gene revealed that together with the IL-4 mRNA a spliced variant with a deletion of exon 2 is synthesized. The latter is a natural antagonist of IL-4 and when expressed in an individual at a level higher than IL-4, the person will resist a microbial infection (e.g. Mycobacterium tuberculosis) or asthma. The present hypothesis suggests that the HIV-1 resistant APSWs produce more IL-4 delta 2 molecules than IL-4 molecules. The binding of IL-4 delta 2 to IL-4 receptors on T and B cells prevents their functions and the infection by HIV-1. The implications of these studies are that treatment of HIV-1 infected people with drugs that will block the IL-4 receptors will stop HIV-1 infections and the determination of the levels of IL-4 and IL-4 delta 2 in the sera of HIV-1+ patients will enable to identify the individuals that have a natural resistance to HIV-l/AIDS and those who need treatments.
PMID: 15965616 [PubMed - indexed for MEDLINE]
Delta 2, Th2 cells prove to be genetic disposition as a resistance to HIV-1
http://www.ncbi.nlm.nih.gov/pubmed/15965616
Virus Genes. 2005 Aug;31(1):113-9.
The molecular mechanism of human resistance to HIV-1 infection in persistently infected individuals--a review, hypothesis and implications.
Becker Y.
Source
Department of Molecular Virology, Faculty of Medicine, The Hebrew University of Jerusalem, Israel. becker@md.huji.ac.il
Abstract
Resistance to HIV-1 infection in Europeans is associated with a mutation in the gene that codes for the CCR5 protein that is present in Th2 cells and serves as a coreceptor for HIV-1 R5 strain. A deletion of 32 amino acids from the cytokine receptor prevents infection. This mutation prevails in Europeans and is absent in Africans. However, duplication of a gene that codes for a chemokine that binds to the CCR5 was discovered in Africans (mean gene copy 6 while in non-Africans the mean gene copy is 3). Higher expression of these genes protects T cells against HIV-1 infection in vitro. It should be noted that resistance to HIV-1 R5 variant does not protect against HIV-1 R4 variant. It was reported that a minority of highly HIV-1 exposed African professional sex workers (APSW) were resistant to the virus infection during a 10 years period. Recently, the analysis of the cytokines in the serum of the persistently infected seronegative women revealed that the latter hypo-expresses the cytokine IL-4. Since the molecular events during HIV-1 infection are associated with a marked increase in the levels of IL-4 and IgE in the sera of the infected individuals, it suggests that AIDS is an allergy. Thus, a very low level of IL-4 production may abrogate the virus infection. Studies on the human IL-4 gene revealed that together with the IL-4 mRNA a spliced variant with a deletion of exon 2 is synthesized. The latter is a natural antagonist of IL-4 and when expressed in an individual at a level higher than IL-4, the person will resist a microbial infection (e.g. Mycobacterium tuberculosis) or asthma. The present hypothesis suggests that the HIV-1 resistant APSWs produce more IL-4 delta 2 molecules than IL-4 molecules. The binding of IL-4 delta 2 to IL-4 receptors on T and B cells prevents their functions and the infection by HIV-1. The implications of these studies are that treatment of HIV-1 infected people with drugs that will block the IL-4 receptors will stop HIV-1 infections and the determination of the levels of IL-4 and IL-4 delta 2 in the sera of HIV-1+ patients will enable to identify the individuals that have a natural resistance to HIV-l/AIDS and those who need treatments.
PMID: 15965616 [PubMed - indexed for MEDLINE]
I also found this bit of info interesting ... Wiki
I also found this bit of info interesting ... Wiki
[edit] Difference between Cannabis indica and Cannabis sativa
Cannabis sativa, Cannabis indica, and Cannabis ruderalisCannabis indica may have a CBD:THC ratio 4–5 times that of Cannabis sativa. Cannabis strains with relatively high CBD:THC ratios are less likely to induce anxiety than vice versa. This may be due to CBD's antagonistic effects at the cannabinoid receptors, compared to THC's partial agonist effect. CBD is also a 5-HT1A receptor agonist, which may also contribute to an anxiolytic effect.[114] This likely means the high concentrations of CBD found in Cannabis indica mitigate the anxiogenic effect of THC significantly.[114] The effects of sativa are well known for its cerebral high, hence used daytime as medical cannabis, while indica are well known for its sedative effects and preferred night time as medical cannabis.[114]
I also found this bit of info interesting ... Wiki
[edit] Difference between Cannabis indica and Cannabis sativa
Cannabis sativa, Cannabis indica, and Cannabis ruderalisCannabis indica may have a CBD:THC ratio 4–5 times that of Cannabis sativa. Cannabis strains with relatively high CBD:THC ratios are less likely to induce anxiety than vice versa. This may be due to CBD's antagonistic effects at the cannabinoid receptors, compared to THC's partial agonist effect. CBD is also a 5-HT1A receptor agonist, which may also contribute to an anxiolytic effect.[114] This likely means the high concentrations of CBD found in Cannabis indica mitigate the anxiogenic effect of THC significantly.[114] The effects of sativa are well known for its cerebral high, hence used daytime as medical cannabis, while indica are well known for its sedative effects and preferred night time as medical cannabis.[114]
Breif Medical Dictionary Reference"
Receptors & Agonists For the purposes of our discussion, receptor refers to a neurotransmitter receptor.
Receptors are present on both postsynaptic and presynaptic neurons – the former being used to receive neurotransmitters, the latter for the purpose of preventing further release of a given neurotransmitter.
Each neurotransmitter has its own receptors. And it’s all about efficient electrical signaling.
synapse /syn·apse/ (sin´aps) the site of functional apposition between neurons, where an impulse is transmitted from one to another, usually by a chemical neurotransmitter released by the axon terminal of the presynaptic neuron. The neurotransmitter diffuses across the gap to bind with receptors on the postsynaptic cell membrane and cause electrical changes in that neuron (depolarization/excitation or hyperpolarization/inhibition).
An anxiolytic (also antipanic or antianxiety agent)[1] is a drug used for the treatment of anxiety and its related psychological and physical symptoms. Anxiolytics have been shown to be useful in the treatment of anxiety disorders.
Beta-receptor blockers such as propranolol and oxprenolol, although not anxiolytics, can be used to combat the somatic symptoms of anxiety.
Anxiolytics are also known as minor tranquilizers.
an·tag·o·nis·tic/anˌtagəˈnistik/
Adjective:
Showing or feeling active opposition or hostility toward someone or something.
Of or relating to an antagonist or its action. Synonyms:
hostile - inimical - adverse - opponent - opposed
Anxiogenic
An anxiogenic substance is one that causes anxiety. Anxiogenic effects can be measured by, for example, the hole-board test in rats and mice.[1] A number of agents are used to provoke anxiety (anxiogens) or panic (panicogens) in experimental models . Some of the most common substances are: sodium lactate, carbon dioxide (as carbogen), L-DOPA, caffeine, Modafinil, GABA antagonists such as DMCM, FG-7142 and ZK-93426, serotonergic agents such as mCPP and LY-293,284, adrenergic agents such as yohimbine, and cholecystokinin (CCK) (especially the tetrapeptide and octapeptide fragments CCK-4 and CCK-8). Studies have shown that 10 mL/kg of 0.5 molar sodium lactate infused intravenously over a 20-minute period will provoke a panic attack in most patients with panic disorder but not healthy control subjects.[2]
Anxiolytic substances have the opposite effect: they reduce anxiety. The most common class of anxiolytic drugs are benzodiazepines.
5-HT (5-hydroxytryptamine) is the chemical designation for the neurotransmitter serotonin. It’s role in the mood and anxiety disorders is huge.
5-HT1A Receptor
A 5-HT1A receptor is a subtype of a 5-HT (serotonin) receptor. In fact, it’s the most widespread of the 5-HT receptors.
Amongst other locations, 5-HT1A receptors are found in high densities in the cerebral cortex, hippocampus, and amygdala – all heavily involved in the mood and anxiety disorders.
Activation of 5-HT1A receptors decreases blood pressure and heart rate, and lowers body temperature. Other activation effects include decreased aggression or an increase in calm behavior, increased sociability, inhibition of addictive behavior, and the facilitation of sexual behavior and arousal.
On the other side of the coin, activation of 5-HT1A receptors generates increased impulsivity, inhibition of penile erection, and the impairment of cognition, learning, and memory.
Resources
Medical Dictionary
http://encyclopedia.thefreedictionary.com/anxiogenic
http://chipur.com/2011/06/18/5ht1a-receptor-agonists-relieve-depression-and-anxiety-what-are-they/
Receptors & Agonists For the purposes of our discussion, receptor refers to a neurotransmitter receptor.
Receptors are present on both postsynaptic and presynaptic neurons – the former being used to receive neurotransmitters, the latter for the purpose of preventing further release of a given neurotransmitter.
Each neurotransmitter has its own receptors. And it’s all about efficient electrical signaling.
synapse /syn·apse/ (sin´aps) the site of functional apposition between neurons, where an impulse is transmitted from one to another, usually by a chemical neurotransmitter released by the axon terminal of the presynaptic neuron. The neurotransmitter diffuses across the gap to bind with receptors on the postsynaptic cell membrane and cause electrical changes in that neuron (depolarization/excitation or hyperpolarization/inhibition).
An anxiolytic (also antipanic or antianxiety agent)[1] is a drug used for the treatment of anxiety and its related psychological and physical symptoms. Anxiolytics have been shown to be useful in the treatment of anxiety disorders.
Beta-receptor blockers such as propranolol and oxprenolol, although not anxiolytics, can be used to combat the somatic symptoms of anxiety.
Anxiolytics are also known as minor tranquilizers.
an·tag·o·nis·tic/anˌtagəˈnistik/
Adjective:
Showing or feeling active opposition or hostility toward someone or something.
Of or relating to an antagonist or its action. Synonyms:
hostile - inimical - adverse - opponent - opposed
Anxiogenic
An anxiogenic substance is one that causes anxiety. Anxiogenic effects can be measured by, for example, the hole-board test in rats and mice.[1] A number of agents are used to provoke anxiety (anxiogens) or panic (panicogens) in experimental models . Some of the most common substances are: sodium lactate, carbon dioxide (as carbogen), L-DOPA, caffeine, Modafinil, GABA antagonists such as DMCM, FG-7142 and ZK-93426, serotonergic agents such as mCPP and LY-293,284, adrenergic agents such as yohimbine, and cholecystokinin (CCK) (especially the tetrapeptide and octapeptide fragments CCK-4 and CCK-8). Studies have shown that 10 mL/kg of 0.5 molar sodium lactate infused intravenously over a 20-minute period will provoke a panic attack in most patients with panic disorder but not healthy control subjects.[2]
Anxiolytic substances have the opposite effect: they reduce anxiety. The most common class of anxiolytic drugs are benzodiazepines.
5-HT (5-hydroxytryptamine) is the chemical designation for the neurotransmitter serotonin. It’s role in the mood and anxiety disorders is huge.
5-HT1A Receptor
A 5-HT1A receptor is a subtype of a 5-HT (serotonin) receptor. In fact, it’s the most widespread of the 5-HT receptors.
Amongst other locations, 5-HT1A receptors are found in high densities in the cerebral cortex, hippocampus, and amygdala – all heavily involved in the mood and anxiety disorders.
Activation of 5-HT1A receptors decreases blood pressure and heart rate, and lowers body temperature. Other activation effects include decreased aggression or an increase in calm behavior, increased sociability, inhibition of addictive behavior, and the facilitation of sexual behavior and arousal.
On the other side of the coin, activation of 5-HT1A receptors generates increased impulsivity, inhibition of penile erection, and the impairment of cognition, learning, and memory.
Resources
Medical Dictionary
http://encyclopedia.thefreedictionary.com/anxiogenic
http://chipur.com/2011/06/18/5ht1a-receptor-agonists-relieve-depression-and-anxiety-what-are-they/
All About Endocannabinoids
Reference
http://emedicine.medscape.com/article/1361971-overview
Humans and animals alike naturally synthesize endocannabinoids, chemical compounds that activate the same receptors as delta-9-tetrahydrocannabinol (THC), the active component of marijuana (Cannabis sativa). Cannabis is famous for its significant psychoactive effects. Its ability to provide relief to chronic pain sufferers, to induce an increase in appetite, to alleviate nausea, and to ease anxiety are only some of the common uses for hemp.
History of endocannabinoid research
When Mechoulam and colleagues isolated THC in 1964, they made it possible to further understand the complex nature of the endocannabinoid system.[1] Other important events in endocannabinoid research are as follows:
1988 - Cannabinoid-binding sites in rat brains identified
1991 - Human cannabinoid receptor CB1 successfully cloned
1992 - Discovery of the first endocannabinoid, arachidonoyl ethanolamide, later named anandamide (a Sanskrit word for “internal bliss”)[2]
1993 - Peripheral CB2 receptor cloned
1995 - Discovery of a second endocannabinoid, 2-arachidonoyl glycerol (2-AG)
In the 21st century, new discoveries of other endocannabinoids, their site distributions, and roles are deepening our understanding of the endocannabinoid system.
Further investigation
Endocannabinoids are crucial to bioregulation. With scientific evidence suggesting their role in inflammation, insulin sensitivity, and fat and energy metabolism, inhibition of endocannabinoids may be a tool in reducing the prevalence of metabolic syndrome. Furthermore, modulation of the endocannabinoid system may be a cure for more chronic neurologic and immune conditions. Many questions are left unanswered about this relatively newly discovered regulatory system. Further investigation into this exciting field promises to shed insights into the mechanisms of health and disease and provide new therapeutic options.
Multiple human and animal studies support that endocannabinoids play a key role in memory, mood, brain reward systems, drug addiction, and metabolic processes, such as lipolysis, glucose metabolism, and energy balance.[3]
Through postsynaptic neuronal depolarization and an influx of calcium, the body activates N- acylphosphatidylethanolamine-hydrolyzing phospholipase D (NAPE-PLD) and diacylglycerol (DAG) lipase, which then build anandamide and 2-AG, respectively. Due to their lipophilic nature, the endocannabinoids act locally and are not synthesized until needed. Central nervous system messengers that act in a retrograde fashion, the endocannabinoids are agonists to CB1 and CB2.
CB1 and CB2 are G-protein receptors. CB1 receptors are abundant in the brain, specifically the mesocorticolimbic system, the spinal cord, and the peripheral neurons. CB1 receptors are particularly concentrated on gamma-aminobutyric acid (GABA) – releasing neurons (inhibitory neurons). Hence, activation of CB1 leads to retrograde suppression of neurotransmitter release. CB2 receptors are located peripherally, with a high density on immune-modulating cells and activated microglial.
CB1 receptor roles
CB1 receptor activation modulates food intake and energy metabolism through coordination of the mesolimbic reward system and the hypothalamus’ appetite control pathway. With fasting or starvation, anandamide and 2-AG levels increase in the limbic forebrain and, to a less significant extent, in the hypothalamus.
CB1 receptors aid in modulating hepatic lipogenesis. Activation in the liver leads to fatty acid synthesis, causing hepatic steatosis and diet-induced obesity.
CB1 activation aids in vasodilation and cardiac contractility, regulating blood pressure and improving left heart function. Activation of CB-1 receptors and, to a lesser extent, CB2 receptors by anandamide also reduces gastrointestinal motility and secretions. CB1 receptor activation inhibits proinflammatory responses in the colon. Moreover, hyperactivity of the endocannabinoid-signaling pathway contributes to the pathophysiology of Parkinson disease.[4, 5]
Obese and overweight individuals may have a mutation in fatty acid amide hydrolase, the enzyme that degrades anandamide.
Even in wild-type mice who develop diet-induced obesity, there is a hyperactive endocannabinoid system, with an increase in receptor availability and an increase in circulation endocannabinoids. In presatiated mice, an intrahypothalamic injection of anandamide induced substantial hyperphagia. Inactivation of CB1 receptors decreases plasma insulin and leptin levels, ultimately leading to more efficient energy metabolism.[6, 7]
CB2 receptor roles
CB2 selective agonists have proven to be helpful in reducing inflammation and undoing established inflammation hypersensitivity involved in peripheral pain and skin disorders. By reducing inflammatory cell infiltration and lipid peroxidation, CB2 receptor activation is protective against hepatic ischemia-reperfusion injury.
In addition to immunomodulatory pathways, CB2 receptors are involved in maintaining proper bone mass.[8] CB2 receptors are abundant in osteocytes, osteoclasts, and osteoblasts. CB2 agonists enhance endocortical osteoblast reproduction and activation, while inhibiting osteoclastogenesis.
Endocannabinoid degradationOnce their job is done at the presynaptic membrane, the endocannabinoids are quickly degraded through transport protein reuptake and hydrolyzation by fatty acid amide hydrolase (FAAH) and monoacylglycerol (MAG) lipase.[9]
Reference
http://emedicine.medscape.com/article/1361971-overview
Humans and animals alike naturally synthesize endocannabinoids, chemical compounds that activate the same receptors as delta-9-tetrahydrocannabinol (THC), the active component of marijuana (Cannabis sativa). Cannabis is famous for its significant psychoactive effects. Its ability to provide relief to chronic pain sufferers, to induce an increase in appetite, to alleviate nausea, and to ease anxiety are only some of the common uses for hemp.
History of endocannabinoid research
When Mechoulam and colleagues isolated THC in 1964, they made it possible to further understand the complex nature of the endocannabinoid system.[1] Other important events in endocannabinoid research are as follows:
1988 - Cannabinoid-binding sites in rat brains identified
1991 - Human cannabinoid receptor CB1 successfully cloned
1992 - Discovery of the first endocannabinoid, arachidonoyl ethanolamide, later named anandamide (a Sanskrit word for “internal bliss”)[2]
1993 - Peripheral CB2 receptor cloned
1995 - Discovery of a second endocannabinoid, 2-arachidonoyl glycerol (2-AG)
In the 21st century, new discoveries of other endocannabinoids, their site distributions, and roles are deepening our understanding of the endocannabinoid system.
Further investigation
Endocannabinoids are crucial to bioregulation. With scientific evidence suggesting their role in inflammation, insulin sensitivity, and fat and energy metabolism, inhibition of endocannabinoids may be a tool in reducing the prevalence of metabolic syndrome. Furthermore, modulation of the endocannabinoid system may be a cure for more chronic neurologic and immune conditions. Many questions are left unanswered about this relatively newly discovered regulatory system. Further investigation into this exciting field promises to shed insights into the mechanisms of health and disease and provide new therapeutic options.
Multiple human and animal studies support that endocannabinoids play a key role in memory, mood, brain reward systems, drug addiction, and metabolic processes, such as lipolysis, glucose metabolism, and energy balance.[3]
Through postsynaptic neuronal depolarization and an influx of calcium, the body activates N- acylphosphatidylethanolamine-hydrolyzing phospholipase D (NAPE-PLD) and diacylglycerol (DAG) lipase, which then build anandamide and 2-AG, respectively. Due to their lipophilic nature, the endocannabinoids act locally and are not synthesized until needed. Central nervous system messengers that act in a retrograde fashion, the endocannabinoids are agonists to CB1 and CB2.
CB1 and CB2 are G-protein receptors. CB1 receptors are abundant in the brain, specifically the mesocorticolimbic system, the spinal cord, and the peripheral neurons. CB1 receptors are particularly concentrated on gamma-aminobutyric acid (GABA) – releasing neurons (inhibitory neurons). Hence, activation of CB1 leads to retrograde suppression of neurotransmitter release. CB2 receptors are located peripherally, with a high density on immune-modulating cells and activated microglial.
CB1 receptor roles
CB1 receptor activation modulates food intake and energy metabolism through coordination of the mesolimbic reward system and the hypothalamus’ appetite control pathway. With fasting or starvation, anandamide and 2-AG levels increase in the limbic forebrain and, to a less significant extent, in the hypothalamus.
CB1 receptors aid in modulating hepatic lipogenesis. Activation in the liver leads to fatty acid synthesis, causing hepatic steatosis and diet-induced obesity.
CB1 activation aids in vasodilation and cardiac contractility, regulating blood pressure and improving left heart function. Activation of CB-1 receptors and, to a lesser extent, CB2 receptors by anandamide also reduces gastrointestinal motility and secretions. CB1 receptor activation inhibits proinflammatory responses in the colon. Moreover, hyperactivity of the endocannabinoid-signaling pathway contributes to the pathophysiology of Parkinson disease.[4, 5]
Obese and overweight individuals may have a mutation in fatty acid amide hydrolase, the enzyme that degrades anandamide.
Even in wild-type mice who develop diet-induced obesity, there is a hyperactive endocannabinoid system, with an increase in receptor availability and an increase in circulation endocannabinoids. In presatiated mice, an intrahypothalamic injection of anandamide induced substantial hyperphagia. Inactivation of CB1 receptors decreases plasma insulin and leptin levels, ultimately leading to more efficient energy metabolism.[6, 7]
CB2 receptor roles
CB2 selective agonists have proven to be helpful in reducing inflammation and undoing established inflammation hypersensitivity involved in peripheral pain and skin disorders. By reducing inflammatory cell infiltration and lipid peroxidation, CB2 receptor activation is protective against hepatic ischemia-reperfusion injury.
In addition to immunomodulatory pathways, CB2 receptors are involved in maintaining proper bone mass.[8] CB2 receptors are abundant in osteocytes, osteoclasts, and osteoblasts. CB2 agonists enhance endocortical osteoblast reproduction and activation, while inhibiting osteoclastogenesis.
Endocannabinoid degradationOnce their job is done at the presynaptic membrane, the endocannabinoids are quickly degraded through transport protein reuptake and hydrolyzation by fatty acid amide hydrolase (FAAH) and monoacylglycerol (MAG) lipase.[9]
http://rstb.royalsocietypublishing.org/site/2012/endocannabinoids.xhtml
Endocannabinoids in nervous system health and disease
The central nervous system is considered by many as the last great frontier of science. Indeed, the brain is the body's "commander-in-chief". What makes the nervous system an even more compelling subject of scientific inquiry, is the recent success medical science has had in other areas of disease. As cancer death rates and cardiovascular disease rates begin to drop, what remains-and what looms even larger as a cause of human disease and disability-are diseases of the nervous system. The latter as a whole account for more hospitalizations, more long-term care, and more chronic suffering than nearly all other disorders combined. We are now witnessing a marked improvement in the treatment of various neurological conditions thanks to the vast advancements in structural and functional neuro-imaging. The answer to all diseases lies at the molecular level - why should the brain be any different?
The Cannabis sativa plant has been exploited for medicinal, agricultural and spiritual purposes in diverse cultures over thousands of years. Indeed, reports of medicinal efficacy of cannabis can be traced back as far as 2700 BC in India. The serendipitous identification of a receptor at which cannabinoid compounds are active in the brain heralded an explosion in endocannabinoid research continuing to this day. The endocannabinoid system in the brain primarily influences communication between neurons, and affects biological functions including eating, anxiety, learning and memory, growth and development via an array of actions throughout the nervous system. In spite of recent scientific findings, much remains to be discovered as to where and when endocannabinoids function, and how endocannabinoid signalling may be exploited for therapeutic benefit. The more we can learn about the endocannabinoid system, the better will be the prospects for capitalizing on endocannabinoid-based therapies in each disease situation. This volume is dedicated to presenting the latest findings dealing with endocannabinoids in development, cellular and molecular neurobiology, behaviour, nervous system disease and aging, and therapeutics.
Issue compiled and edited by Stephen D. Skaper and Vincenzo Di Marzo
Issue will be published online in 2012.
Endocannabinoids in nervous system health and disease
The central nervous system is considered by many as the last great frontier of science. Indeed, the brain is the body's "commander-in-chief". What makes the nervous system an even more compelling subject of scientific inquiry, is the recent success medical science has had in other areas of disease. As cancer death rates and cardiovascular disease rates begin to drop, what remains-and what looms even larger as a cause of human disease and disability-are diseases of the nervous system. The latter as a whole account for more hospitalizations, more long-term care, and more chronic suffering than nearly all other disorders combined. We are now witnessing a marked improvement in the treatment of various neurological conditions thanks to the vast advancements in structural and functional neuro-imaging. The answer to all diseases lies at the molecular level - why should the brain be any different?
The Cannabis sativa plant has been exploited for medicinal, agricultural and spiritual purposes in diverse cultures over thousands of years. Indeed, reports of medicinal efficacy of cannabis can be traced back as far as 2700 BC in India. The serendipitous identification of a receptor at which cannabinoid compounds are active in the brain heralded an explosion in endocannabinoid research continuing to this day. The endocannabinoid system in the brain primarily influences communication between neurons, and affects biological functions including eating, anxiety, learning and memory, growth and development via an array of actions throughout the nervous system. In spite of recent scientific findings, much remains to be discovered as to where and when endocannabinoids function, and how endocannabinoid signalling may be exploited for therapeutic benefit. The more we can learn about the endocannabinoid system, the better will be the prospects for capitalizing on endocannabinoid-based therapies in each disease situation. This volume is dedicated to presenting the latest findings dealing with endocannabinoids in development, cellular and molecular neurobiology, behaviour, nervous system disease and aging, and therapeutics.
Issue compiled and edited by Stephen D. Skaper and Vincenzo Di Marzo
Issue will be published online in 2012.
http://www.ncbi.nlm.nih.gov/pubmed/23008748
Dtsch Arztebl Int. 2012 Jul;109(29-30):495-501. Epub 2012 Jul 23.
The therapeutic potential of cannabis and cannabinoids.
Grotenhermen F, Müller-Vahl K.
Source
nova-Institut GmbH, Chemiepark Knapsack, Hürth.
Abstract
BACKGROUND:
Cannabis-based medications have been a topic of intense study since the endogenous cannabinoid system was discovered two decades ago. In 2011, for the first time, a cannabis extract was approved for clinical use in Germany.
METHODS:
Selective literature review
RESULTS:
Cannabis-based medications exert their effects mainly through the activation of cannabinoid receptors (CB1 and CB2). More than 100 controlled clinical trials of cannabinoids or whole-plant preparations for various indications have been conducted since 1975. The findings of these trials have led to the approval of cannabis-based medicines (dronabinol, nabilone, and a cannabis extract [THC:CBD=1:1]) in several countries. In Germany, a cannabis extract was approved in 2011 for the treatment of moderate to severe refractory spasticity in multiple sclerosis. It is commonly used off label for the treatment of anorexia, nausea, and neuropathic pain. Patients can also apply for government permission to buy medicinal cannabis flowers for self-treatment under medical supervision. The most common side effects of cannabinoids are tiredness and dizziness (in more than 10% of patients), psychological effects, and dry mouth. Tolerance to these side effects nearly always develops within a short time. Withdrawal symptoms are hardly ever a problem in the therapeutic setting.
CONCLUSION:
There is now clear evidence that cannabinoids are useful for the treatment of various medical conditions.
Dtsch Arztebl Int. 2012 Jul;109(29-30):495-501. Epub 2012 Jul 23.
The therapeutic potential of cannabis and cannabinoids.
Grotenhermen F, Müller-Vahl K.
Source
nova-Institut GmbH, Chemiepark Knapsack, Hürth.
Abstract
BACKGROUND:
Cannabis-based medications have been a topic of intense study since the endogenous cannabinoid system was discovered two decades ago. In 2011, for the first time, a cannabis extract was approved for clinical use in Germany.
METHODS:
Selective literature review
RESULTS:
Cannabis-based medications exert their effects mainly through the activation of cannabinoid receptors (CB1 and CB2). More than 100 controlled clinical trials of cannabinoids or whole-plant preparations for various indications have been conducted since 1975. The findings of these trials have led to the approval of cannabis-based medicines (dronabinol, nabilone, and a cannabis extract [THC:CBD=1:1]) in several countries. In Germany, a cannabis extract was approved in 2011 for the treatment of moderate to severe refractory spasticity in multiple sclerosis. It is commonly used off label for the treatment of anorexia, nausea, and neuropathic pain. Patients can also apply for government permission to buy medicinal cannabis flowers for self-treatment under medical supervision. The most common side effects of cannabinoids are tiredness and dizziness (in more than 10% of patients), psychological effects, and dry mouth. Tolerance to these side effects nearly always develops within a short time. Withdrawal symptoms are hardly ever a problem in the therapeutic setting.
CONCLUSION:
There is now clear evidence that cannabinoids are useful for the treatment of various medical conditions.
eurasian_farmer
Member
Awesome thread!! Keep it going
^^^
agreed, interesting thead, but its gotten waaaaay off topic, looking for STRAINS known to be high in CBD, (often times are low-ish in TCH)
agreed, interesting thead, but its gotten waaaaay off topic, looking for STRAINS known to be high in CBD, (often times are low-ish in TCH)
Anyone in Colorado know if the Phnom Pehn high CBD cutting is alive and around?
http://herbalsynergyllc.com/mmj-tested-products/sample-1085-phomn-penn
^ second highest CBD content bud tested from those guys and highest overall cannabinoid content for a CBD rich strain.
Its a Thai Haze x Cambodian.
http://herbalsynergyllc.com/mmj-tested-products/sample-1085-phomn-penn
^ second highest CBD content bud tested from those guys and highest overall cannabinoid content for a CBD rich strain.
Its a Thai Haze x Cambodian.
village green
Member
I've been reading smoke reports on Outdoor Mix and Z7. Some people felt it didn't help with pain and anxiety in the way they hoped it would. I think they were expecting something more sedating but instead got something that was more like an ADHD stimulant without feeling wired. I think CBD varieties will differ in the effect according to the indica/sativa percentages. I'll probably get CBD Critical Mass and CBD Yummy to allow more sedation and alertness, respectively. Any smoke reports?
Nirvana_Papaya
Member
I just invested quite a bit into high cbd strains.
Got:
Night Queen - Mostly Indica
CBD Skunk Haze - Mostly Sativa
CBD Shark - Mostly Indica
CBD Nordle - Mostly Indica
Otto #1 ( little to no THC ) - Mostly Sativa
Blue Mystic - Mostly Indica
All of them claim to have medium to high CBD. Will be posting smoke reports in like 4 months. Not very helpful right now I know. I'm hoping it can help keep me stable, been going crazy lately.
Got:
Night Queen - Mostly Indica
CBD Skunk Haze - Mostly Sativa
CBD Shark - Mostly Indica
CBD Nordle - Mostly Indica
Otto #1 ( little to no THC ) - Mostly Sativa
Blue Mystic - Mostly Indica
All of them claim to have medium to high CBD. Will be posting smoke reports in like 4 months. Not very helpful right now I know. I'm hoping it can help keep me stable, been going crazy lately.
blue mystic is high in CBDs? i wonder about Blue dream.
