Ok As Promised - Suggestions To Halt...
Society & Culture0 min ago
cannabis
32 Answers
can someone answer my question i put in the science section. Just realised i could be asking the wrong people ! ta
Answers
Best Answer
No best answer has yet been selected by darrensmith. Once a best answer has been selected, it will be shown here.
For more on marking an answer as the "Best Answer", please visit our FAQ.
The active compound in herbal cannabis, 9-tetrahydrocannabinol, exerts all of its known central effects through the CB1 cannabinoid receptor. Research on cannabinoid mechanisms has been facilitated by the availability of selective antagonists acting at CB1 receptors and the generation of CB1 receptor knockout mice. Particularly important classes of neurons that express high levels of CB1 receptors are GABAergic interneurons in hippocampus, amygdala and cerebral cortex, which also contain the neuropeptides cholecystokinin. Activation of CB1 receptors leads to inhibition of the release of amino acid and monoamine neurotransmitters. The lipid derivatives anandamide and 2-arachidonylglycerol act as endogenous ligands for CB1 receptors (endocannabinoids). They may act as retrograde synaptic mediators of the phenomena of depolarization-induced suppression of inhibition or excitation in hippocampus and cerebellum. Central effects of cannabinoids include disruption of psychomotor behaviour, short-term memory impairment, intoxication, stimulation of appetite, antinociceptive actions (particularly against pain of neuropathic origin) and anti-emetic effects. Although there are signs of mild cognitive impairment in chronic cannabis users there is little evidence that such impairments are irreversible, or that they are accompanied by drug-induced neuropathology. A proportion of regular users of cannabis develop tolerance and dependence on the drug. Some studies have linked chronic use of cannabis with an increased risk of psychiatric illness, but there is little evidence for any causal link. The potential medical applications of cannabis in the treatment of painful muscle spasms and other symptoms of multiple sclerosis are currently being tested in clinical trials. Medicines based on drugs that enhance the function of endocannabinoids may offer novel therapeutic approaches in the future.
lol my son is 25, he smoke3d it for at least 5 years and i went thru the living hell you would expect, he says i made out he was some crack sniffing junkie and it was 'only cannabis', now he never touches it but he does have some obsessive compulsive tendancies what even he is becomning aware of, and so i do sometimes feel there has been damage, but he was not a daily user and he has found his senses, if he had been using it for pain relief that would have been another matter, but him and his mates were just like thousands of other teenagers who have tried it and are still trying it regularly.
drugs are controled crete.... if i were in need on a bit of skunk or ANY other drug to cure pain, ide take it.... no iffs and no buts.
but there are laws governing what we can and cant consume !
in my own defence.... i didnt read dots full and very informative answer... i read the title "cannabis".... nothing more.
but there are laws governing what we can and cant consume !
in my own defence.... i didnt read dots full and very informative answer... i read the title "cannabis".... nothing more.
So which part was from memory Dot ? It looks remarkably like a yahoo answer. Naughty Dot. Ah , the wonder of google hee hee. Have to split it up to fit the whole answer in.
Best Answer - Chosen by Asker
The active compound in herbal cannabis, Delta(9)-tetrahydrocannabinol, exerts all of its known central effects through the CB(1) cannabinoid receptor. Research on cannabinoid mechanisms has been facilitated by the availability of selective antagonists acting at CB(1) receptors and the generation of CB(1) receptor knockout mice. Particularly important classes of neurons that express high levels of CB(1) receptors are GABAergic interneurons in hippocampus, amygdala and cerebral cortex, which also contain the neuropeptides cholecystokinin. Activation of CB(1) receptors leads to inhibition of the release of amino acid and monoamine neurotransmitters. The lipid derivatives anandamide and 2-arachidonylglycerol act as endogenous ligands for CB(1) receptors (endocannabinoids). They may act as retrograde synaptic mediators of the phenomena of depolarization-induced suppression of inhibition or excitation in hippocampus and cerebellum.
Best Answer - Chosen by Asker
The active compound in herbal cannabis, Delta(9)-tetrahydrocannabinol, exerts all of its known central effects through the CB(1) cannabinoid receptor. Research on cannabinoid mechanisms has been facilitated by the availability of selective antagonists acting at CB(1) receptors and the generation of CB(1) receptor knockout mice. Particularly important classes of neurons that express high levels of CB(1) receptors are GABAergic interneurons in hippocampus, amygdala and cerebral cortex, which also contain the neuropeptides cholecystokinin. Activation of CB(1) receptors leads to inhibition of the release of amino acid and monoamine neurotransmitters. The lipid derivatives anandamide and 2-arachidonylglycerol act as endogenous ligands for CB(1) receptors (endocannabinoids). They may act as retrograde synaptic mediators of the phenomena of depolarization-induced suppression of inhibition or excitation in hippocampus and cerebellum.
(Next bit) Central effects of cannabinoids include disruption of psychomotor behaviour, short-term memory impairment, intoxication, stimulation of appetite, antinociceptive actions (particularly against pain of neuropathic origin) and anti-emetic effects. Although there are signs of mild cognitive impairment in chronic cannabis users there is little evidence that such impairments are irreversible, or that they are accompanied by drug-induced neuropathology. A proportion of regular users of cannabis develop tolerance and dependence on the drug. Some studies have linked chronic use of cannabis with an increased risk of psychiatric illness, but there is little evidence for any causal link. The potential medical applications of cannabis in the treatment of painful muscle spasms and other symptoms of multiple sclerosis are currently being tested in clinical trials. Medicines based on drugs that enhance the function of endocannabinoids may offer novel therapeutic approaches in the future.
The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body�s natural morphines.
The sensations of slight euphoria, relaxation, and amplified auditory and visual perceptions produced by marijuana are due almost entirely to its effect on the cannabinoid receptors in the brain. These receptors are present almost everywhere in the brain, and an endogenous molecule that binds to them naturally has been identified: anandamide. We are thus dealing with the same kind of mechanism as in the case of opiates that bind directly to the receptors for endorphins, the body�s natural morphines.
Anandamide is involved in regulating mood, memory, appetite, pain, cognition, and emotions. When cannabis is introduced into the body, its active ingredient, Delta-9-tetrahydrocannabinol (THC), can therefore interfere with all of these functions.
THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain�s neural networks is thus reduced as well.
However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain�s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
Research teams from Louisiana, Japan and Scotland report on endocannabinoids as a novel neural messenger in various stress-related situations with possible applications in eating, disease treatment and social behavior. Led by Shi Di, the Tulane/LSU team found that endocannabinoids acted as an intrabrain messenger to shutdown the neuroendocrine stress response. The Japanese team, headed by Atsushi Soya, said it next would look at endocannabinoids involvement in autonomic, endocrine and immune function. The Edinburgh group led by Nancy Sabatier is studying endocannabinoids' influence on
THC begins this process by binding to the CB1 receptors for anandamide. These receptors then modify the activity of several intracellular enzymes, including cAMP, whose activity they reduce. Less cAMP means less protein kinase A. The reduced activity of this enzyme affects the potassium and calcium channels so as to reduce the amount of neurotransmitters released. The general excitability of the brain�s neural networks is thus reduced as well.
However, in the reward circuit, just as in the case of other drugs, more dopamine is released. As with opiates, this paradoxical increase is explained by the fact that the dopaminergic neurons in this circuit do not have CB1 receptors, but are normally inhibited by GABAergic neurons that do have them. The cannabis removes this inhibition by the GABA neurons and hence activates the dopamine neurons.
In chronic consumers of cannabis, the loss of CB1 receptors in the brain�s arteries reduces the flow of blood, and hence of glucose and oxygen, to the brain. The main results are attention deficits, memory loss, and impaired learning ability.
Research teams from Louisiana, Japan and Scotland report on endocannabinoids as a novel neural messenger in various stress-related situations with possible applications in eating, disease treatment and social behavior. Led by Shi Di, the Tulane/LSU team found that endocannabinoids acted as an intrabrain messenger to shutdown the neuroendocrine stress response. The Japanese team, headed by Atsushi Soya, said it next would look at endocannabinoids involvement in autonomic, endocrine and immune function. The Edinburgh group led by Nancy Sabatier is studying endocannabinoids' influence on
"Rapid glucocorticoid-mediated endocannabinoid release and opposing regulation of glutamate and GABA inputs to hypothalamic magnocellular neurons." Funded by NIH. Shi Di, Victor Marcheselli, Nicolas Bazan, Jeffrey Tasker. Di and Tasker are at the Neurobiology Division and Cell & Molecular Biology Department at Tulane University, New Orleans; Tasker is also at the Neuroscience Program; Marcheselli and Bazan are at the Neuroscience Center, Louisiana State University Health Sciences Center, New Orleans.
"Cannabinoid modulates synaptic inputs to the supraoptic nucleus neuron in rats." Atsushi Soya, Ryota Serino, Tatsushi Onaka, Takeshi Terao, Jun Nakamura, Yoichi Ueta. Soya and Ueta are at Dept. of Physiology School of Medicine, University of Occupational & Environmental Health (UOEH), Kitakyushu; Serino is at the UOEH Dept. of Internal Medicine; Onaka is at Division of Integrative Physiology, Dept. of Physiology, Jichi Medical School; Terao is at Dept. of Psychiatry, Oita University School of Medicine; and Nakaura is at UOEH Dept. of Psychiatry.
"Cannabanoids inhibit excitatory responses of supraoptic neurons to stimulation of OVLT in vivo." Nancy Sabatier, Gareth Leng, University of Edinburgh, Scotland.
Source(s):
http://www.greatindianspices.com...
5 days ago - Report Abuse
What would Bibatha T say about you copying her answer to what is brain Cannabis ? on Yahoo. Naughty Dot. You could have at least referenced her.
"Cannabinoid modulates synaptic inputs to the supraoptic nucleus neuron in rats." Atsushi Soya, Ryota Serino, Tatsushi Onaka, Takeshi Terao, Jun Nakamura, Yoichi Ueta. Soya and Ueta are at Dept. of Physiology School of Medicine, University of Occupational & Environmental Health (UOEH), Kitakyushu; Serino is at the UOEH Dept. of Internal Medicine; Onaka is at Division of Integrative Physiology, Dept. of Physiology, Jichi Medical School; Terao is at Dept. of Psychiatry, Oita University School of Medicine; and Nakaura is at UOEH Dept. of Psychiatry.
"Cannabanoids inhibit excitatory responses of supraoptic neurons to stimulation of OVLT in vivo." Nancy Sabatier, Gareth Leng, University of Edinburgh, Scotland.
Source(s):
http://www.greatindianspices.com...
5 days ago - Report Abuse
What would Bibatha T say about you copying her answer to what is brain Cannabis ? on Yahoo. Naughty Dot. You could have at least referenced her.
