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上瘾这事,社会学家怎么说我不在乎
我是药理学的,我不信这些social scientist
大麻药理如下,自己看,资料源于
Rang HP, Ritter JM, Flower RJ, Henderson G (2014). Rang & Dale's Pharmacology: With student consult online access. edn. Elsevier Health Sciences.
Cannabinoids, being highly lipid soluble, were originally thought to act in a similar way to general anaesthetics. However, in 1988, saturable high-affinity binding of a tri- tiated cannabinoid was demonstrated in membranes prepared from homogenised rat brain. This led to the identification of specific cannabinoid receptors in brain. These are now termed CB 1 receptors to distinguish them from the CB 2 receptors subsequently identified in peripheral tissues. Cannabinoid receptors are typical members of the family of G-protein-coupled receptors (Ch. 3). CB 1 receptors are linked via G i/o to inhibition of adenylyl cyclase and of voltage-operated calcium channels, and to activation of G-protein-sensitive inward-rectifying potassium (GIRK) channels, causing hyperpolarisation (Fig. 18.2). These effects are similar to those mediated by opioid receptors (Ch. 41). CB 1 receptors are located in the plasma membrane of nerve endings and inhibit transmitter release from presynaptic terminals, which is caused by depolarisation and Ca 2+ entry (Ch. 4). CB receptors also influence gene expression, both directly by activating mitogen-activated protein kinase, and indirectly by reducing the activity of protein kinase A as a result of reduced adenylyl cyclase activity (see Ch. 3). CB 1 receptors are among the most abundant receptors in the brain, being comparable in this regard with receptors for glutamate and GABA— the main central excitatory and inhibitory neurotransmitters (Ch. 37). They are not homogeneously distributed, being concentrated in the hippocampus (relevant to effects of cannabinoids on memory), cerebellum (relevant to loss of coordination), hypothalamus (important in control of appetite and body temperature; see Ch. 29 and below), substantia nigra, mesolimbic dopamine pathways that have been implicated in psychological ‘reward’ (Ch. 48), and in association areas of the cerebral cortex. There is a relative paucity of CB 1 receptors in the brain stem, perhaps explaining the lack of serious respiratory or cardiovascular toxicity of the cannabinoids. At a cellular level, CB 1 receptors are localised presynaptically, and inhibit transmitter release as explained above. Like opioids, they can, however, increase the activity of some neuronal pathways by inhibiting inhibitory connections, including GABA-ergic interneurons in the hippocampus and amygdala.
In addition to their well-recognised location in the CNS, CB 1 receptors are also expressed in peripheral tissues, for example on endothelial cells, adipocytes and peripheral nerves. Cannabinoids promote lipogenesis through activation of CB 1 receptors, an action that could contribute to their effect on body weight (Cota et al., 2003). The CB 2 receptor has only approximately 45% amino acid homology with CB 1 and is located mainly in lymphoid tissue (spleen, tonsils and thymus as well as circulating lymphocytes, monocytes and tissue mast cells). CB 2 receptors are also present on microglia— immune cells in the CNS (Ch. 36). The localisation of CB 2 receptors on cells of the immune system was unexpected, but may account for inhibitory effects of cannabis on immune function. CB 2 receptors differ from CB 1 receptors in their responsiveness to cannabinoid ligands (see Table 18.1). They are linked via G i/o to adenylyl cyclase, GIRK channels and mitogenactivated protein kinase similarly to CB 1 , but not to voltageoperated calcium channels (which are not expressed in immune cells). So far, rather little is known about their function. They are present in atherosclerotic lesions (see Ch. 22), and CB 2 agonists have antiatherosclerotic effects (Mach & Steffens, 2008). Some endocannabinoids turned out, surprisingly, 1 to activate vanilloid receptors, ionotropic receptors that stim1 Surprising because capsaicin, the active principle of chilli peppers, causes intense burning pain, whereas the endocannabinoid anandamide is associated with pleasure, or even bliss … so perhaps not so surprising after all! ulate nociceptive nerve endings (see Ch. 41). Other asyet-unidentified G-protein-coupled receptors are also implicated, because cannabinoids exhibit analgesic actions and activate G-proteins in the brain of CB 1 knockout mice despite the absence of CB 1 receptors.
最后一句关于总结的:
Tolerance to cannabis, and physical dependence, occur to a minor degree and mainly in heavy users. The abstinence symptoms are similar to those of ethanol or opiate withdrawal, namely nausea, agitation, irritability, confusion, tachycardia and sweating, but are relatively mild and do not result in a compulsive urge to take the drug.
成不成瘾,不是社会学家研究的,他们不懂。 |
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