PCDVD數位科技討論區 - 涉吸大麻傳拘庹宗康屈中恆

引用:

作者FD3STYPER

大麻, 抽了頂多就覺得莫名其妙很愉快.
拉K或是MDMA這種抗鬱劑也差不多, 濫用頂多中心神經失調.
安非他命頂多竟是騙過大腦可以超時工作.

以上都是軟性毒品, 也是二級毒品, 其實都沒啥重罪.

4號或是古柯鹼, 高檔也致命, 不過這種東西就是循序漸進,
嚐過軟的就會想來硬的, 下場通常很悽慘.

有看過四號巴很大的人就知道, 手臂上都洞, 沒得走最後走手指指縫. 古柯鹼用鼻子吸,
搞到最後氣管纖毛會直接失去作用, 就不用說黏膜被破壞殆盡, 當然, 人也爛了.

至於藝人, 就不用提了, 過太爽錢好賺, 當吃喝**賭都沒辦法滿足自己的時候,
就是走上吸毒.

也不用舉例, 他們很多都是轟啪, 最喜歡找漂亮大學女生同歡.

有這些寶貝 , 自己享用都來不及了 , 應該沒人會去找女人才對 .

THC (Tetrahydrocannabinol) 四氫大麻酚
http://en.wikipedia.org/wiki/Tetrahydrocannabinol
Recent research has shown that many adverse side effects, generally known as the "stoner" stereotype, fail to hold up to the scientific method. Recent studies with synthetic cannabinoids show that activation of CB1 receptors can facilitate neurogeneration, as well as neuroprotection, and can even help prevent natural neural degredation from neurodegenerative diseases such as MS, Parkinson's, and Alzheimer's. This, along with research into the CB2 receptor (throughout the immune system), has given the case for medical marijuana more support.

http://en.wikipedia.org/wiki/Ketamine
Ketamine/PCP 是所謂的解離性麻醉劑 , 其主要作用機制是 NMDA 接受器 (N-methyl d-aspartate, 氮-甲基左旋天門冬胺酸) 的非競爭性拮抗劑 . NMDA 接受器的主要功用是接受麩胺酸 (MSG/味精/單鈉麩胺酸) 之後就開啟 . Ketamine/NMDA receptor 主導的鎮痛作用不被 naloxone 所抑制 .

Ketamine, like Phencyclidine, is primarily a non-competitive antagonist of the NMDA receptor, which opens in response to binding of the neurotransmitter glutamate. This NMDA receptor mediates the analgesic (reduction of pain) effects of ketamine at low doses. Evidence for this is reinforced by the fact that naloxone, an opioid antagonist, does not reverse the analgesia. Studies also seem to indicate that ketamine is 'use dependent' meaning it only initiates its blocking action once a glutamate binds to the NMDA receptor.

At high, fully anesthetic level doses, ketamine has also been found to bind to opioid mu receptors and sigma receptors. Thus, loss of consciousness that occurs at high doses may be partially due to binding at the opioid mu and sigma receptors.

http://en.wikipedia.org/wiki/MDMA 安非他命 (苯丙胺)
Serotonin is a neurotransmitter believed to play a role in the regulation of mood and pleasure. MDMA causes serotonin vesicles in the neurons to release quantities of serotonin into the synapses. Although popular press accounts focus on the role of serotonin release, the mechanism by which MDMA causes its unusual psychoactivity is largely unknown. In vitro and nonhuman animal studies have established that MDMA also induces dopamine, norepinephrine, and acetylcholine release and can act directly on a number of receptors, including a2-adrenergic (adrenaline) and 5HT2A (serotonin) receptors. MDMA promotes the release of several hormones including prolactin and the antidiuretic hormone vasopressin, which may be important in its occasional production of water intoxication or hyponatremia.

http://en.wikipedia.org/wiki/Cocaine
The pharmacodynamics of cocaine are complex. One significant effect of cocaine on the central nervous system is the blockage of the dopamine transporter protein (DAT), hence cocaine is called a dopamine reuptake inhibitor. Brain regions that are rich with dopaminergic neurons are the ventral tegmental area (VTA), and the substantia nigra (SN). The dopamine (DA) neurons of the VTA send axons to the nucleus accumbens (nAC) and the prefrontal cortex (PFC) and release DA presynaptically on the neurons in these regions. While the precise role of DA in the subjective experience of reward is controversial among neuroscientists, the release of DA in the nAC is widely considered to be responsible for cocaine's rewarding effects. This conclusion is largely based on laboratory data involving rats that are trained to self-administer cocaine intravenously (i.v.). If DA antagonists are infused directly into the nAC, well-trained rats self-administering cocaine will undergo extinction (i.e., initially increase responding only to stop completely) thereby indicating that cocaine is no longer reinforcing (i.e., rewarding) drug-seeking behavior.