Balster R L
Department of Pharmacology and Toxicology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA.
Drug Alcohol Depend. 1998 Jun-Jul;51(1-2):207-14. doi: 10.1016/s0376-8716(98)00078-7.
It should be apparent from this review that far less is known about the neural basis for inhalant abuse than for other forms of drug abuse. This reflects a lack of research interest in this area (Balster, 1997). Indeed, conclusions are difficult to draw. In the case of the volatile alkyl nitrites, the most reasonable hypothesis at this time is that the cellular basis for their abuse resides in their actions on smooth muscles to produce vasodilation and relaxation, however, direct effects on the brain cannot be ruled out. Although there is some evidence that analgesic effects of nitrous oxide may involve opiate systems, even this conclusion is controversial. There is no evidence that opiate systems play a role in nitrous oxide intoxication or reinforcement. The mechanisms for these effects are unknown. They may reflect the same actions on lipid membranes or on hydrophobic sites on unspecified proteins that have been proposed as mechanisms for nitrous oxide anesthesia. In the case of the volatile solvents, fuels and anesthetics we are faced with a wide variety of specific chemicals which may produce different profiles of pharmacological effects. There is evidence that the prototypic abused solvents toluene and trichloroethane produce acute effects similar to subanesthetic concentrations of general anesthetics, as well as to the effects of classical CNS depressant drugs, such as alcohol and the barbiturates. For the anesthetics, evidence suggests that enhancement of GABAergic inhibition may be an important cellular target for their acute effects, just as it is for alcohol and other depressant drugs. For toluene, as with alcohol, recent evidence suggests a possible role for inhibition of glutamatergic neurotransmission involving NMDA receptors. Toluene has also been shown to have some dopaminergic effects which may be important to its abuse. As for the large number of other abused vapors, practically no information can be found on their cellular actions, and certainly not on actions that may be relevant to their abuse. This entire area would seem an important direction for future research.
从这篇综述中可以明显看出，与其他形式的药物滥用相比，人们对吸入剂滥用的神经基础了解得要少得多。这反映出该领域缺乏研究兴趣（巴尔斯特，1997年）。确实，很难得出结论。就挥发性亚硝酸烷基酯而言，目前最合理的假设是，其滥用的细胞基础在于它们对平滑肌的作用，从而产生血管舒张和松弛，然而，对大脑的直接影响也不能排除。尽管有一些证据表明一氧化二氮的镇痛作用可能涉及阿片系统，但即使这一结论也存在争议。没有证据表明阿片系统在一氧化二氮中毒或强化作用中起作用。这些作用的机制尚不清楚。它们可能反映了对脂质膜或未指明蛋白质上疏水位点的相同作用，这些作用已被提出作为一氧化二氮麻醉的机制。就挥发性溶剂、燃料和麻醉剂而言，我们面临着各种各样的特定化学物质，它们可能产生不同的药理作用谱。有证据表明，典型的滥用溶剂甲苯和三氯乙烷产生的急性效应类似于亚麻醉浓度的全身麻醉剂，以及经典中枢神经系统抑制药物（如酒精和巴比妥类药物）的效应。对于麻醉剂，有证据表明增强GABA能抑制可能是其急性效应的一个重要细胞靶点，就像对酒精和其他抑制药物一样。对于甲苯，与酒精一样，最近的证据表明，抑制涉及NMDA受体的谷氨酸能神经传递可能起作用。甲苯还被证明具有一些多巴胺能效应，这可能对其滥用很重要。至于大量其他滥用的蒸汽，几乎找不到关于它们细胞作用的信息，当然也找不到可能与其滥用相关的作用的信息。这整个领域似乎是未来研究的一个重要方向。
