What We're Not Talking about When We Talk about Addiction

The landscape of addiction is dominated by two rival models: a moral model and a model that characterizes addiction as a neurobiological disease of compulsion. Against both, I offer a scientifically and clinically informed alternative. Addiction is a highly heterogenous condition that is ill-characterized as involving compulsive use. On the whole, drug consumption in addiction remains goal directed: people take drugs because drugs have tremendous value. This view has potential implications for the claim that addiction is, in all cases, a brain disease. But more importantly, it has implications for clinical and policy interventions. To help someone overcome addiction, you need to understand and address why they persist in using drugs despite negative consequences. If they are not compelled, then the explanation must advert to the value of drugs for them as an individual. What blocks us from acknowledging this reality is not science but fear: that it will ignite moralism about drugs and condemnation of drug users. The solution is not to cleave to the concept of compulsion but to fight moralism directly.     

‘Hot’ vs. ‘cold’ behavioural‐cognitive styles: motivational‐dopaminergic vs. cognitive‐cholinergic processing of a Pavlovian cocaine cue in sign‐ and goal‐tracking rats

Discrete Pavlovian reward cues acquire more potent incentive motivational properties (incentive salience) in some animals (sign‐trackers; STs) compared to others (goal‐trackers; GTs). Conversely, GTs appear to be better than STs in processing more complex contextual cues, perhaps reflecting their relatively greater bias for goal‐directed cue processing. Here, we investigated the activity of two major prefrontal neuromodulatory input systems, dopamine (DA) and acetylcholine (ACh), in response to a discrete Pavlovian cue that was previously paired with cocaine administration in STs and GTs. Rats underwent Pavlovian training in which light cue presentations were either paired or unpaired with an intravenous cocaine infusion. Following a 10‐day abstinence period, prefrontal dialysates were collected in STs and GTs during cue presentations in the absence of cocaine. In STs, the cue previously paired with cocaine significantly increased prefrontal DA levels. DA levels remained elevated over baseline across multiple cue presentation blocks, and DA levels and approaches to the cue were significantly correlated. In STs, ACh levels were unaffected by cue presentations. In contrast, in GTs, presentations of the cocaine cue increased prefrontal ACh, but not DA, levels. GTs oriented towards the cue at rates similar to STs, but they did not approach it and elevated ACh levels did not correlate with conditioned orientation. The results indicate a double dissociation between the role of prefrontal DA and ACh in STs and GTs, and suggest that these phenotypes will be useful for studying the role of neuromodulator systems in mediating opponent behavioural‐cognitive styles.     

大学生电脑游戏成瘾问卷的编制

目的编制大学生电脑游戏成瘾问卷。方法通过对546名大学生调查数据的探索性因素分析和242名大学生数据的验证性因素分析,检验大学生电脑游戏成瘾问卷的信度和效度。结果大学生电脑游戏成瘾问卷包含24个项目,可聚合为时间管理、情绪体验、生活冲突、牺牲社交和戒断困难五个因子。24个项目的载荷范围是0.513-0.838,五个因子解释了总方差的59.62%。量表各维度的内部一致性系数为0.78-0.84,分半信度为0.68-0.91,重测信度为0.79-0.88。验证性因素分析结果显示问卷的RMSEA小于0.08,CFI、RFE、IFI、NFI、NNFI都在0.90以上。结论该问卷的因素结构清晰,信度和效度较好。     

Effects of 9 -tetrahydrocannabinol and ethyl alcohol on adjunctive behavior and the lateral hypothalamus

The fact that electrical stimulation of the lateral hypothalamus (LH) can be substituted for the delivery of a food pellet in typical schedule induced polydipsia was established and demonstrated the role of this part of the brain in the mediation of adjunctive behavior. The assumption that Δ⁹-tetrahydrocannabinol (Δ⁹-THC) and ethyl alcohol affect behavior because of a differential effect on the same LH mechanism was supported by the following evidence. Relatively small doses of Δ⁹-THC, 0.25, 0.375, and 0.50 mg/kg, enhanced adjunctive drinking; whereas, larger quantities of 0.625 and 0.75 mg/kg had no appreciable effects. The effect is somewhat specific, as it did not occur with strychnine sulfate, and rate dependent within limits as it was most pronounced in animals with low rates of responding or in animals when responding at a low rate. The effect of rate dependency was also apparent with fixed interval schedules of 2 and 4 min and a multiple schedule of a fixed interval and a signalled timed out period of nonreinforcement. Low rates of responding were enhanced by all doses of Δ⁹-THC, 1.0, 1.5, 2.0, 2,5, and 3.0 mg/kg, and there was an obvious dose related decrease in high rates. A similar effect was observed with low and high rates of electrical self-stimulation through implanted LH electrodes. The hypothesis that some drugs such as Δ⁹-THC and ethyl alcohol can enhance the positive feedback in an LH mediated motor control system by the facilitation of the same mechanism which initially generated the behavior was confirmed. Oral self administration of ethyl alcohol in a saccharin sweetened fluid enhanced recovered adjunctive drinking of the solution in quantities which should be sufficient to produce physical dependence if continued for relatively long periods. Recovered adjunctive drinking occurs in animals without food or water deprivation and it is an intense and persistent phenomenon.     

Microanatomy of dendritic spines: emerging principles of synaptic pathology in psychiatric and neurological disease.

Psychiatric and neurologic disorders ranging from mental retardation to addiction are accompanied by structural and functional alterations of synaptic connections in the brain. Such alterations include abnormal density and morphology of dendritic spines, synapse loss, and aberrant synaptic signaling and plasticity. Recent work is revealing an unexpectedly complex biochemical and subcellular organization of dendritic spines. In this review, we highlight the molecular interplay between functional domains of the spine, including the postsynaptic density, the actin cytoskeleton, and membrane trafficking domains. This research points to an emerging level of analysis--a microanatomical understanding of synaptic physiology--that will be critical for discerning how synapses operate in normal physiologic states and for identifying and reversing microscopic changes in psychiatric and neurologic disease.