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Legal distinctions are made in the Opium Law between drugs with a low risk of harm and/or addiction, called 'soft drugs', and drugs with a high risk of harm and/or addiction, called 'hard drugs'. Soft drugs include hash, marijuana, sleeping pills and sedatives, while hard drugs include heroin, cocaine, amphetamine, LSD and ecstasy. Policy has been to largely tolerate the sale of soft drugs while strongly suppressing the sale, circulation and use of hard drugs, effectively separating it into two markets. Establishments that have been permitted to sell soft drugs under certain circumstances are called coffee shops.[3] Laws established in January 2013 required visitors of coffee shops to be Dutch residents, but these laws were only applied in Zeeland, North Brabant and Limburg after much local criticism.[4][5] Possession of a soft drug for personal use in quantities below a certain threshold (5 grams of cannabis or 5 cannabis plants) is tolerated, but larger quantities or possession of hard drugs may lead to prosecution. Prosecution for possession, trade and (in some rare cases) use are typically handled by the municipal government except where large-scale criminal activity is suspected.[6][7]

The initiation of psychostimulant sensitization depends on the mesocorticolimbic dopamine (DA) system. Although many cellular adaptations has been reported to be associated with this addictive behavior, the overall influence of these adaptations on the network regulation of DA neurons has not been established. Here, we profile a network-driven slow oscillation (SO) in the firing activity of ventral tegmental area (VTA) putative DA and non-DA neurons and their correlation with locomotor sensitization induced by repeated administration of cocaine. One day after the last cocaine injection, the power of SO (Pso) significantly increased both in DA and non-DA neurons. Interestingly, the Pso in DA neurons was positively correlated, while Pso in non-DA neurons was negatively correlated with the level of locomotor sensitization. On the other hand, the firing rates of DA and non-DA neurons were both elevated, but none exhibited any correlation with the level of sensitization. Fourteen days after the last injection, the Pso of DA neurons dissipated but still positively correlated with the level of sensitization. In contrast, the Pso in non-DA neurons lost correlation with locomotor sensitization. These results suggest that cocaine-induced locomotor sensitization is associated with long-term network adaptation in DA system and that DA and non-DA neurons may corporately facilitate/hamper the initiation of locomotor sensitization.

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The mesocorticolimbic dopamine (DA) circuit, as the center for drug abuse and addiction1,2, undergoes long-term adaptations in response to repeated drug use, which promotes a risk of relapse after drug withdrawal3. Abusive drugs exert their rewarding effects, in part, by modulating the activity of DA and non-DA neurons within the ventral tegmental area (VTA)4,5. In rodents, repeated administration of many abusive drugs (i.e. cocaine, amphetamine and opioids) produces locomotor sensitization: a progressive and persistent augmentation of behavioral response to psychostimulants6. This behavioral phenomenon resembles some addiction-related features in humans6,7.

The development of locomotor sensitization is associated with increased activity in the mesocorticolimbic DA circuit, particularly in the VTA8. Several studies in brain slices have demonstrated that exposure to psychostimulants elicits drug-evoked synaptic plasticity in both excitatory and inhibitory inputs in VTA DA and non-DA neurons3,9,10,11,12. Another important mechanism that the altered activity is through intrinsic regulation of ion channels such as GABAB receptor (GABABR)-dependent G-protein-gated inwardly-rectifying K (GirK) channel13,14. Together, these neuroadaptations lead to significant alterations of firing activity in VTA neurons. VTA DA neurons fire in two patterns in vivo: irregular single-spike firing and burst firing15,16,17. Repeated cocaine administration results in an initial increase and later decrease over withdrawal time in the number of spontaneously active VTA DA neurons and in their mean firing rate18,19. It also facilitates the switch of DA neuron firing from single-spike to burst, which augments DA release in the VTA and nucleus accumbens20,21. These changes of firing activity in VTA DA neurons are believed to be involved in the development of behavioral sensitization induced by repeated cocaine exposure. Besides significant changes in DA neuronal activity, emerging evidence indicates that other brain regions also contribute to the initiation of behavioral sensitization, most likely through regulation of VTA neurons. For instance, ventral hippocampus activation increases DA neuronal population activity and facilitates locomotor sensitization22. By contrast, lesions of prelimbic cortex (PFC) prevent the development of behavioral sensitization to cocaine23,24,25.

Non-DA neurons, in the present study, are mostly GABAergic inhibitory neurons38, as glutamatergic neurons largely localize in the medial VTA42. Many addictive drugs inhibit VTA GABA neurons, which disinhibit DA neuron activity in the acute phase12,43,44,45,46. However, after repetitive exposure, addictive drugs may increase VTA GABA neuron firing by depressing GABABR signaling, thus enhancing GABA mediated inhibition of DA neurons14,45,47. In the present study, the increase in DA firing rate and bursting does not seem to result from disinhibition from local GABAergic input, because firing rate of non-DA neurons is always positively correlated with that of DA neurons in naive, saline-, and cocaine-treated rats. Rather, the strong positive correlation in the firing may represent an attempt to counteract the excitation of DA neurons.

The family dentist should know that the injection of local anesthetic with epinephrine must be avoided for at least six hours after cocaine consumption.18 Some sources suggest the use of epinephrine in either local anesthetic or retraction cord is contraindicated for at least 24 hours after cocaine use to prevent "sympathetic overload" resulting in a hypertensive crisis, cerebrovascular bleed, myocardial infarction, tachydysrhythmias, and/or cardiac arrest.21,28 Lidocaine without vasoconstrictors will have an additive effect with existing cocaine in reducing the patients threshold for seizure activity.4,5 As well, general anesthesia poses significant cardiovascular risk and should be avoided with the chronic cocaine user.4 be457b7860