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Taco J De Vries

Publications and source records attributed to Taco J De Vries.

11 recordsLinked to original sources
PubMed2006

Enhanced cortical and accumbal molecular reactivity associated with conditioned heroin, but not sucrose-seeking behaviour.

Re-exposure to drug-related cues elicits drug-seeking behaviour and relapse in both humans and laboratory animals even after months of abstinence. Identifying neural and molecular substrates underlying conditioned heroin-seeking behaviour will be helpful in understanding mechanisms behind opiate relapse. In humans and animals, brain areas activated by natural reward-related stimuli (e.g. food, sex) do not show a complete overlap with those activated by stimuli associated with drugs of abuse, suggesting the involvement of different circuitry. To that end, we investigated neural reactivity by measuring immediate early gene (IEG) expression patterns in mesocorticolimbic system target areas following cue-induced reinstatement of heroin seeking and compared those IEG expression patterns to what was measured during natural reward (sucrose)-seeking behaviour. Animals were trained to administer heroin associated with a compound audio-visual cue. Re-exposure to the cue after 3 weeks of withdrawal reinstated heroin-seeking behaviour, which resulted in IEG expression of ania-3, MKP-1, c-fos and Nr4a3 in the medial prefrontal cortex (mPFC), and of ania-3 in the orbital frontal cortex (OFC) and nucleus accumbens core (NAC). The expression patterns for heroin-seeking behaviours did not generalize to sucrose-seeking behaviours, indicating that the two behaviours involve different connectivity pathways of neuronal signalling.

Animals↗
PubMed2006

Beta-adrenoceptor mediated inhibition of long-term reward-related memory reconsolidation.

Well-consolidated fear-related memories, once retrieved, are susceptible to disruption and require reconsolidation in order to be maintained. We examined whether reactivated reward-related memories are also susceptible to interference by evaluating the effect of propranolol (PROP), a beta-adrenergic antagonist known to impair reconsolidation of fear-related memories, on context-induced sucrose seeking. PROP administration upon reactivation reduced sucrose seeking behaviour 3 weeks post-training, indicating that reconsolidation of reward-related memories can be disrupted after a long post-training interval.

Adrenergic beta-Antagonists↗
PubMed2006

A proteomics approach to identify long-term molecular changes in rat medial prefrontal cortex resulting from sucrose self-administration.

The medial prefrontal cortex (mPFC) is involved in the processing and retrieval of reward-related information. Here, we investigated long-lasting changes in protein composition of the mPFC in rats with a history of sucrose self-administration. Protein levels were analyzed using 2-D PAGE and MALDI-TOF sequencing. From approximately 1500 spots, 28 regulated proteins were unambiguously identified and were involved in cytoskeleton organization, energy metabolism, oxidative stress, neurotransmission, and neuronal outgrowth and differentiation. For several proteins, this change was also found as a long-lasting alteration in gene expression. We show that self-administration of sucrose produces long-lasting molecular neuroadaptations in the mPFC that may be involved in reward-related information processing.

Animals↗
PubMed2005

Suppression of conditioned nicotine and sucrose seeking by the cannabinoid-1 receptor antagonist SR141716A.

The present study shows that the selective cannabinoid CB1 receptor antagonist SR141716A attenuated responding for both nicotine- and sucrose-associated stimuli in a long-term extinction-reinstatement model. The results suggest that endocannabinoids play a general role in modulating cue reactivity or conditioned reinforcement following prolonged abstinence of both drug and natural reinforcers. In line with previous preclinical and recent clinical observations, our results provide a strong rationale for the use of CB1 antagonists in the treatment of addictive behaviors.

Animals↗
PubMed2005

Molecular reactivity of mesocorticolimbic brain areas of high and low grooming rats after elevated plus maze exposure.

High and low grooming rats (HG and LG), selected by extremities in stress-induced self-grooming on the elevated plus maze (EPM), display differences in stress coping style on the EPM, their motivation to self-administer cocaine, and differences in the reactivity of dopaminergic nerve terminals in mesocorticolimbic brain areas. This indicates a link between coping with a stressful/anxiogenic situation and drug intake. Here, we aimed to determine the molecular correlates of these differences by analyzing the reactivity of the mesocorticolimbic brain areas (the medial prefrontal cortex (mPFC) nucleus accumbens shell (NAS) and ventral tegmental area (VTA)) of HG and LG rats in response to EPM exposure. We report by measuring levels of immediate early gene (IEG) transcripts that EPM exposure-induced IEG expression was not significantly different between HG and LG rats. On the other hand, novel IEG expression patterns upon stress (EPM exposure) were apparent in all three areas including arc induction in the mPFC and NAS, CRH, BDNF, and Nr4a3 induction in the NAS, and serum glucocorticoid-regulated kinase (sgk) induction in the VTA. It is concluded that although the mPFC, NAS, and VTA play a role in modulating stress and grooming behavior, the neuronal reactivity in these regions measured by the IEG response is not related with behavioral extremities in stress coping style displayed on the EPM.

Adaptation, Psychological↗
PubMed2005

Cannabinoid CB1 receptors control conditioned drug seeking.

Recent developments have implicated cannabinoid CB1 receptors as a novel target for a new class of therapeutic agents used to treat drug addiction. CB1 receptors are expressed in the motivational circuitry of the brain and modulate drug seeking. Blockade of the CB1 receptor is particularly effective in reducing cue-induced reinstatement of drug seeking, an animal analogue of cue-induced relapse in human addicts. These relapse-preventing properties are observed with different classes of abused drug (i.e. psychostimulants, opiates, nicotine and alcohol). In addition, recent evidence indicates a more general role of CB1 receptors in reward-related memories, which is consistent with the proposed role of endocannabinoids in memory-related plasticity. Relapse-preventing actions and inhibitory effects on weight gain were confirmed recently in clinical trials with the CB1 antagonist rimonabant. Collectively, these clinical and preclinical studies suggest that antagonists of CB1 receptors offer a novel approach in the treatment of addictive behaviours.

Animals↗
PubMed2005

Differential involvement of the prelimbic cortex and striatum in conditioned heroin and sucrose seeking following long-term extinction.

Relapse to drug taking is triggered by stimuli previously associated with consumption of drugs of misuse (cues) and involves brain systems controlling motivated behaviour towards natural reinforcers. In this study, we aimed to identify and compare neuronal pathways in corticostriatal systems that control conditioned heroin or natural reward (sucrose) seeking. To that end, rats were trained to self-administer heroin or sucrose in association with an identical compound cue. After more than 3 weeks of abstinence during extinction training, cue exposure robustly reinstated heroin and sucrose seeking, but induced distinct and even opposing changes in the expression of the neuronal activation marker zif268 in the prelimbic cortex and striatal complex, respectively. Because in the prelimbic area zif268 expression was enhanced during cue-induced heroin seeking but unaffected during sucrose seeking, a pharmacological intervention was aimed at this prefrontal region. Injection of a GABA agonist mixture within the prelimbic area enhanced conditioned heroin seeking, but had no effect on conditioned sucrose seeking. Our findings suggest a differential role of the prelimbic area and the striatum in the persistence of heroin vs. sucrose seeking following long-term extinction.

Analysis of Variance↗
PubMed2003

Cannabinoid modulation of the reinforcing and motivational properties of heroin and heroin-associated cues in rats.

RATIONALE: Recently, we provided evidence for a cannabinoid mechanism in relapse to cocaine seeking in rats. There is also increasing evidence for functional cross-talk between cannabinoid and opioid systems in several physiological processes. OBJECTIVES: This study was designed to evaluate whether the cannabinoid system plays a role in mediating the reinforcing and motivational effects of heroin and heroin-paired stimuli. METHODS: Male Wistar rats were trained to self-administer heroin (50 microg/kg per infusion) on fixed (FR5) or progressive ratio schedules of reinforcement in the presence of a discriminative and discrete heroin-associated cue. The selective cannabinoid CB1 antagonist SR141716A was given 30 min before the session to determine its effect on responding for heroin. Separate groups of rats were subjected to extinction training during which heroin-associated cues were absent and no heroin was delivered. During subsequent reinstatement tests, the effects of the cannabinoid agonist HU210 and the antagonist SR141716A on reinstatement of heroin seeking were evaluated. RESULTS: The cannabinoid antagonist dose-dependently reduced responding for heroin on the FR5 schedule and to a greater extent on the progressive ratio schedule. HU210 (20 microg/kg) reinstated heroin seeking behaviour following a 2-week extinction period, whereas SR141716A dose-dependently attenuated heroin seeking that was provoked by a priming injection of heroin (0.25 mg/kg) and heroin seeking that was triggered by re-exposure to heroin paired stimuli. CONCLUSIONS: The results show that the reinforcing and motivational effects of heroin and heroin-paired stimuli are mediated, at least in part, by activation of cannabinoid CB1 receptors. Therefore, the present study provides a rationale for the use of cannabinoid antagonists in the treatment of opiate addiction.

Animals↗
PubMed2002

Psychostimulant-induced behavioral sensitization depends on nicotinic receptor activation.

Animal studies have shown that nicotine and psychostimulant drugs (amphetamine and cocaine) share the property of inducing long-lasting behavioral and neurochemical sensitization, which is thought to contribute to their addictive properties. Neuroplasticity subserving learning and memory mechanisms is considered to be involved in psychostimulant-induced sensitization and addiction behavior. Because nicotinic receptors in the brain play a role in the storage of drug-related information underlying reinforcement learning, we evaluated the possibility that activation of central nicotinic receptors may underlie psychostimulant-induced sensitization. Repeated exposure of rats to nicotine profoundly enhanced the psychomotor effects of nicotine and amphetamine 3 weeks after nicotine pretreatment. Moreover, the nicotinic receptor antagonist mecamylamine completely blocked the induction, but not the long-term expression, of behavioral sensitization to amphetamine in amphetamine-pretreated rats. Mecamylamine also prevented the development of cocaine-induced behavioral sensitization. Behavioral sensitization induced by nicotine, amphetamine, or cocaine was associated with an increase in the electrically evoked release of [(3)H]dopamine from nucleus accumbens slices. Coadministration of mecamylamine during pretreatment with nicotine, amphetamine, or cocaine prevented the development of this long-term hyperreactivity of nucleus accumbens dopamine neurons. Similarly, the high-affinity non-alpha7 subtype nicotinic receptor antagonist dihydro-beta-erythroidine prevented the development of amphetamine-induced behavioral and neurochemical sensitization. These data indicate that nicotinic receptor activation (by endogenously released acetylcholine) is a common denominator initiating neuroplasticity involved in the development of amphetamine, as well as cocaine-induced sensitization.

Amphetamine↗
PubMed2002

Relapse to cocaine- and heroin-seeking behavior mediated by dopamine D2 receptors is time-dependent and associated with behavioral sensitization.

The sensitizing properties of drugs of abuse have been proposed to play an important role in the persistence of drug seeking behavior. We decided to evaluate the temporal relationship of dopamine D2 receptor-mediated drug seeking behavior and behavioral sensitization in animals with a history of cocaine and heroin self-administration. During early phases of withdrawal (<1 week), activation of dopamine D2 receptors with quinpirole resulted in robust, dose-dependent, reinstatement of (non-reinforced) responding in both cocaine- and heroin-trained rats. Cocaine and heroin seeking induced by quinpirole was associated with a dramatic enhancement of the psychomotor stimulant effects of the D2 agonist, indicating that sensitization to D2-mediated events had developed. During the late phase of withdrawal (>3 weeks), reinstatement of cocaine seeking by quinpirole was still apparent, but less robust. In heroin-trained rats, increases of responding were no longer observed. Interestingly, behavioral sensitization to quinpirole was still observed in cocaine-trained rats, but was absent in heroin-trained rats. Thus, it appears that dopamine D2 receptors have a time-dependent role in relapse to cocaine and heroin seeking which is strongly associated with a behaviorally sensitized state.

Animals↗