Effects of lesions of prefrontal cortex, amygdala, or fornix on behavioral sensitization to amphetamine: Comparison with N-methyl-d-aspartate antagonists

Wolf, Marina E.; Dahlin, S.L.; Hu, Xiu‐Ti; Xue, Chang Jiang; White, K. Geoffrey

doi:10.1016/0306-4522(95)00248-h

Cited by 248 publications

(203 citation statements)

References 125 publications

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“…Initiation of sensitization involves both D1 dopamine (DA) receptor and glutamate receptor activation within ventral tegmentum and substantia nigra (Bjijou et al, 1996;Wolf et al, 1995;Kalivas and Alesdatter, 1993). Projections from prefrontal cortex and amygdala also participate in the initiation of sensitization (Wolf, 1998).…”

Section: Development Vs Expression Of Behavioral Sensitizationmentioning

confidence: 99%

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Richtand

2006

Neuropsychopharmacol

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Behavioral sensitization, the progressive and enduring augmentation of certain behaviors following repetitive drug use, alters rodent locomotion in a long-standing manner. The same dopamine pathways playing an important role in drug dependence and psychosis also play a critical role in sensitization. Individual dopamine receptor subtypes have markedly different functional responses to stimulation, with D3 dopamine receptor stimulation inhibiting rodent locomotion. The D3 receptor has highest affinity of the dopamine receptor subtypes for dopamine, and is occupied to a greater degree following stimulant drug administration. D3 receptor activity may be regulated through the expression of an alternatively spliced, truncated receptor isoform (termed 'D3nf') altering receptor localization and function via dimerization with the full-length subunit. The expected physiological response to repetitive drug administration is tolerance. Tolerance of D3 receptor inhibition of locomotion would contribute to sensitization to stimulant drugs. We hypothesize that repetitive D3 receptor stimulation contributes to the development of behavioral sensitization through decreased responsivity of D3-receptor-mediated locomotor inhibition. Increased D3nf expression may direct altered receptor localization and subsequent release of D3-receptormediated inhibition, contributing to the expression of sensitization. These hypotheses follow directly from the affinities of the receptor subtypes for dopamine; dopamine concentrations following stimulant administration; the effects of individual dopamine receptor subtype stimulation on locomotion; and the expected homeostatic response of the system to perturbation by drug. Clarifying these mechanisms underlying sensitization may suggest new interventions for neuropsychiatric conditions in which dopamine plays an important role, including psychosis, drug dependence, and Parkinson's disease. This information may also elucidate a previously unrecognized mechanism regulating receptor trafficking and desensitization.

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Section: Development Vs Expression Of Behavioral Sensitizationmentioning

confidence: 99%

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Richtand

2006

Neuropsychopharmacol

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“…The systemic administration of either NMDA (Karler et al, 1989;Wolf et al, 1995) or AMPA/kainate (Karler et al, 1991a;Li et al, 1997;cf Akiyama et al, 1998) receptor antagonists as well as the application into the VTA of either NMDA (Cador et al, 1999;Vezina and Queen, 2000) or mGlu (Kim and Vezina, 1998) receptor antagonists has been shown to prevent the induction of AMPH-induced locomotor sensitization. Moreover, systemically administering NMDA receptor antagonists with AMPH during preexposure also prevents cellular correlates of locomotor Figure 6 Injection cannula tip placements in the VTA.…”

Section: Induction Of Sensitization By Amph Requires Activation Of Glmentioning

confidence: 99%

“…Indeed, induction of locomotor sensitization by AMPH has been shown to be dependent on activation of Nmethyl-D-aspartate (NMDA: Cador et al, 1999;Vezina and Queen, 2000) and metabotropic glutamate (mGlu: Kim and Vezina, 1998) receptors in the VTA. Systemic administration of NMDA (Karler et al, 1989;Wolf et al, 1995) or a-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA)/kainate receptor antagonists (Karler et al, 1991a;Li et al, 1997) also prevents the development of locomotor sensitization by systemic AMPH. Moreover, induction of locomotor sensitization by AMPH is blocked by lesions of the PFC, which provides major glutamatergic afferentation to the VTA Cador et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Previous Exposure to VTA Amphetamine Enhances Cocaine Self-Administration under a Progressive Ratio Schedule in an NMDA, AMPA/Kainate, and Metabotropic Glutamate Receptor-Dependent Manner

Suto

Tanabe

Austin

et al. 2003

Neuropsychopharmacol

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Previous exposure to amphetamine (AMPH) in the ventral tegmental area (VTA) enhances cocaine self-administration in a D 1 dopamine receptor-dependent manner. The present study examined the contribution of VTA NMDA, AMPA/kainate, and metabotropic glutamate (mGlu) receptors to this effect. Rats in different groups received three intra-VTA injections, one every third day, of either saline (0.5 ml/ side), AMPH (2.5 mg/0.5 ml/side), AMPH+CPP (NMDA receptor antagonist; 10 mM or 100 mM/0.5 ml/side), AMPH+CNQX (AMPA/ kainate receptor antagonist; 0.3 mM or 1 mM/0.5 ml/side), AMPH+MCPG (mGlu receptor antagonist; 0.5 mM or 50 mM/0.5 ml/side), or the glutamate receptor antagonists alone. Starting 7-10 days after the last pre-exposure injection, rats were trained to self-administer cocaine (0.3 mg/kg/infusion) and then tested under a progressive ratio (PR) schedule of reinforcement for 6 consecutive days. As reported previously, VTA AMPH pre-exposed rats worked more and obtained more infusions of cocaine than saline pre-exposed animals. Coadministration of CPP, CNQX, or MCPG with AMPH during pre-exposure dose-dependently blocked this enhancement of cocaine self-administration. Rats pre-exposed to the glutamate receptor antagonists alone did not differ on the test days from the saline pre-exposed controls. These results indicate that, in a manner paralleling the induction of sensitization of the locomotor stimulating effects of AMPH, activation of NMDA, AMPA/kainate, and mGlu receptors during pre-exposure to AMPH in the VTA is necessary for the enhancement of cocaine self-administration to develop.

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“…A few studies have used cleaner, competitive NMDAR antagonists in examining AMPH-induced sensitization. For example, Wolf et al (1995) used CGS19755 and found a "clean block" of AMPH sensitization -i.e., stereotyped and locomotor behavior did not increase with repeated administration in rats co-administered CGS19755 with AMPH. However, CGS19755 dramatically altered the acute locomotor response to AMPH, in particular the time course of the drug response.…”

Section: Discussionmentioning

confidence: 99%

“…This difference in time course makes a later sensitization challenge test diffi cult to interpret. It seems that most competitive NMDAR antagonists interfere with the acute behavioral response to AMPH; CPP, CGS19755, and AP5 have all been shown to alter the acute responses to AMPH (Wolf et al 1995, Cador et al 1999, Battisti et al 2000. These fi ndings highlight the need for more studies …”

Section: Discussionmentioning

confidence: 99%

Antioxidant effect of simvastatin throught oxidative imbalance caused by lisdexamfetamine dimesylate

Eger

Ferreira

Batista

et al. 2016

An. Acad. Bras. Ciênc.

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The present study aims to directly investigate the behavioral and antioxidant effects of simvastatin in a model of bipolar mania induced by lisdexamfetamine dimesylate. Wistar rats were treated for 30 days with simvastatin. On the 24th day after the start of treatment, each rat was administered lisdexamfetamine dimesylate for 7 days. The results suggest that simvastatin combined with lisdexamfetamine dimesylate induced a signifi cant increased locomotion and lisdexamfetamine dimesylate administration causes an oxidative imbalance determined by an increment in lipid peroxidation, protein oxidation and alterations in the activities of antioxidant enzymes in brain areas; moreover, in the presence of simvastatin, most of these effects were prevented. These fi ndings contribute to a better understanding of the critical roles of lisdexamfetamine dimesylate in the treatment of neuropsychiatric disorders, associated with increased oxidative stress and changes in antioxidant enzymatic defense. In view of the central role played by lisdexamfetamine dimesylate, the established antioxidant effect of simvastatin therapy is of major interest.

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Effects of lesions of prefrontal cortex, amygdala, or fornix on behavioral sensitization to amphetamine: Comparison with N-methyl-d-aspartate antagonists

Cited by 248 publications

References 125 publications

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Behavioral Sensitization, Alternative Splicing, and D3 Dopamine Receptor-Mediated Inhibitory Function

Previous Exposure to VTA Amphetamine Enhances Cocaine Self-Administration under a Progressive Ratio Schedule in an NMDA, AMPA/Kainate, and Metabotropic Glutamate Receptor-Dependent Manner

Antioxidant effect of simvastatin throught oxidative imbalance caused by lisdexamfetamine dimesylate

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