Subchronic methamphetamine treatment enhances methamphetamine- or cocaine-induced dopamine efflux in vivo

Kazahaya, Yasuko; Akimoto, Kiyoshi; Otsuki, Saburo

doi:10.1016/0006-3223(89)90270-9

Cited by 114 publications

(42 citation statements)

References 19 publications

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“…Furthermore, the seizure-induced elevation of DA release could be enhanced if seizures were induced repeatedly (Strecker and Moneta, 1994;Dazzi et al, 1997;Becker et al, 2000). This phenomenon is comparable to the process of 'behavioral sensitization', in which repeated administration of DA agonists augment abnormal behaviors with the concominant enhancement of DA release (Kazahaya et al, 1989;Hamamura et al, 1991; also see review of Kalivas and Stewart, 1991). In our study, the prolonged seizure activity associated with limbic status epilepticus might produce excessive DA release and have such sensitization-like effects on DA systems.…”

Section: Seizure-induced Pathological Sensitization Of the Da Systemsupporting

confidence: 65%

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Ando

Morimoto

Watanabe

et al. 2004

Neuropsychopharmacol

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There is an increased incidence of schizophrenia-like psychosis in temporal lobe epilepsy (TLE), and several risk factors have been implicated, including the duration of epilepsy and temporal lobe neuropathology. To investigate the biological mechanism of epileptic psychosis, we examined alterations of central dopaminergic systems in the kainate model of TLE. In adult rats, kainate was microinjected into the left amygdala to induce status epilepticus. An indirect dopamine agonist methamphetamine (MAP, 2 mg/kg, i.p.) was administered before and 1 month after the kainate treatment. MAP-induced locomotor activity was significantly enhanced in the kainate group compared with the baseline (pre-kainate) level, which was antagonized by pretreatment with haloperidol. The enhancement of locomotor activity in the kainate group was significantly correlated with the density of hippocampal CA1 neurons. Although the basal extracellular dopamine concentration was significantly lower in the striatum in the kainate group than in the control group (5.5 vs 39.2 fmol/20-min sample), the maximal concentration following MAP administration did not differ between the two groups. These results clearly demonstrate that hypersensitivity of the dopamine systems develops in the chronic phase of the kainate-induced TLE model, which may be responsible for the mechanism of epileptic psychosis.

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Section: Seizure-induced Pathological Sensitization Of the Da Systemsupporting

confidence: 65%

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Ando

Morimoto

Watanabe

et al. 2004

Neuropsychopharmacol

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“…For example, many early studies on the neurobiology of sensitization found that repeated treatment with psychostimulant drugs increases evoked DA release from striatal slices, which consisted primarily of CPu (Kolta et al, 1985;Robinson and Becker, 1982), and later microdialysis studies showed increased DA release in both the NAcc and CPu (Kazahaya et al, 1989;Paulson and Robinson, 1995). Indeed, repeated treatment with drugs of abuse causes neuroadaptations in many brain regions (Robinson and Berridge, 2000;Vanderschuren and Kalivas, 2000), which presumably account for the diversity of behaviors and psychological processes that are altered by these drugs.…”

Section: Resultsmentioning

confidence: 99%

The Location of Persistent Amphetamine-Induced Changes in the Density of Dendritic Spines on Medium Spiny Neurons in the Nucleus Accumbens and Caudate-Putamen

Kolb

Robinson

2002

Neuropsychopharmacol

141

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Repeated intermittent treatment with amphetamine increases the density of dendritic spines on medium spiny neurons (MSNs) in the nucleus accumbens (NAcc). The purpose of this study was two-fold: (1) to determine whether amphetamine has similar effects on MSNs in the caudate-putamen (CPu) and (2) to determine if this effect is localized to distal dendrites, the site of convergence of dopamine (DA) and glutamate synapses in the striatum. An amphetamine treatment regimen that produced behavioral sensitization increased the density of dendritic spines on MSNs in both the NAcc and dorsolateral CPu. This effect was long lasting, because it was evident 3.5 months after the discontinuation of drug treatment. The increase in spine density was confined to distal dendrites of MSNs, and was not apparent on dendrites close to the cell body. It is concluded that amphetamine may preferentially reorganize synapses at the site of DAglutamate interaction in the striatum, which may alter DA-glutamate signaling and thereby contribute to some of the persistent behavioral and psychological consequences of repeated exposure to psychostimulant drugs.

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“…Results from in vivo microdialysis [38][39][40] and in vitro superfusion [41,42] studies indicate that METH directly stimulates DA release in the striatum, which in turn could stimulate pep tide release from DYN-containing neurons. This would account for the METH-induced decrease in striatal DYN A-ir concentrations observed in the present studies and extends previous data showing that a single injection of AMPH or apomorphine (a D i/D 2 DA ago nist) causes a rapid and transient decline in DYN-ir peptides [7,43].…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine-lnduced Changes in AP-1 Binding and Dynorphin in the Striatum: Correlated, Not Causally Related Events?

Bronstein

Pennypacker²,

Lee³

et al. 1996

Neurosignals

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Activation of D₁ dopamine (DA) receptors in the striatum increases the expression of the opioid neuropeptide, dynorphin (DYN). While cAMP is generally accepted as a second messenger in this signal transduction pathway, the role of Fos/FRA proteins and AP-1 binding in mediating D₁ receptor-induced changes in DYN expression remains uncertain. In this study, DYN peptide and mRNA levels, as well as Fos/FRA proteins and AP-1 DNA binding activity, were measured in individual animals following acute challenge with the psychostimulant drug methamphetamine (METH). METH caused an initial decrease in striatal levels of DYN A, reflecting increased peptide release. Six hours postinjection, DYN mRNA levels were significantly elevated by METH as compared to vehicle-injected controls. At the same time, these drugs increased the expression of Fos/FRA-ir proteins, in particular the 35- and 40-kDa molecular weight species, and increased binding to the AP-1 DNA element. Analyses of the time course of METH''s effects revealed that DYN mRNA levels, Fos/FRA proteins and AP-1 binding activity showed variable increases by 3 h but all were significantly elevated above control levels by 6 h post-treatment. The D₁-specific antagonist, SCH 23390, completely blocked the METH-induced changes in DYN peptide and mRNA levels while a D₂ receptor antagonist (sulpiride) had little or no effect. These data indicate that stimulant drugs such as METH increase the expression of DYN and AP-1 factors in the striatum via a D₁ receptor-mediated mechanism. However, the finding that AP-1 binding merely paralleled but did not precede, the increase in DYN expression, as would be expected if it were mediating increased gene transcription, suggests these may be correlative, not causally related events.

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Subchronic methamphetamine treatment enhances methamphetamine- or cocaine-induced dopamine efflux in vivo

Cited by 114 publications

References 19 publications

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

Enhancement of Central Dopaminergic Activity in the Kainate Model of Temporal Lobe Epilepsy: Implication for the Mechanism of Epileptic Psychosis

The Location of Persistent Amphetamine-Induced Changes in the Density of Dendritic Spines on Medium Spiny Neurons in the Nucleus Accumbens and Caudate-Putamen

Methamphetamine-lnduced Changes in AP-1 Binding and Dynorphin in the Striatum: Correlated, Not Causally Related Events?

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