Influence of novel versus home environments on sensitization to the psychomotor stimulant effects of cocaine and amphetamine

Badiani, Aldo; Browman, Kaitlin E.; Robinson, Terry E.

doi:10.1016/0006-8993(95)00028-o

Cited by 191 publications

(135 citation statements)

References 34 publications

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“…Mere placement of an animal into the drug-paired environment elicits a conditioned locomotor response (4,6,26,27), indicating that animals learn to associate environmental cues with the drug experience. To test whether GluRA(Ϫ͞Ϫ) mice were able to make such associations, we examined their conditioned locomotor response after a single cocaine exposure.…”

Section: Discussionmentioning

confidence: 99%

“…When animals are given an injection in the context in which they previously received drug, part of the enhanced behavioral response is due to ''sensitization'' (i.e., a nonassociative increase in responsiveness), but part is due to drug-context conditioning (i.e., a conditioned locomotor response) (4,6,(26)(27)(28). To test whether GluRA(Ϫ͞Ϫ) mice learned to associate context with the drug experience, we initially used a protocol in which on day 1 the animals received cocaine or saline and were placed in the test apparatus, but on day 2 both groups received only saline before being tested.…”

Section: Cocaine and Stress Do Not Potentiate Synaptic Strength Inmentioning

confidence: 99%

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Cocaine-induced potentiation of synaptic strength in dopamine neurons: Behavioral correlates in GluRA(–/–) mice

Dong

Saal

Thomas

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

145

138

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Synaptic plasticity in the mesolimbic dopamine (DA) system is thought to contribute to the neural adaptations that mediate behavioral sensitization, a model for core aspects of addiction. Recently, it has been demonstrated that multiple classes of drugs of abuse, as well as acute stress, enhance strength at excitatory synapses on midbrain DA neurons. Here, we show that both the cocaine-and stress-induced synaptic enhancement involves an up-regulation of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This enhancement requires the ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor subunit GluRA as evidenced by its absence in mice lacking this subunit. The cocaine-elicited, but not the stress-elicited, synaptic potentiation in DA neurons was blocked by a D1-like receptor antagonist, indicating that the in vivo triggering mechanisms differ for these forms of experience-dependent synaptic modification. Surprisingly, behavioral sensitization to cocaine was elicited in GluRA(؊͞؊) mice, indicating that potentiation of excitatory synaptic transmission in DA neurons is not necessary for this form of behavioral plasticity. However, GluRA(؊͞؊) mice did not exhibit a conditioned locomotor response when placed in a context previously paired with cocaine, nor did they exhibit conditioned place preference in response to cocaine. We suggest that the drug-induced enhancement of excitatory synaptic transmission in midbrain DA neurons, although not required for behavioral sensitization per se, may contribute to the attribution of incentive value to drug-associated cues.

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Section: Discussionmentioning

confidence: 99%

Section: Cocaine and Stress Do Not Potentiate Synaptic Strength Inmentioning

confidence: 99%

Cocaine-induced potentiation of synaptic strength in dopamine neurons: Behavioral correlates in GluRA(–/–) mice

Dong

Saal

Thomas

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

145

138

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“…Another explanation for the lack of behavioral sensitization in WT animals could be related to the paradigm of behavioral recording employed in this study. There is some lines of evidence in the literature suggesting that behavioral sensitization is context-dependent (Badiani et al, 1995). As mentioned in the methodology, our animals were recorded and injected in their home cage throughout the entire COC repeated treatment.…”

Section: Coc-induced Ngfi-b Expression In Tg Micementioning

confidence: 99%

Effects of Cocaine on c-Fos and NGFI-B mRNA Expression in Transgenic Mice Underexpressing Glucocorticoid Receptors

St-Hilaire

Tremblay

Lévesque

et al. 2002

Neuropsychopharmacol

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Numerous evidences suggest that stress and stress-related hormones can modulate the activity of the brain reward pathway and thus may account for individual vulnerability towards the reinforcing effects of drugs of abuse. Transgenic (TG) mice expressing an antisense mRNA against the glucocorticoid receptor (GR), which partially blocks GR expression, were used to assess the role of GR dysfunction on cocaine (COC)-induced c-fos and Nerve-Growth Factor Inducible-B (NGFI-B, or Nur77) gene expression. These two genes belong to different families of transcription factors and have been shown to be modulated by various dopaminergic drugs. TG and wild-type (WT) mice were both acutely and repeatedly treated with COC (20 mg/kg, i.p.). In the chronic experiment, mice received a 5-day treatment of COC and were challenged 5 days later with COC or vehicle. Locomotor activity was assessed during the entire chronic experiment in the mouse home cages. Animals were sacrificed 1 h after the last injection and NGFI-B and c-fos mRNA levels in the prefrontal cortex, the nucleus accumbens and the striatum were measured by in situ hybridization. Acute COC administration led to significantly smaller c-fos increases in TG mice compared to WT, whereas repeated COC treatment potentiated c-fos induction both in TG and WT mice to equivalent levels. TG mice displayed higher basal NGFI-B expression in the nucleus accumbens and the level of NGFI-B mRNA was differently modulated by COC in TG mice compared to WT mice. In accordance with data on c-fos expression, behavioral data indicate a blunted locomotor effect on the first COC injection in TG mice, a phenomenon corrected by the repeated COC treatment. These results suggest that an alteration of the hypothalamus-pituitary-adrenal axis can modify COC-induced regulation of the transcription factors c-fos and NGFI-B, and that these changes parallel those seen at the behavioral level. It also demonstrates that the differences at the behavioral and molecular levels noted between TG and WT mice after acute COC injection disappear following repeated COC administration, suggesting that repeated COC has a greater impact in TG mice underexpressing GRs.

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“…The acquisition of sensitization is facilitated by associative learning that links a specific context to drug exposure (Badiani et al, 1995). Specific alterations in immediate early gene expression and neuronal morphology are observed following such contextspecific sensitization (Robinson and Kolb, 1997;Mattson et al, 2008;Koya et al, 2009;Singer et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Altered Acquisition and Extinction of Amphetamine-Paired Context Conditioning in Genetic Mouse Models of Altered NMDA Receptor Function

Benneyworth

Coyle

2012

Neuropsychopharmacol

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Repeated intermittent exposure to amphetamine (AMPH) results in the development of persistent behavioral and neurological changes. When drug exposure is paired with a specific environment, contextual cues can control conditioned responses, context-specific sensitization, and alterations in dendritic morphology in the nucleus accumbens (NAc). Intact N-methyl-D-aspartate (NMDA) glutamate receptor signaling is thought to be required for associative learning. The acquisition of context-specific behavioral sensitization to AMPH and extinction of conditioned hyperactivity have been investigated in two genetically modified mouse strains: the serine racemase homozygous knockout (SRÀ/À) and glycine transporter 1 heterozygous mutant (GlyT1À/ + ). These strains have reciprocally altered NMDA receptor co-agonists, D-serine and glycine, levels that result in decreased (SRÀ/À) or increased (GlyT1À/ + ) NMDA receptor signaling. AMPH-induced changes in dendritic morphology in the NAc were also examined. SRÀ/À mice showed reduced expression of context-specific sensitization and conditioned hyperactivity. However, the conditioned hyperactivity in these mice is completely resistant to extinction. Extinction reversed AMPH-induced increased in NAc spine density in wild-type but not SRÀ/À mice. GlyT1 À/ + mice showed a more rapid acquisition of sensitization, but no alteration in the extinction of conditioned hyperactivity. The SRÀ/À data demonstrate that a genetic model of NMDA receptor hypofunction displays a reduced ability to extinguish conditioned responses to drug-associated stimuli. Findings also demonstrate that the morphological changes in the NAc encode conditioned responses that are sensitive to extinction and reduced NMDA receptor activity. NMDA receptor hypofunction may contribute to the comorbidity of substance abuse in schizophrenia.

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Influence of novel versus home environments on sensitization to the psychomotor stimulant effects of cocaine and amphetamine

Cited by 191 publications

References 34 publications

Cocaine-induced potentiation of synaptic strength in dopamine neurons: Behavioral correlates in GluRA(–/–) mice

Cocaine-induced potentiation of synaptic strength in dopamine neurons: Behavioral correlates in GluRA(–/–) mice

Effects of Cocaine on c-Fos and NGFI-B mRNA Expression in Transgenic Mice Underexpressing Glucocorticoid Receptors

Altered Acquisition and Extinction of Amphetamine-Paired Context Conditioning in Genetic Mouse Models of Altered NMDA Receptor Function

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