Inhibition by MK-801 of cocaine-induced sensitization, conditioned place preference, and dopamine-receptor supersensitivity in mice

Kim, Hack-Seang; Park, Woo-Kyu; Jang, Choon‐Gon; Oh, Seikwan

doi:10.1016/0361-9230(96)00006-8

Cited by 76 publications

(40 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Selective ablation of NR1 expression in striatal neurons has been used to study the role of NMDA receptor signaling in the acquisition of behavioral sensitization and conditioned place preference (Heusner and Palmiter, 2005;Agatsuma et al, 2010). These studies clarify previous research showing that blockade of NMDA receptor is disruptive to the development of sensitization and place preference (Haracz et al, 1995;Kim et al, 1996;Li and Wolf, 1999).…”

Section: Introductionsupporting

confidence: 55%

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

Benneyworth

Coyle

2012

Neuropsychopharmacol

View full text Add to dashboard Cite

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.

show abstract

Section: Introductionsupporting

confidence: 55%

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

Benneyworth

Coyle

2012

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Previous work has shown that peripheral or intra-VTA administration of glutamate antagonists is rewarding (Steinpreis et al, 1995;David et al, 1998;Panos et al, 1999) and can increase the rewarding properties of established cocaine reinforcement (Ranaldi et al, 1996;Pierce et al, 1997). Similar treatments, however, have also been shown to block learning reinforced by psychostimulants (Schenk et al, 1993;Cervo and Samanin, 1996;Kim et al, 1996) and to attenuate locomotor sensitization to psychostimulants (Kalivas and Alesdatter, 1993;Wolf and Jeziorski, 1993;Karler et al, 1994;Kim et al, 1996;Cornish et al, 2001). These findings indicate that glutamate antagonists do not alter the learning of cocaine reward because they are aversive (in fact they are rewarding), or because they decrease cocaine reward (they actually increase it if it has already been established).…”

Section: Resultsmentioning

confidence: 99%

“…Previous studies showed that systemic administration of glutamate antagonists blocked cocaine-induced locomotor sensitization (Wolf and Jeziorski, 1993;Karler et al, 1994), acquisition of self-administration (Schenk et al, 1993) and conditioned place preference (Cervo and Samanin, 1995;Kim et al, 1996). In addition, intra-VTA injections of NMDA antagonists have been reported to block locomotor sensitization to both cocaine (Kalivas and Alesdatter, 1993) and amphetamine (Cador et al, 1999).…”

Section: Introductionmentioning

confidence: 98%

Critical Role for Ventral Tegmental Glutamate in Preference for a Cocaine-Conditioned Environment

Harris

Aston‐Jones

2003

Neuropsychopharmacol

140

View full text Add to dashboard Cite

Cocaine administration induces glutamatergic activation within the mesolimbic-accumbens system. This activation has been linked to the behavioral effects of cocaine and recently to the induction of long-term potentiation in dopamine neurons within the ventral tegmental area (VTA). We sought to determine if glutamate receptor activation is also crucial to the development of a conditioned place preference (CPP) to cocaine's rewarding effects. Two groups of rats were given intra-VTA injections of either vehicle or a combination of NMDA (N-methyl-D-aspartate) and AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor antagonists (AP5 0.24 nmol plus CNQX 0.12 nmol per side) prior to each cocaine place-conditioning trial. Microinjections of the glutamate antagonists completely blocked the development of a cocaine CPP when given within, but not when given outside of, the VTA. These data indicate that glutamatergic activity in the VTA may be crucial for learning to associate environmental stimuli with cocaine exposure.

show abstract

“…It has been accepted that NMDARs are critical for the development of cocaine-induced sensitization. This notion is primarily based on evidence that co-administration of MK801 with cocaine completely blocks [15][16][17][18][19][20][21][22][23] or reduces [16,33,49,76,77] cocaine-induced sensitization. However, this conclusion is still highly controversial and the role of NMDARs in addiction remains unclear [78].…”

Section: Discussionmentioning

confidence: 99%

“…Co-administration of MK801 prevents the development of sensitization to cocaine [15][16][17][18][19][20][21][22][23], amphetamine [24][25][26][27][28] and methamphetamine [29,30]. Moreover, MK801 similarly prevents the development of cocaine, amphetamine, and methamphetamineinduced conditioned place preference, a prominent associative memory model of drug seeking behavior [31][32][33].…”

Section: Introductionmentioning

confidence: 99%

The competitive NMDA receptor antagonist CPP disrupts cocaine-induced conditioned place preference, but spares behavioral sensitization

Carmack

Kim²,

Sage³

et al. 2013

Behavioural Brain Research

View full text Add to dashboard Cite

h i g h l i g h t sCPP co-administration with cocaine altered the acute response to cocaine. NMDAR antagonism with CPP had no effect on cocaine-induced behavioral sensitization. NMDAR antagonism with CPP abolished cocaine-induced conditioned place preference. a r t i c l e i n f o a b s t r a c tRecently, the notion that memory and addiction share similar neural substrates has become widely accepted. N-methyl-d-aspartate receptors (NMDAR) are the cornerstones of synaptic models of memory. The present study examined the effect of the competitive NMDAR antagonist CPP on the induction of behavioral sensitization and conditioned place preference to cocaine. Conditioned place preference is an associative memory model of drug seeking, while sensitization is a non-associative model of the transition from casual to compulsive use. There were three principal findings: (1) co-administration of CPP and cocaine altered the acute response to cocaine, suggesting a direct interaction between the two drugs; (2) NMDAR antagonism had no effect on behavioral sensitization; and (3) NMDAR antagonism abolished conditioned place preference. A review of prior evidence supporting a role for NMDARs in sensitization suggests that NMDAR antagonists directly interfere with cocaine's psychostimulant effects, and this interaction could be misinterpreted as a disruption of sensitization. Finally, we suggest that addiction recruits multiple kinds of plasticity, with sensitization recruiting NMDAR-independent mechanisms.

show abstract

Inhibition by MK-801 of cocaine-induced sensitization, conditioned place preference, and dopamine-receptor supersensitivity in mice

Cited by 76 publications

References 48 publications

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

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

Critical Role for Ventral Tegmental Glutamate in Preference for a Cocaine-Conditioned Environment

The competitive NMDA receptor antagonist CPP disrupts cocaine-induced conditioned place preference, but spares behavioral sensitization

Contact Info

Product

Resources

About