Implication of NMDA receptors in behavioural sensitization to psychostimulants: A short review

Landa, Leoš; Máchalová, Alena; Šulcová, Alexandra

doi:10.1016/j.ejphar.2014.02.028

Cited by 20 publications

(14 citation statements)

References 80 publications

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“…However, infusions of the higher volume (1 ml) of MK 801 in sexually naïve males caused a significantly increased CPP score compared to vehicle-infused sexually naïve males (p ¼ 0.016). This finding is in agreement with effects of systemic MK 801 on psychostimulant sensitization (Rung et al, 2005;Eyjolfsson et al, 2006;Landa et al, 2014), but in sharp contrast to the effect of NMDA receptor blockade in sexually experienced males in the current study.…”

Section: Intra-nac Mk 801 Prevented Sex Experience-induced Amph Cppsupporting

confidence: 92%

“…It is well established that systemic administration of MK 801 leads to Amph locomotor sensitization in rats (Rung et al, 2005;Eyjolfsson et al, 2006;Landa et al, 2014) but its effects on cross-sensitization to drug CPP has not been demonstrated. Therefore, the current findings expand on this knowledge by showing that MK 801 results in sensitization of Amph reward, and specifically by acting in the NAc.…”

Section: Discussionmentioning

confidence: 99%

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Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats

et al. 2016

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Section: Intra-nac Mk 801 Prevented Sex Experience-induced Amph Cppsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats

et al. 2016

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“…Early on, most researchers focused on the mesolimbic dopamine system and they established that dopamine and dopamine receptors (DRs) play a key role in neurobiological mechanisms of addiction [29,30]. However, experiments have increasingly suggested that glutamate receptors, especially NMDARs, also contribute to neurobiological changes of addiction to psychomotor stimulants [9,10]. Building on these previous findings, we used ifenprodil, a selective antagonist of the GluN2B subunit, to explore the role of GluN2B-containing NMDARs in METH-induced behavioral sensitization and potential downstream signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…N-Methyl-d-aspartate receptors (NMDARs), a kind of glutamate receptor, have been frequently reported to participate in psychomotor stimulants-induced behavioral sensitization [9,10]. Functional NMDARs contain heteromeric combinations of the GluN1 subunit and various subunits of the GluN2 subfamily [11].…”

Section: Locomotionmentioning

confidence: 99%

Ifenprodil Attenuates Methamphetamine-Induced Behavioral Sensitization and Activation of Ras-ERK-∆FosB Pathway in the Caudate Putamen

Liu

Qiao

et al. 2016

Neurochem Res

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Addiction is a debilitating, chronic psychiatric disorder that is difficult to cure completely owing to the high rate of relapse. Behavioral sensitization is considered to may underlie behavioral changes, such as relapse, caused by chronic abuse of psychomotor stimulants. Thus, its animal models have been widely used to explore the etiology of addiction. Recently, increasing evidence has demonstrated that N-methyl-D-aspartate receptors (NMDARs) play an important role in addiction to psychomotor stimulants. However, the role of GluN2B-containing receptors and their downstream signaling pathway(s) in behavioral sensitization induced by methamphetamine (METH) have not been investigated yet. In this study, we used different doses of ifenprodil (2.5, 5, 10 mg/kg), a selective antagonist of the GluN2B subunit, to investigate the role of GluN2B-containing NMDARs in METH-induced behavioral sensitization. We then examined changes in the levels of Ras, phosphorylated extracellular signal-regulated kinase (pERK)/ERK, and ∆FosB in the caudate putamen (CPu) by western blot. We found that 2.5 or 10 mg/kg ifenprodil significantly attenuated METH-induced behavioral sensitization, whereas the mice treated with a moderate dose of ifenprodil (5 mg/kg) displayed no significant changes. Further results of western blot experiments showed that repeated administration of METH caused the increases in the levels of Ras, pERK/ERK and ∆FosB in the CPu, and these changes were inhibited by only the 2.5 mg/kg dose of ifenprodil. In conclusion, these results demonstrated that 2.5 mg/kg ifenprodil could attenuate METH-induced behavioral sensitization. Moreover, GluN2B-containing NMDARs and their downstream Ras-ERK-∆FosB signaling pathway in the CPu might be involved in METH-induced behavioral sensitization.

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“…Its neurobiological background consists in drug-induced neuroadaptive changes in a circuit involving dopaminergic and glutamatergic interconnections between the ventral tegmental area, the nucleus accumbens, prefrontal cortex and amygdala (Vanderschuren and Kalivas 2000;Nestler 2001;Landa et al 2014a). A simultaneous impact of both endogenous opioid and cannabinoid systems on the development of behavioural sensitisation can be the result of a cross-talk between opioid and cannabinoid receptors (Robledo et al 2008).…”

mentioning

confidence: 99%

Interaction of CB<sub>1</sub> receptor agonist arachidonylcyclopropylamide with behavioural sensitisation to morphine in mice

Landa¹,

Šlais²,

Máchalová³

et al. 2014

Vet. Med. - Czech

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Activities of the endocannabinoid system are believed to be substantially involved in psychostimulant and opioid addiction. Nevertheless, interactions between cannabinoid and opioid systems are not yet fully understood. Thus, the aim of the present study was to investigate the interaction between morphine and the cannabinoid CB 1 receptor agonist arachidonylcyclopropylamide (ACPA) in behavioural sensitisation. Sensitisation occurs after repeated exposure to drugs of abuse including morphine and cannabinomimetics and it has been suggested to mediate craving and relapses. Male mice were randomly allocated into three groups and were seven times (from the 7 th to 13 th day of the experiment) administered drugs as follows: (a) n 1 : vehicle at the dose of 10 ml/kg/day; (b) n 2 : morphine at the dose of 10.0 mg/kg/day; (c) n 3 : ACPA at the dose of 1.0 mg/kg/day. Changes in locomotor behaviour were measured in the Open Field Test: (a) after administration of vehicle on the 1 st experimental day, (b) after the 1 st dose of drugs given on the 7 th day, and (c) on the 14 th day after "challenge doses" given in the following way: n 1 : saline at the dose of 10 ml/kg, n 2, 3 : morphine at the dose of 10.0 mg/kg. Registered behavioural changes unambiguously showed the development of behavioural sensitisation to the stimulatory effects of morphine on locomotion after its repeated administration (P < 0.05). However, surprisingly, taking into account reports on synergistic effects of opioids and cannabinoid receptor stimulation, a significant decrease (P < 0.05) in behavioural sensitisation to morphine occurred when the drug challenge dose was given following repeated pre-treatment with the CB 1 receptor agonist ACPA, i.e. suppression of cross-sensitisation to morphine. Keywords

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Implication of NMDA receptors in behavioural sensitization to psychostimulants: A short review

Cited by 20 publications

References 80 publications

Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats

Nucleus accumbens NMDA receptor activation regulates amphetamine cross-sensitization and deltaFosB expression following sexual experience in male rats

Ifenprodil Attenuates Methamphetamine-Induced Behavioral Sensitization and Activation of Ras-ERK-∆FosB Pathway in the Caudate Putamen

Interaction of CB<sub>1</sub> receptor agonist arachidonylcyclopropylamide with behavioural sensitisation to morphine in mice

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