Effects of acute cocaine on ERK and DARPP-32 phosphorylation pathways in the caudate-putamen of Fischer rats

Sun, Wei-Lun; Zhou, Luyi; Hazim, Ruhal; Quiñones-Jenab, Vanya; Jenab, Shirzad

doi:10.1016/j.brainres.2007.07.051

Cited by 35 publications

(37 citation statements)

References 63 publications

(83 reference statements)

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“…However, because we saw only a 32% increase in phosphoThr 34 -DARPP-32 after cocaine in simultaneously studied adult mice, it is difficult to make a firm conclusion as to whether these data are reflective of age and/or background strain (Sun et al, 2007). However, there were marked age-related differences in levels of phosphoThr 34 -DARPP-32 both at baseline and after a cocaine injection, despite equal total DARPP-32 levels.…”

Section: Discussionmentioning

confidence: 57%

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

Niculescu¹,

Perrine²,

Miller³

et al. 2008

J. Neurosci.

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Responses to psychostimulants vary with age, but the molecular etiologies of these differences are largely unknown. The goal of the present research was to identify age-specific behavioral and molecular adaptations to cocaine and to elucidate the mechanisms involved therein. Postweanling, periadolescent, and adult male CD-1 mice were exposed to cocaine (20 mg/kg) for 7 d. The rewarding effects of cocaine were assessed, as were the response to a Trk antagonist and the regulation of dopamine and cAMP-regulated phosphoprotein, 32 kDa (DARPP-32). Cocaine was rewarding in both periadolescent and adult mice using a conditioned place preference procedure. In contrast, postweanling mice failed to demonstrate significant cocaine-induced place preference. Because components of the neurotrophin system including brain-derived neurotrophic factor and TrkB are developmentally regulated, their role in the age-specific effects of cocaine was determined using the Trk receptor antagonist K252a. Postweanling mice that received K252a before daily cocaine showed a significant place preference to the cocaine-paired environment that was not seen in the absence of K252a. DARPP-32 protein levels were significantly upregulated in the lateral region of the caudate-putamen exclusively in postweanling mice after chronic cocaine. Daily pretreatment with K252a attenuated the induction of DARPP-32 in the postweanling striatum. These data indicate that Trk neurotransmission plays a role in age-specific behavioral and molecular responses to cocaine and concurrently modulates DARPP-32 levels.

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Section: Discussionmentioning

confidence: 57%

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

Niculescu¹,

Perrine²,

Miller³

et al. 2008

J. Neurosci.

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“…We found that 2.5 mg/kg ifenprodil significantly attenuated these increases, while the dose in the CPu by western blot. The results found that, similar to cocaine [41], acute METH administration significantly increased the protein level of pERK/ERK in the CPu, but ifenprodil did not result in an inhibitory effect. Interestingly, we found that acute pre-injections of ifenprodil at doses of 5 and 10 mg/kg significantly increased the protein level of Ras although 2.5 mg/kg ifenprodil or METH alone did not affect it.…”

Section: Effect Of Ifenprodil On Meth-induced Behavioral Sensitizatiomentioning

confidence: 64%

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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“…In addition, mGluR activation has been shown to induce rapid translation of striatal-enriched protein tyrosine phosphatase (STEP), which also downregulates AMPAR surface expression and may actively maintain endocytosis rates (Luscher and Huber, 2010;Zhang et al, 2008). Acute exposure to both amphetamine and cocaine alters phosphorylation of STEP in striatal regions and inactivation of STEP prevents cocaineinduced reductions in AMPAR-mediated currents in MSNs (Chiodi et al, 2014;Sun et al, 2007;Tashev et al, 2009;Valjent et al, 2005). However, the degree to which alterations in STEP activity may occur in response to psychostimulant re-exposure is unknown.…”

Section: Mechanisms Underlying Synaptic Depotentiationmentioning

confidence: 99%

Cocaine and Amphetamine Induce Overlapping but Distinct Patterns of AMPAR Plasticity in Nucleus Accumbens Medium Spiny Neurons

Jedynak

Hearing

Ingebretson

et al. 2015

Neuropsychopharmacol

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Repeated exposure to psychostimulant drugs such as cocaine or amphetamine can promote drug-seeking and -taking behavior. In rodent addiction models, persistent changes in excitatory glutamatergic neurotransmission in the nucleus accumbens (NAc) appear to drive this drug-induced behavioral plasticity. To study whether changes in glutamatergic signaling are shared between or exclusive to specific psychostimulant drugs, we examined synaptic transmission from mice following repeated amphetamine or cocaine administration. Synaptic transmission mediated by AMPA-type glutamate receptors was potentiated in the NAc shell 10-14 days following repeated amphetamine or cocaine treatment. This synaptic enhancement was depotentiated by re-exposure to amphetamine or cocaine. By contrast, in the NAc core only repeated cocaine exposure enhanced synaptic transmission, which was subsequently depotentiated by an additional cocaine but not amphetamine injection during drug abstinence. To better understand the drug-induced depotentiation, we replicated these in vivo findings using an ex vivo model termed 'challenge in the bath,' and showed that drug-induced decreases in synaptic strength occur rapidly (within 30 min) and require activation of metabotropic glutamate receptor 5 (mGluR5) and protein synthesis in the NAc shell, but not NAc core. Overall, these data demonstrate the specificity of neuronal circuit changes induced by amphetamine, introduce a novel method for studying drug challenge-induced plasticity, and define NAc shell medium spiny neurons as a primary site of persistent AMPA-type glutamate receptor plasticity by two widely used psychostimulant drugs.

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Effects of acute cocaine on ERK and DARPP-32 phosphorylation pathways in the caudate-putamen of Fischer rats

Cited by 35 publications

References 63 publications

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

Trk: A Neuromodulator of Age-Specific Behavioral and Neurochemical Responses to Cocaine in Mice

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

Cocaine and Amphetamine Induce Overlapping but Distinct Patterns of AMPAR Plasticity in Nucleus Accumbens Medium Spiny Neurons

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