Alterations in AMPA receptor phosphorylation in the rat striatum following acute and repeated cocaine administration

Kim, S.M.; Ahn, Sung Min; Go, Bok Soon; Wang, J.Q.; Choe, Eun Sang

doi:10.1016/j.neuroscience.2009.06.054

Cited by 23 publications

(24 citation statements)

References 34 publications

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“…Among these substrates are dopamine transporters and glutamate receptors which are the major central sites of action of psychostimulants. Available data show that PKC-mediated phosphorylation of these substrates is highly sensitive to cocaine (Cervinski et al, 2005; Wang et al, 2006; Bakshi et al, 2009; Kim et al, 2009; Zahniser and Sorkin, 2009). Thus, by regulating phosphorylation and thus function of these substrates and others, PKC is deemed to contribute substantially to neural plasticity and drug addiction.…”

Section: Discussionmentioning

confidence: 99%

Cocaine facilitates PKC maturation by upregulating its phosphorylation at the activation loop in rat striatal neurons in vivo

et al. 2012

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Newly synthesized protein kinase C (PKC) undergoes a series of phosphorylation to render a mature form of the enzyme. It is this mature PKC that possesses the catalytic competence to respond to second messengers for activation and downstream signaling. The first and rate-limiting phosphorylation occurs at a threonine residue in the activation loop (AL), which triggers the rest maturation processing of PKC and regulates PKC activity in response to cellular stimulation. Given the fact that PKC is enriched in striatal neurons, we investigated the regulation of PKC phosphorylation at the AL site in the rat striatum by the psychostimulant cocaine in vivo. We found that PKC was phosphorylated at the AL site at a moderate level in the normal rat brain. Acute systemic injection of cocaine increased the PKC-AL phosphorylation in the two striatal structures (caudate putamen and nucleus accumbens). Cocaine also elevated the PKC-AL phosphorylation in the medial prefrontal cortex. The cocaine-stimulated PKC phosphorylation in the striatum is rapid and transient. A reliable increase in PKC phosphorylation was seen 7 min after drug injection, which declined to the normal level by 1 h. This kinetics corresponds to that seen for another striatum-enriched protein kinase, mitogen-activated protein kinase/extracellular signal-regulated kinase, in response to cocaine. This study suggests a new model for exploring the impact of cocaine on protein kinases in striatal neurons. By modifying PKC phosphorylation at the AL site, cocaine is believed to possess the ability to alter the maturation processing of the kinase in striatal neurons in vivo.

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Section: Discussionmentioning

confidence: 99%

Cocaine facilitates PKC maturation by upregulating its phosphorylation at the activation loop in rat striatal neurons in vivo

et al. 2012

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“…Immunoreactive protein bands visualized on X-ray films or BiP immunoreactivity on brain sections were semi-quantified with NIH image 1.62 software and a digital imaging camera as previously described [1,6,13]. Briefly, the background of X-ray films or brain sections was measured and saved as a "blank field" to correct for uneven illumination.…”

Section: Methodsmentioning

confidence: 99%

Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Ryu

Choe

2014

Neuroscience Letters

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“…With the exception of xestospongin C (Millipore Bioscience Research, Billerica, MA, USA), all pharmacological drugs were purchased from Tocris Bioscience (Bristol, UK). The concentrations of drugs used were determined from previous studies [1,6,12,15,21]. The PKG inhibitor, KT5823 (2 nmol), the neuronal nitric oxide synthase (nNOS) inhibitor, N -propyl (0.1 nmol), the Ca 2+ chelator, BAPTA-AM (50 pmol), the Na + channel blocker, tetrodotoxin citrate (TTX, 1 pmol), the N-methyl-d-aspartate (NMDA) receptor antagonists, AP5 (2 nmol) and MK801 (2 nmol), the ryanodine-sensitive Ca 2+ channel blocker, dantrolene (20 nmol), the L-type voltage operated Ca 2+ channel blocker, nifedipine (60 nmol), and the IP 3 -sensitive Ca 2+ channel blocker, xestospongin C (0.004 nmol), were dissolved in artificial cerebro-spinal fluid (aCSF) containing (mM) 123 NaCl, 0.86 CaCl 2 , 3.0 KCl, 0.89 MgCl 2 , 0.50 NaH 2 PO 4 , and 0.25 Na 2 HPO 4 aerated with 95% O 2 /5% CO 2 (pH 7.2-7.4) or dimethylsulfoxide (DMSO).…”

Section: Methodsmentioning

confidence: 99%

Protein kinase G regulates β-synuclein in response to repeated exposure to cocaine in the rat dorsal striatum in a Ca2+-dependent manner

Yang

Choe

2014

Neuroscience Letters

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Alterations in AMPA receptor phosphorylation in the rat striatum following acute and repeated cocaine administration

Cited by 23 publications

References 34 publications

Cocaine facilitates PKC maturation by upregulating its phosphorylation at the activation loop in rat striatal neurons in vivo

Cocaine facilitates PKC maturation by upregulating its phosphorylation at the activation loop in rat striatal neurons in vivo

Cocaine challenge increases the expression of immunoglobulin heavy chain binding protein in the rat nucleus accumbens

Protein kinase G regulates β-synuclein in response to repeated exposure to cocaine in the rat dorsal striatum in a Ca2+-dependent manner

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