Behavioral and Morphological Responses to Cocaine Require Kalirin7

Kiraly, Drew D.; Ma, Xin−Ming; Mazzone, Christopher M.; Xin, Xiaonan; Mains, Richard E.; Eipper, Betty A.

doi:10.1016/j.biopsych.2010.03.024

Cited by 78 publications

(168 citation statements)

References 53 publications

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“…For all experiments, animals were given a saline or cocaine injection and had their locomotor activity monitored for the subsequent 45 min. In the experiments in which RNA from NAc lysates was used for miRNA-Seq library preparation, animals were given injections of 20 mg/kg cocaine or saline (10 mL/kg) intraperitoneally for 7 d. Our group and others have demonstrated the efficacy of this method at eliciting robust locomotor sensitization (Hiroi et al 1999;Kiraly et al 2010). For all other experiments (both RNA and protein), animals received a lower dose of cocaine (10 mg/kg) on the first and last (seventh) day, with the standard 20 mg/kg cocaine dose on days 2-6 (Kalivas and Duffy 1993; Pierce et al 1996).…”

Section: Cocaine Treatment Of Micementioning

confidence: 98%

“…After extraction of the PSD-enriched fraction with 0.5% Triton X-100, PSDs were pelleted and subjected to Western blot analysis as described (Ma et al 2008;Kiraly et al 2010). The protocol is similar to that of Lugli et al (2008) and was modified to protect against RNA degradation as follows: All rotors, homogenizers, pestles, and ultracentrifuge tubes were rinsed with RNaseZAP (Applied Biosystems) and DEPC water and air dried prior to use; fractionation buffers were prepared using DEPC water and were treated with RNASecure (1:25 dilution from stock; Applied Biosystems) at 60°C for 10 min; aliquots of different subcellular fractions were diluted into TRIzol for preparation of total RNA as described previously.…”

Section: Whole Tissue Lysate Preparation and Subcellular Fractionationmentioning

confidence: 99%

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microRNA-Seq reveals cocaine-regulated expression of striatal microRNAs

Eipper-Mains

Kiraly²,

Palakodeti³

et al. 2011

RNA

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120

138

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MicroRNAs (miRNAs) are small RNAs that modulate gene expression by binding target mRNAs. The hundreds of miRNAs expressed in the brain are critical for synaptic development and plasticity. Drugs of abuse cause lasting changes in the limbic regions of the brain that process reward, and addiction is viewed as a form of aberrant neuroplasticity. Using next-generation sequencing, we cataloged miRNA expression in the nucleus accumbens and at striatal synapses in control and chronically cocainetreated mice. We identified cocaine-responsive miRNAs, synaptically enriched and depleted miRNA families, and confirmed cocaine-induced changes in protein expression for several predicted synaptic target genes. The miR-8 family, known for its roles in cancer, is highly enriched and cocaine regulated at striatal synapses, where its members may affect expression of cell adhesion molecules. Synaptically enriched cocaine-regulated miRNAs may contribute to long-lasting drug-induced plasticity through finetuning regulatory pathways that modulate the actin cytoskeleton, neurotransmitter metabolism, and peptide hormone processing.

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Section: Cocaine Treatment Of Micementioning

confidence: 98%

Section: Whole Tissue Lysate Preparation and Subcellular Fractionationmentioning

confidence: 99%

microRNA-Seq reveals cocaine-regulated expression of striatal microRNAs

Eipper-Mains

Kiraly²,

Palakodeti³

et al. 2011

RNA

Self Cite

120

138

View full text Add to dashboard Cite

show abstract

“…All behavior experiments were performed as described previously (Ma et al, 2008;Kiraly et al, 2010). Mice were moved to the behavior room in their home cages at least 1 h before training or testing.…”

Section: Methodsmentioning

confidence: 99%

“…Golgi staining of hippocampal CA1 pyramidal neurons from mature male mice shows decreased spine density in Kal7 knockout [Kal7(KO)] mice (Ma et al, 2008). Kal7 plays an essential role in the behavioral response of male mice to cocaine; Kal7(KO) mice display increased cocaine locomotor sensitization and impaired cocaine-induced spinogenesis (Kiraly et al, 2010). Expression of Kal7 in rat hippocampal neurons in culture is increased by 17␤-estradiol .…”

Section: Introductionmentioning

confidence: 99%

Analysis of Kalirin-7 Knockout Mice Reveals Different Effects in Female Mice

et al. 2012

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Estradiol treatment of ovariectomized rodents is known to affect the morphology of dendritic spines and produce behavioral and cognitive effects. Kalirin-7 (Kal7), a postsynaptic density (PSD)-localized Rho-guanine nucleotide exchange factor, is important for dendritic spine formation and stability. Male Kal7 knockout [Kal7(KO)] mice exhibit a number of abnormal behavioral and biochemical phenotypes. Given that chronic 17␤-estradiol (E2) replacement of ovariectomized rats enhanced Kal7 expression in the hippocampus and primary hippocampal cultures, we assessed the behavioral and biochemical effects of chronic E2 treatment of ovariectomized female wild-type and Kal7(KO) mice. Both intact and ovariectomized Kal7(KO) female mice exhibited decreased anxiety-like behavior compared with the corresponding wild type in the elevated zero maze and were unaffected by E2 treatment. Chronic E2 decreased locomotor activity in the open field and enhanced performance in a passive-avoidance fear conditioning task, which were both unaffected by genotype. Kal7(KO) female mice engaged in significantly more object exploration, both familiar and novel, than did wild-type females. E2 enhanced the acute locomotor response to cocaine, with no significant effect of genotype. Similar to Kal7(KO) males, Kal7(KO) females had decreased levels of Nmethyl-D-aspartate receptor 2B in hippocampal PSD fractions with no effect of E2 treatment. The differing behavioral effects of Kal7 ablation in female and male mice may offer insight into the molecular underpinnings of these differences.

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“…In adults, Kalirin-7 is the major isoform in mature neurons, whereas Kalirin-9 and Kalirin-12 are primarily found at lower levels in peripheral tissues (87). Genetic disruption of Kalirin-7 reduced spine density and induced several motor and behavior deficits (71,(147)(148)(149). Depletion of Kalirin-7 also impairs synaptic plasticity, probably through alteration of glutamate receptors and Rac1 signaling (150,151).…”

Section: Potential Mediators Of Xbp1 Signaling In Neuronsmentioning

confidence: 99%

The Transcription Factor XBP1 in Memory and Cognition: implications in Alzheimer’s Disease

Cissé

Duplan

Checler

2016

Mol Med

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X-box binding protein 1 (XBP1) is a unique basic region leucine zipper transcription factor that was isolated two decades ago in a search for regulators of major histocompatibility complex class II gene expression. XBP1 is a very complex protein that regulates many physiological functions, including the immune system, inflammatory responses and lipid metabolism. Evidence over the past few years suggests that XBP1 also plays an important role in pathological settings, since its activity as a transcription factor has profound effects on the prognosis and progression of diseases such as cancer, neurodegeneration and diabetes. Here we provide an overview of recent advances in our understanding of this multifaceted molecule, particularly in regulating synaptic plasticity and memory function, and the implications in neurodegenerative diseases, with an emphasis on Alzheimer's disease.

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Behavioral and Morphological Responses to Cocaine Require Kalirin7

Cited by 78 publications

References 53 publications

microRNA-Seq reveals cocaine-regulated expression of striatal microRNAs

microRNA-Seq reveals cocaine-regulated expression of striatal microRNAs

Analysis of Kalirin-7 Knockout Mice Reveals Different Effects in Female Mice

The Transcription Factor XBP1 in Memory and Cognition: implications in Alzheimer’s Disease

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