Involvement of protein kinase A in ethanol-induced locomotor activity and sensitization

Fee, Jon R.; Knapp, Darin J.; Sparta, Dennis R.; Breese, George R.; Picker, Mitchell J.; Thiele, Todd E.

doi:10.1016/j.neuroscience.2006.02.002

Cited by 10 publications

(15 citation statements)

References 54 publications

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“…The paradigm used in this study has been described previously (Fee et al, 2006) and was adapted from a design commonly used to study ethanol-induced behavioral sensitization (Lessov et al, 2001). On test day 1-3, all mice received an i.p.…”

Section: The Effect Of Cp-154526 On the Expression Of Ethanol-inducementioning

confidence: 99%

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice

et al. 2007

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Rationale-Manipulation of glucocorticoid receptor signaling has been shown to alter the acquisition and expression of ethanol-induced locomotor sensitization in mice. It is unknown if other components of the hypothalamic-pituitary-adrenal (HPA)-axis modulate locomotor sensitization resulting from repeated ethanol administration. In the present investigation, we determined if pretreatment with an intraperitoneal (i.p.) injection of CP-154,526, a selective corticotropin releasing factor (CRF) type-1 receptor antagonist, would block the acquisition and/or expression of ethanolinduced locomotor sensitization in male DBA/2J mice.Methods-To assess the role of the CRF 1 receptor in the acquisition of behavioral sensitization, mice were pretreated with an i.p. injection of CP-154,526 30 minutes before each of 10 sensitizing i.p. injections of ethanol. To determine the role of the CRF 1 receptor in modulating the expression of ethanol-induced sensitization, mice that had previously been sensitized to the locomotor stimulant effects of ethanol were pretreated with CP-154,526 30 minutes before an i.p. injection of ethanol on the test day. In a third study, ethanol-naïve mice were pretreated with CP-154,526 30 minutes before an initial i.p. injection of ethanol to determine the combined effects of the CRF 1 receptor antagonist and ethanol on locomotor activity. Blood ethanol concentrations were assessed at the termination of sensitization studies.Results-Pretreatment with CP-154,526 blocked the expression of ethanol-induced locomotor sensitization in DBA/2J mice but did not prevent the acquisition of sensitization. The ability of CP-154,526 to block the expression of ethanol-induced locomotor sensitization was not attributable to alterations in blood ethanol levels or possible sedative effects produced by the combined administration of CP-154,526 and ethanol.Conclusions-These data provide novel evidence that CRF 1 receptor signaling modulates the expression of ethanol-induced locomotor sensitization, and adds to a growing literature suggesting a role for neurochemicals and hormones associated with the HPA-axis in behavioral sensitization resulting from repeated exposure to drugs of abuse.

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Section: The Effect Of Cp-154526 On the Expression Of Ethanol-inducementioning

confidence: 99%

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice

et al. 2007

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“…Defined by the progressive augmentation of locomotor responses to a given dose of ethanol following repeated administration, ethanol-induced locomotor sensitization has been observed in both rodent and human populations (Lessov and Phillips, 1998, Newlin and Thomson, 1991, Fee et al, 2006). Indeed, repeated drug exposure is thought to usurp natural reward circuitry within the mesolimbic dopaminergic pathway, leading to a hypersensitized state (Pierce and Kalivas, 1997, White and Kalivas, 1998, Robinson and Berridge, 2003).…”

Section: Introductionmentioning

confidence: 99%

Histone Acetylation in the Nucleus Accumbens Shell Modulates Ethanol‐Induced Locomotor Activity inDBA/2JMice

Sprow

Rinker

Thiele

2014

Alcoholism Clin & Exp Res

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Background A growing body of literature suggests that epigenetic mechanisms, including histone acetylation, may play key roles in drug abuse and the development of addiction. Experiments in the present study were designed to investigate the role of histone acetylation in ethanol-induced locomotor sensitization. Methods Immunohistochemical, western blotting, and site-directed pharmacological techniques were used to explore the roles of histone acetylation at histone H3 (acH3K9) in both the expression of and acquisition of ethanol-induced locomotor sensitization. A commonly used sensitization protocol, in which animals were exposed to repeated injections of a low dose of ethanol while in their home cage, was used to examine this behavioral phenomenon. Additionally, site-directed administration of the histone deacetylase inhibitor (HDACi) Trichostatin A (TSA), in the absence of repeated ethanol injections, was used to examine the role of hyperacetylation in the nucleus accumbens shell in ethanol-induced locomotor sensitization. Results Sensitized mice displayed elevated acH3K9 immunoreactivity (IR) localized to the shell of the nucleus accumbens. This augmentation in acH3K9 IR was confirmed, in a separate experiment, using western blot analyses. Next, repeated intra-accumbal infusions of TSA, in the absence of repeated ethanol injections, were sufficient to induce an augmented locomotor response to a later injection of a low dose (2.0 g/kg, i.p.) of ethanol, indicative of cross-sensitization to this locomotor stimulation between TSA and ethanol. Finally, a local infusion of TSA into the shell of the accumbens was also associated with a significant increase in acH3K9 IR within this region. Conclusions Together, the present observations suggest that histone acetylation, particularly within the shell of the nucleus accumbens, is important for the development and expression of ethanol-induced locomotor sensitization.

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“…We focused on these 2 families because of their putative role in the long-lasting neuroadaptations induced by EtOH (Bhutada et al, 2012;McGough et al, 2004;Pandey et al, 2008). There is considerable evidence that targets involved in signal transduction such as protein kinase A, brain-derived neurotrophic factor (BDNF), neuropeptide Y, and the transcription factor cAMP responsive element-binding protein 1 may play a role in EIBS and behavioral responses to drugs of abuse (Fee et al, 2006;Hayes et al, 2012;Madsen et al, 2012;Rueda et al, 2012). In addition, overexpression and genetic deletion of specific histone deacetylases (HDACs) or histone acetyltransferases affect behavioral responses to cocaine (Kumar et al, 2005;Levine et al, 2005;Renthal et al, 2007).…”

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confidence: 99%

Blockade of Ethanol-Induced Behavioral Sensitization by Sodium Butyrate: Descriptive Analysis of Gene Regulations in the Striatum

Legastelois

Botia

Naassila

2013

Alcohol Clin Exp Res

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Involvement of protein kinase A in ethanol-induced locomotor activity and sensitization

Cited by 10 publications

References 54 publications

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice

Histone Acetylation in the Nucleus Accumbens Shell Modulates Ethanol‐Induced Locomotor Activity inDBA/2JMice

Blockade of Ethanol-Induced Behavioral Sensitization by Sodium Butyrate: Descriptive Analysis of Gene Regulations in the Striatum

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