Temporal and Behavioral Variability in Cannabinoid Receptor Expression in Outbred Mice Submitted to Ethanol-Induced Locomotor Sensitization Paradigm

Coelhoso, Cássia Canha; Engelke, Douglas Senna; Filev, Renato; Silveira, Dartiu Xavier da; Mello, Luiz E.; Santos-Junior, Jair Guilherme

doi:10.1111/acer.12130

Cited by 17 publications

(20 citation statements)

References 44 publications

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“…Another study found that withdrawal from CIE increased CB 1 transcript in the rat prefrontal cortex (Rimondini et al, 2002). Other work suggests that withdrawal from CIE causes increased CB 1 protein in the hippocampus (Mitrirattanakul et al, 2007; Ceccarini et al, 2013; Coelhoso et al, 2013), striatum (Ceccarini et al, 2013; Coelhoso et al, 2013), and NAc (Coelhoso et al, 2013) that persist for up to 40 days. These results suggest that persistent upregulation of CB 1 occurs during acute withdrawal and protracted abstinence.…”

Section: Effects Of Chronic Ethanol On Cb1 Couplingmentioning

confidence: 99%

Roles for the endocannabinoid system in ethanol-motivated behavior

Henderson-Redmond

Guindon

Morgan

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Alcohol use disorder represents a significant human health problem that leads to substantial loss of human life and financial cost to society. Currently available treatment options do not adequately address this human health problem, and thus, additional therapies are desperately needed. The endocannabinoid system has been shown, using animal models, to modulate ethanol-motivated behavior, and it has also been demonstrated that chronic ethanol exposure can have potentially long-lasting effects on the endocannabinoid system. For example, chronic exposure to ethanol, in either cell culture or preclinical rodent models, causes an increase in endocannabinoid levels that results in down-regulation of the cannabinoid receptor 1 (CB1) and uncoupling of this receptor from downstream G protein signaling pathways. Using positron emission tomography (PET), similar down-regulation of CB1 has been noted in multiple regions of the brain in human alcoholic patients. In rodents, treatment with the CB1 inverse agonist SR141716A (Rimonabant), or genetic deletion of CB1 leads to a reduction in voluntary ethanol drinking, ethanol-stimulated dopamine release in the nucleus accumbens, operant self-administration of ethanol, sensitization to the locomotor effects of ethanol, and reinstatement/relapse of ethanol-motivated behavior. Although the clinical utility of Rimonabant or other antagonists/inverse agonists for CB1 is limited due to negative neuropsychiatric side effects, negative allosteric modulators of CB1 and inhibitors of endocannabinoid catabolism represent therapeutic targets worthy of additional examination.

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Section: Effects Of Chronic Ethanol On Cb1 Couplingmentioning

confidence: 99%

Roles for the endocannabinoid system in ethanol-motivated behavior

Henderson-Redmond

Guindon

Morgan

2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…During EtOH‐induced behavioral sensitization (EIBS) paradigm in mice, one robust result is the variability in the rodent's response, with some animals being sensitized at the end of the procedure and others not showing sensitization (called resistant). Although most of the literature on EtOH‐induced behavioral sensitization was dedicated to the mesolimbic circuitry, it has been shown that the dorsal hippocampus may endure some changes after EtOH‐ or other drugs of abuse‐induced sensitization (Degoulet et al, ; Botia et al, ; Coelhoso et al, ; Soares‐Simi et al, ; Legastelois et al, ; Nona et al, ). Different targets have been identified, such as the transcription factor CREB (Soares‐Simi et al, ; Nona et al, ), cannabinoid receptor expression (Coelhoso et al, ), low level of chromatin remodeling (Botia et al, ), BDNF and trkB receptor mRNA expression (Nona et al, ).…”

Section: Introductionmentioning

confidence: 99%

“…Although most of the literature on EtOH‐induced behavioral sensitization was dedicated to the mesolimbic circuitry, it has been shown that the dorsal hippocampus may endure some changes after EtOH‐ or other drugs of abuse‐induced sensitization (Degoulet et al, ; Botia et al, ; Coelhoso et al, ; Soares‐Simi et al, ; Legastelois et al, ; Nona et al, ). Different targets have been identified, such as the transcription factor CREB (Soares‐Simi et al, ; Nona et al, ), cannabinoid receptor expression (Coelhoso et al, ), low level of chromatin remodeling (Botia et al, ), BDNF and trkB receptor mRNA expression (Nona et al, ). It is known that drugs of abuse alter NMDA‐dependent bidirectional synaptic plasticity, i.e., long‐term synaptic depression (LTD) and long‐term potentiation (LTP) in the mesolimbic circuit (Lüscher and Malenka, ) and in particular in the nucleus accumbens (NAc) where NMDA receptor‐dependent LTD is abolished by different drugs of abuse (Kasanetz et al, ; Abrahao et al, ).…”

Section: Introductionmentioning

confidence: 99%

Resistance to ethanol sensitization is associated with a loss of synaptic plasticity in the hippocampus

Coune

Ferron

González-Marín

et al. 2016

Synapse

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Behavioral sensitization to repeated ethanol (EtOH) exposure induces an increase in locomotor activity in mice. However, not all animals express such sensitization. Although the literature indicated that the hippocampus may play a role in EtOH sensitization, it is not known whether behavioral sensitization to EtOH is associated with preferential changes in bidirectional synaptic plasticity, i.e., LTP and LTD, two markers of learning capabilities that have also been shown to be involved in addictive behavior. In the present study, we examined whether the vulnerability to develop and express behavioral sensitization to EtOH is associated with altered bidirectional synaptic plasticity in the CA1 area of the dorsal hippocampus. For this purpose, we analyzed both LTP and LTD in resistant and sensitized mice during the expression phase, i.e., 7 days after 10 days of repeated EtOH i.p. administration. We found that resistant mice showed a lack of LTD without changes in LTP. The lack of LTD was associated with an increase in GluN2A protein level and was not due to an altered level of neuronal activity, since no difference was observed between the number of c-FOS positive neurons in sensitized and resistant mice. Given that both types of synaptic plasticity signals may have distinct roles in specific learning and behaviors, our results suggest that resistant mice could exhibit different phenotypes in terms of learning/memory and addictive behaviors compared to sensitized ones. Synapse 71:e21899, 2017. © 2016 Wiley Periodicals, Inc.

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“…Interestingly, a prolonged withdrawal period after sensitization development is necessary for the establishment of neuroadaptations underlying long-term maintenance of the behavioral response (Vanderschuren and Kalivas, 2000). Such neuroadaptations are related to various neurobiological systems including dopaminergic (Heidbreder et al, 1996), GABAergic (Zhang et al, 2006), glutamatergic (Boudreau and Wolf, 2005), cannabinoidergic (Coelhoso et al, 2013), and opioidergic (Magendzo and Bustos, 2003). More specifically, inhibition of GABA transmission in the NAc persists 28 days after locomotor sensitization to methamphetamine (Zhang et al, 2006), suggesting a long-term disruption of this system after chronic treatment to drug of abuse.…”

Section: Discussionmentioning

confidence: 99%

“…To do so, we took advantage of the high level of individual variability in response to both EIBS (Botia et al, 2012;Legastelois et al, 2014) and anxiety tests (Bahi, 2013;Correia et al, 2009) in mice. Interestingly, we and others reported that significant signs of sensitization following chronic EtOH injections are only observed in a subset of mice, allowing the distinction between sensitized and resistant (nonsensitized) animals (Abrahao et al, 2012;Botia et al, 2012;Coelhoso et al, 2013).…”

mentioning

confidence: 88%

Basal Anxiety Negatively Correlates with Vulnerability to Ethanol‐Induced Behavioral Sensitization in DBA/2J Mice: Modulation by Diazepam

Botia

Legastelois

Houchi

et al. 2015

Alcoholism Clin & Exp Res

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This study shows that, in mice, basal anxiety predicts the vulnerability to EIBS. Mice exhibiting low basal anxiety will develop higher EIBS than mice with elevated anxiety levels. Modulation of anxiety by a diazepam treatment during the development of EIBS enhances its expression after 1 week postinduction. Altogether, we demonstrated an inverse relationship between basal anxiety-like behaviors and EIBS vulnerability and that resistance to EIBS vanishes after anxiolytic treatment.

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Temporal and Behavioral Variability in Cannabinoid Receptor Expression in Outbred Mice Submitted to Ethanol-Induced Locomotor Sensitization Paradigm

Cited by 17 publications

References 44 publications

Roles for the endocannabinoid system in ethanol-motivated behavior

Roles for the endocannabinoid system in ethanol-motivated behavior

Resistance to ethanol sensitization is associated with a loss of synaptic plasticity in the hippocampus

Basal Anxiety Negatively Correlates with Vulnerability to Ethanol‐Induced Behavioral Sensitization in DBA/2J Mice: Modulation by Diazepam

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