Central Amygdala Neuroplasticity in Alcohol Dependence

Roberto, Marisa; Gilpin, Nicholas W.

doi:10.1016/b978-0-12-405941-2.00011-0

Cited by 4 publications

(4 citation statements)

References 217 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of both acute EtOH and chronic EtOH/acute in vitro withdrawal on glutamatergic signaling are primarily centered on postsynaptic glutamate receptors (Bliss et al, 2014; Lovinger and Roberto, 2013; Roberto and Gilpin, 2014; Szumliski and Woodward, 2014). Glutamate receptors include three major classes of ionotropic receptors (iGluRs), 1) α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors or AMPARs), 2) N -methyl-D-aspartate receptors (NMDA receptors or NMDARs) and 3) kainate receptors (KARs), as well as various sub-classes of metabotropic glutamate receptors (mGluRs) that are G protein-coupled receptors (GPCRs) (Lovinger and Roberto, 2013).…”

Section: 1 Glutamate and Etoh Effectsmentioning

confidence: 99%

Synaptic targets: Chronic alcohol actions

2017

Self Cite

View full text Add to dashboard Cite

Alcohol acts on numerous cellular and molecular targets to regulate neuronal communication within the brain. Chronic alcohol exposure and acute withdrawal generate prominent neuroadaptations at synapses, including compensatory effects on the expression, localization and function of synaptic proteins, channels and receptors. The present article reviews the literature describing the synaptic effects of chronic alcohol exposure and their relevance for synaptic transmission in the central nervous system. This review is not meant to be comprehensive, but rather to highlight the effects that have been observed most consistently and that are thought to contribute to the development of alcohol dependence and the negative aspects of withdrawal. Specifically, we will focus on the major excitatory and inhibitory neurotransmitters in the brain, glutamate and GABA, respectively, and how their neuroadaptations after chronic alcohol exposure contributes to alcohol reinforcement, dependence and withdrawal.

show abstract

Section: 1 Glutamate and Etoh Effectsmentioning

confidence: 99%

Synaptic targets: Chronic alcohol actions

2017

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Backg Rou N Dmentioning

confidence: 99%

“…Anker and Kushner (2019) describe how the overlapping neurobiological architecture of INTD and AUD, particularly concerning systems that regulate stress and reward such as the hypothalamic pituitary adrenal system (HPA) and the limbic system (Gilpin et al, 2015; Vinkers et al, 2021), may be relevant to the high rate of comorbidity between these conditions. For example, dysfunction in the central amygdala, which serves as an integrative hub for stress and reward systems and consequently plays a major role in emotional processing (Agoglia & Herman, 2018; Breese et al, 2011; Gilpin et al, 2015; Noronha et al, 2014; Roberto & Gilpin, 2014), is a neurobiological correlate of both INTD and AUD (Agoglia & Herman, 2018; Breese et al, 2011; Gilpin et al, 2015). Also, the central amygdala has been shown to regulate depressive‐ and anxiety‐like states in both humans and rodents (Han et al, 2018; Koob, 2013; Koob & Le Moal, 2001; VanElzakker et al, 2014) and serves a functional role in the acquisition and maintenance of alcohol self‐administration in nondependent rodents (Dyr & Kostowski, 1995; Hyytiä & Koob, 1995; Möller et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Evidence for an alcohol‐related “harm paradox” in individuals with internalizing disorders: Test and replication in two independent community samples

Anker

Thuras

Shuai

et al. 2023

Alcohol: Clinical and Experimental Research

View full text Add to dashboard Cite

Background Internalizing (anxiety and mood) disorders (INTD) commonly co‐occur (are “comorbid”) with alcohol use disorder (AUD). The literature suggests that excessive alcohol use aimed at coping with INTD symptoms is, at best, a partial explanation for the high comorbidity rates observed. We hypothesized that individuals with INTD experience greater susceptibility to developing AUD symptoms due to the partially shared neurobiological dysfunctions underlying both conditions. We probe this hypothesis by testing the prediction that, after accounting for the volume of alcohol intake, individuals with INTD experience higher levels of alcohol‐related symptoms. Methods Data from the National Epidemiological Survey on Alcohol‐Related Conditions (NESARC) Wave 3 were used for the primary analyses, and NESARC Wave 1 data were used for independent replication analyses. Individuals who reported any alcohol use in the prior year were categorized as: (1) never having had an INTD diagnosis (“INTD‐Never”); (2) having a remitted INTD diagnosis only (“INTD‐Remitted”); or (3) having current INTD diagnosis (“INTD‐Current”). Between‐group contrasts of alcohol‐related symptoms controlled for total alcohol intake (past year), drinking pattern (e.g., binging) and variables previously shown to mark exaggerated AUD symptoms relative to drinking amount (e.g., SES, gender, and family history). Results With all covariates in the model, individuals in the INTD‐Current group and the INTD‐Remitted group reported significantly greater alcohol‐related symptoms than those in the INTD‐Never group but did not themselves differ in level of alcohol‐related symptoms. These results were replicated in the NESARC 1 dataset. Conclusions Individuals with INTD experience more alcohol‐related symptoms than those who drink at the same level. While considering other explanations, we argue that this “harm paradox” is best explained by the view that INTD confers a neurobiologically mediated susceptibility to the development of AUD symptoms.

show abstract

“…Thus, CRF, dynorphin, and alcohol have been hypothesized to augment the inhibition of CeA projection interneurons (co-containing CRF, opioids, or NPY), leading to the excitation of downstream neurons through disinhibition (see Roberto review, this issue). Thus, the cellular actions parallel the neuropharmacological effects in animal models of compulsive drug taking and seeking, leading to a powerful preclinical framework for future drug development (Roberto and Gilpin, 2014). A focus on restoring motivational homeostasis by reversing acute withdrawal and protracted abstinence associated with the withdrawal/negative affect and preoccupation/anticipation (craving) stages of the addiction cycle reveals numerous preclinical targets for medications development for addiction.…”

Section: Neurobiological Mechanisms In Alcohol Use Disorder That Are mentioning

confidence: 99%

Emerging pharmacotherapies for alcohol use disorder

Mason

2017

Neuropharmacology

View full text Add to dashboard Cite

The identification of different stages within the alcohol use disorder (AUD) cycle that are linked to neurocircuitry changes in pathophysiology associated with the negative emotional states of abstinence has provided a view of medication development for AUD that emphasizes changes in the brain reward and stress systems. Alcohol use disorder can be defined as a chronic relapsing disorder that involves compulsive alcohol seeking and taking, loss of control over alcohol intake, and emergence of a negative emotional state during abstinence. The focus of early medications development was to block the motivation to seek alcohol in the binge/intoxication stage. More recent work has focused on reversing the motivational dysregulations associated with the withdrawal/negative affect and preoccupation/anticipation stages during protracted abstinence. Advances in our understanding of the neurocircuitry and neuropharmacological mechanisms that are involved in the development and maintenance of the withdrawal/negative affect stage using validated animal models have provided viable targets for future medications. Another major advance has been proof-of-concept testing of potential therapeutics and clinical validation of relevant pharmacological targets using human laboratory models of protracted abstinence. This review focuses on future targets for medication development associated with reversal of the loss of reward function and gain in brain stress function that drive negative reinforcement in the withdrawal/negative affect stage of addiction. Basic research has identified novel neurobiological targets associated with the withdrawal/negative affect stage and preoccupation/anticipation stage, with a focus on neuroadaptive changes within the extended amygdala that account for the transition to dependence and vulnerability to relapse.

show abstract

Central Amygdala Neuroplasticity in Alcohol Dependence

Cited by 4 publications

References 217 publications

Synaptic targets: Chronic alcohol actions

Synaptic targets: Chronic alcohol actions

Evidence for an alcohol‐related “harm paradox” in individuals with internalizing disorders: Test and replication in two independent community samples

Emerging pharmacotherapies for alcohol use disorder

Contact Info

Product

Resources

About