Selective alterations of NMDAR function and plasticity in D1 and D2 medium spiny neurons in the nucleus accumbens shell following chronic intermittent ethanol exposure

Renteria, Rafael; Maier, Esther Y.; Buske, Tavanna R.; Morrisett, Richard A.

doi:10.1016/j.neuropharm.2016.03.004

Cited by 55 publications

(72 citation statements)

References 50 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To investigate how CIE modulates plasticity in D1 and D2 MSNs of a mouse strain that has a well-documented drinking phenotype, we used Drd1a -tdTomato transgenic mice on a C57Bl/6J background (Ade, Wan, Chen, Gloss, & Calakos, 2011). Similar to what we observed in transgenic mice on the Swiss Webster background, LTD was expressed only in D1 MSNs of ethanol–naïve mice (Renteria, Maier, Buske, & Morrisett, 2016). Twenty-four hours after CIE treatment, the pairing protocol resulted in LTP in D1 MSNs and LTD in D2 MSNs.…”

Section: Chronic Intermittent Ethanol Exposure Differentially Modulatsupporting

confidence: 85%

Using In Vitro Electrophysiology to Screen Medications

Renteria¹,

Jeanes²,

Mangieri³

et al. 2016

International Review of Neurobiology

View full text Add to dashboard Cite

The nucleus accumbens (NAc) is a central component of the mesocorticolimbic reward system. Increasing evidence strongly implicates long-term synaptic neuroadaptations in glutamatergic excitatory activity of the NAc shell and/or core medium spiny neurons in response to chronic drug and alcohol exposure. Such neuroadaptations likely play a critical role in the development and expression of drug-seeking behaviors. We have observed unique cell-type-specific bidirectional changes in NAc synaptic plasticity (metaplasticity) following acute and chronic intermittent ethanol exposure. Other investigators have also previously observed similar metaplasticity in the NAc following exposure to psychostimulants, opiates, and amazingly, even following an anhedonia-inducing experience. Considering that the proteome of the postsynaptic density likely contains hundreds of biochemicals, proteins and other components and regulators, we believe that there is a large number of potential molecular sites through which accumbal metaplasticity may be involved in chronic alcohol abuse. Many of our companion laboratories are now engaged in identifying and screening medications targeting candidate genes and its products previously linked to maladaptive alcohol phenotypes. We hypothesize that if manipulation of such target genes and their products change NAc plasticity, then that observation constitutes an important validation step for the development of novel therapeutics to treat alcohol dependence.

show abstract

Section: Chronic Intermittent Ethanol Exposure Differentially Modulatsupporting

confidence: 85%

Using In Vitro Electrophysiology to Screen Medications

Renteria¹,

Jeanes²,

Mangieri³

et al. 2016

International Review of Neurobiology

View full text Add to dashboard Cite

show abstract

“…Notably, chronic intermittent ethanol (CIE) induced a significant increase in NMDAR function in dopamine D1 receptor-containing medium spiny neurons (MSNs) during acute in vitro withdrawal, as measured by the NMDA/AMPA ratio and input-output curves of isolated NMDAR currents and a decrease in D1- MSNs in the mouse nucleus accumbens (NAcc) shell (Renteria et al, 2016). This reversal of NMDAR function may account for the CIE-induced alterations in neuronal plasticity.…”

Section: 1 Glutamate and Etoh Effectsmentioning

confidence: 99%

“…This reversal of NMDAR function may account for the CIE-induced alterations in neuronal plasticity. In fact, in ethanol naïve mice, low frequency stimulation induced synaptic depression (LTD) in D1+ MSNs, but induced synaptic potentiation (LTP) in these cells after chronic ethanol exposure (Renteria et al, 2016). These cell-type specific alterations in excitatory signaling in the NAcc shell may constitute an important neuroadaptation for the expression of increased ethanol consumption induced by intermittent ethanol vapor exposure.…”

Section: 1 Glutamate and Etoh Effectsmentioning

confidence: 99%

“…Additionally, Marty and Spigelman (2012) reported that the amplitude and conductance of AMPAR-mediated miniature EPSCs were enhanced in the NAcc of CIE-treated rats during acute in vitro withdrawal, due to an increase in a small fraction of functional postsynaptic GluA2-lacking AMPARs (Marty and Spigelman, 2012). Similarly, CIE/acute in vitro withdrawal induced a significant increase in baseline AMPAR-mediated signaling in D1+ MSNs, but not D1- MSNs, in the rat NAcc (Renteria et al, 2016). Other studies have demonstrated similar increases in AMPAR function in cerebellar Purkinje neurons (Netzeband et al, 1999), and AMPAR-mediated synaptic responses in the BLA during in vivo withdrawal (Lack et al, 2007).…”

Section: 1 Glutamate and Etoh Effectsmentioning

confidence: 99%

See 1 more Smart Citation

Synaptic targets: Chronic alcohol actions

2017

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

“…Chronic drug use consistently causes changes in dendrite spines and synaptic proteins. Several synaptic mechanisms, e.g., AMPA receptor trafficking, mGluR signaling and dynamics of actin in spine, are affected by chronic drug taking [159]. Parkinson's disease is a chronic and progressive neurological disorder.…”

Section: Amylloid Beta (Ab) Homeostasis As a Target Of Environmental mentioning

confidence: 99%

Disruption of Neurosynaptic Physiology and Neuron Network Dysfunction in Brain Disorders: An Environmental and Occupational Health Perspective

Pandey¹

2017

AND

View full text Add to dashboard Cite

Networks of signaling cascades regulate synaptic transmission and morphology. Signaling molecules and their dynamics are subject to impact of environmental insults as well as genes predisposing to disease risks. Pollutants may impact brain through cellular, molecular and inflammatory pathways, causing direct damage or predisposing to damage by other insults, leading to diseases. Disruptions in structure and function of neurotransmission elements and protein networks contribute to pathogenesis of neuropsychiatric diseases. Different affected brain regions and/or synaptic connections between excitatory and inhibitory neurons charecterise specific clinical states. Functional identification of synaptic signaling networks and specific neuronal pathways would facilitate understanding of specific pathomechanisms relevant to preventive and corrective interventions. Physiology of neural networks and pathogenesis, therapeutics and prevention of diseases arising of their disruption, specially with environmental afflictions, deserve holistic and not fragmentary understanding. Present article attempts to present such diverse information with possible coherence to emphasize necessary address in contemporary medical teaching and continuing education for young researchers. The mounting challenge of prevention and management of pollution inflicted disruption of neurophysiology associated with brain dysfunction and diseases in contemporary world may be better addressed by integrated interdisciplinary understanding of the problems.

show abstract

Selective alterations of NMDAR function and plasticity in D1 and D2 medium spiny neurons in the nucleus accumbens shell following chronic intermittent ethanol exposure

Cited by 55 publications

References 50 publications

Using In Vitro Electrophysiology to Screen Medications

Using In Vitro Electrophysiology to Screen Medications

Synaptic targets: Chronic alcohol actions

Disruption of Neurosynaptic Physiology and Neuron Network Dysfunction in Brain Disorders: An Environmental and Occupational Health Perspective

Contact Info

Product

Resources

About