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Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala.
Neuropharmacology. 2016 09; 108:474-84.N

Abstract

The endogenous cannabinoid (eCB) system has been suggested to play a key role in ethanol preference and intake, the acute effects of ethanol, and in the development of withdrawal symptoms following ethanol dependence. Ethanol-dependent alterations in glutamatergic signaling within the lateral/basolateral nucleus of the amygdala (BLA) are critical for the development and expression of withdrawal-induced anxiety. Notably, the eCB system significantly regulates both glutamatergic and GABAergic synaptic activity within the BLA. Chronic ethanol exposure significantly alters eCB system expression within regions critical to the expression of emotionality and anxiety-related behavior, including the BLA. Here, we investigated specific interactions between the BLA eCB system and its functional regulation of synaptic activity during acute and chronic ethanol exposure. In tissue from ethanol naïve-rats, a prolonged acute ethanol exposure caused a dose dependent inhibition of glutamatergic synaptic activity via a presynaptic mechanism that was occluded by CB1 antagonist/inverse agonists SR141716a and AM251. Importantly, this acute ethanol inhibition was attenuated following 10 day chronic intermittent ethanol vapor exposure (CIE). CIE exposure also significantly down-regulated CB1-mediated presynaptic inhibition at glutamatergic afferent terminals but spared CB1-inhibition of GABAergic synapses arising from local inhibitory-interneurons. CIE also significantly elevated BLA N-arachidonoylethanolamine (AEA or anandamide) levels and decreased CB1 receptor protein levels. Collectively, these data suggest a dynamic regulation of the BLA eCB system by acute and chronic ethanol.

Authors+Show Affiliations

Department of Physiology & Pharmacology, Winston-Salem NC, USA; Neuroscience and Alcohol Research Training Programs Wake Forest School Medicine, Winston-Salem NC, USA.Department of Physiology & Pharmacology, Winston-Salem NC, USA.Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA.Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA; Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN, USA; Vanderbilt-Kennedy Center for Research on Human Development, Vanderbilt University School of Medicine, Nashville, TN, USA; Department Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA.Department of Physiology & Pharmacology, Winston-Salem NC, USA; Neuroscience and Alcohol Research Training Programs Wake Forest School Medicine, Winston-Salem NC, USA. Electronic address: bmccool@wakehealth.edu.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

26707595

Citation

Robinson, Stacey L., et al. "Acute and Chronic Ethanol Exposure Differentially Regulate CB1 Receptor Function at Glutamatergic Synapses in the Rat Basolateral Amygdala." Neuropharmacology, vol. 108, 2016, pp. 474-84.
Robinson SL, Alexander NJ, Bluett RJ, et al. Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala. Neuropharmacology. 2016;108:474-84.
Robinson, S. L., Alexander, N. J., Bluett, R. J., Patel, S., & McCool, B. A. (2016). Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala. Neuropharmacology, 108, 474-84. https://doi.org/10.1016/j.neuropharm.2015.12.005
Robinson SL, et al. Acute and Chronic Ethanol Exposure Differentially Regulate CB1 Receptor Function at Glutamatergic Synapses in the Rat Basolateral Amygdala. Neuropharmacology. 2016;108:474-84. PubMed PMID: 26707595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala. AU - Robinson,Stacey L, AU - Alexander,Nancy J, AU - Bluett,Rebecca J, AU - Patel,Sachin, AU - McCool,Brian A, Y1 - 2015/12/18/ PY - 2015/08/13/received PY - 2015/11/02/revised PY - 2015/12/08/accepted PY - 2015/12/29/entrez PY - 2015/12/29/pubmed PY - 2017/7/19/medline KW - Anandamide KW - Basolateral amygdala KW - CB1 KW - Dependence KW - Endogenous cannabinoid KW - Ethanol SP - 474 EP - 84 JF - Neuropharmacology JO - Neuropharmacology VL - 108 N2 - The endogenous cannabinoid (eCB) system has been suggested to play a key role in ethanol preference and intake, the acute effects of ethanol, and in the development of withdrawal symptoms following ethanol dependence. Ethanol-dependent alterations in glutamatergic signaling within the lateral/basolateral nucleus of the amygdala (BLA) are critical for the development and expression of withdrawal-induced anxiety. Notably, the eCB system significantly regulates both glutamatergic and GABAergic synaptic activity within the BLA. Chronic ethanol exposure significantly alters eCB system expression within regions critical to the expression of emotionality and anxiety-related behavior, including the BLA. Here, we investigated specific interactions between the BLA eCB system and its functional regulation of synaptic activity during acute and chronic ethanol exposure. In tissue from ethanol naïve-rats, a prolonged acute ethanol exposure caused a dose dependent inhibition of glutamatergic synaptic activity via a presynaptic mechanism that was occluded by CB1 antagonist/inverse agonists SR141716a and AM251. Importantly, this acute ethanol inhibition was attenuated following 10 day chronic intermittent ethanol vapor exposure (CIE). CIE exposure also significantly down-regulated CB1-mediated presynaptic inhibition at glutamatergic afferent terminals but spared CB1-inhibition of GABAergic synapses arising from local inhibitory-interneurons. CIE also significantly elevated BLA N-arachidonoylethanolamine (AEA or anandamide) levels and decreased CB1 receptor protein levels. Collectively, these data suggest a dynamic regulation of the BLA eCB system by acute and chronic ethanol. SN - 1873-7064 UR - https://www.unboundmedicine.com/medline/citation/26707595/Acute_and_chronic_ethanol_exposure_differentially_regulate_CB1_receptor_function_at_glutamatergic_synapses_in_the_rat_basolateral_amygdala_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(15)30201-X DB - PRIME DP - Unbound Medicine ER -