Calcium imaging of central amygdala activity after escalation of fentanyl self-administration

IF 4.6 2区 医学 Q1 NEUROSCIENCES
Samantha G. Malone , Navid S. Tavakoli , Peggy S. Keller , Michael T. Bardo , Pavel I. Ortinski
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引用次数: 0

Abstract

The central amygdala (CeA) is involved in opioid relapse-associated behaviors. This study determined if escalation of fentanyl intake as modeled by long-access (LgA) self-administration (SA) alters ex vivo neuronal activity in CeA in response to fentanyl during acute withdrawal and protracted abstinence. Adult male and female Sprague-Dawley rats were trained to self-administer fentanyl or saline across 7 daily 1-h short access (ShA) sessions, followed by 21 6-h long access (LgA) sessions. Following acute (17 h) or protracted (30 days) withdrawal, withdrawal signs were assessed and rats were euthanized for CeA calcium imaging in brain slices. Fentanyl rats demonstrated reduced basal frequency of activity after 30 days withdrawal, but not after 17 h withdrawal. Regardless of SA group, acute fentanyl application in slices reduced activity (frequency, duration, active cell number) of CeA neurons. In acute withdrawal, the magnitude to which acute fentanyl suppressed CeA neuronal activity was smaller in fentanyl SA rats, relative to saline SA controls. However, the magnitude of acute fentanyl effect on suppression of CeA activity was greater in fentanyl SA rats (vs. saline SA controls) after protracted abstinence.
芬太尼自我给药升级后中央杏仁核活动的钙显像。
中央杏仁核(CeA)参与阿片类药物复发相关行为。本研究确定了芬太尼摄入量的增加是否会改变急性戒断和长期戒断期间芬太尼对CeA的体外神经元活性。成年雄性和雌性Sprague-Dawley大鼠被训练在每天7个1小时的短通道(ShA)中自我施用芬太尼或生理盐水,随后是21个6小时的长通道(LgA)。急性戒断(17小时)或长期戒断(30天)后,评估戒断体征,并对大鼠实施安乐死,进行脑切片CeA钙显像。芬太尼大鼠在停药30天后显示出基础活动频率降低,但在停药17小时后没有。无论SA组,急性芬太尼切片应用降低CeA神经元的活性(频率、持续时间、活性细胞数)。在急性戒断时,芬太尼SA大鼠急性芬太尼抑制CeA神经元活性的程度比盐水SA对照组小。然而,长期戒断后,芬太尼SA大鼠(与生理盐水SA对照组相比)急性芬太尼对CeA活性抑制的影响程度更大。
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来源期刊
Neuropharmacology
Neuropharmacology 医学-神经科学
CiteScore
10.00
自引率
4.30%
发文量
288
审稿时长
45 days
期刊介绍: Neuropharmacology publishes high quality, original research and review articles within the discipline of neuroscience, especially articles with a neuropharmacological component. However, papers within any area of neuroscience will be considered. The journal does not usually accept clinical research, although preclinical neuropharmacological studies in humans may be considered. The journal only considers submissions in which the chemical structures and compositions of experimental agents are readily available in the literature or disclosed by the authors in the submitted manuscript. Only in exceptional circumstances will natural products be considered, and then only if the preparation is well defined by scientific means. Neuropharmacology publishes articles of any length (original research and reviews).
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