Effects of acute ethanol on opioid peptide release in the central amygdala: an in vivo microdialysis study

Lam, Minh P.; Marinelli, Peter W.; Bai, Li; Gianoulakis, Christina

doi:10.1007/s00213-008-1267-8

Cited by 84 publications

(92 citation statements)

References 54 publications

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“…We and others have previously shown that acute ethanol administration enhances GABA release at CeA synapses from rats and mice (Roberto et al, 2003;Nie et al, 2004;Kang-Park et al, 2007). In addition, our previous physiologic studies indicate that acute ethanol administration induces release of such neuropeptides as endogenous opioids and CRF in CeA (Nie et al, 2004;Lam et al, 2008), and these peptides may further modulate GABA release (Nie et al, 2004;Kang-Park et al, 2007Roberto et al, 2010). We hypothesize that acute ethanol releases dynorphin in CeA that acts at presynaptic KORs by decreasing GABA release and partially ameliorating the overall effect of ethanol on such release.…”

Section: Methodsmentioning

confidence: 84%

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Kang-Park

Kieffer

Roberts

et al. 2013

J Pharmacol Exp Ther

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Section: Methodsmentioning

confidence: 84%

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Kang-Park

Kieffer

Roberts

et al. 2013

J Pharmacol Exp Ther

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“…Because changes were observed at concentrations as low as those of endogenous m-opioids in the rat brain (Lam et al, 2008), these changes might reflect the modulation of SWRs by endogenous opioids. In the hippocampus, MORs are almost exclusively located on GABAergic inhibitory interneurons (Drake and Milner, 2002) and opioid agonists modulate inhibition (Nicoll et al, 1980;Lupica, 1995) and increase the excitability of the pyramidal cells (Zieglgansberger et al, 1979;Masukawa and Prince, 1982;Swearengen and Chavkin, 1987).…”

Section: Interpretation Of Drug Effects -Implications For the Mechanimentioning

confidence: 98%

“…We then studied the effects of the three MOR agonists, morphine, DAMGO and fentanyl, used in a wide range of concentrations (1 nM-10 mM ), which includes concentrations similar to brain extracellular levels of endogenous opioids and clinically relevant concentrations of exogenous opioid agonists. Thus morphine, fentanyl and DAMGO were applied at concentrations (10 -9 to 10 -5 M) that included the nanomole regime covering the range of clinically relevant brain concentrations (Bouw et al, 2001), the opioid concentrations found in the cerebrospinal fluid (Bernards et al, 2003) or the plasma/serum (Veselis et al, 1994;Klepstad et al, 2003;Gunnar et al, 2004;Solassol et al, 2005) as well as the extracellular levels of endogenous brain opioids (~1 to 10 nM) (Lam et al, 2008).…”

Section: Figurementioning

confidence: 99%

Effects of μ‐opioid receptor modulation on the hippocampal network activity of sharp wave and ripples

Giannopoulos

Papatheodoropoulos

2013

British J Pharmacology

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BACKGROUND AND PURPOSEHippocampus-dependent memory involves the activity of sharp wave ripples (SWRs), which are thought to participate in the process of memory consolidation. The hippocampus contains high levels of endogenous opioids and of m-opioid receptors (MORs). Here, we have assessed the role of MOR agonists in the modulation of SWRs. EXPERIMENTAL APPROACHUsing recordings of extracellular potentials from the CA1 field of rat hippocampal slices, we examined the pharmacological actions of morphine, DAMGO and fentanyl on SWRs and on network excitability and paired-pulse inhibition. KEY RESULTSAll three MOR agonists (1 nM-10 mM) significantly increased the amplitude of sharp waves and the occurrence of SWR sequences, but reduced the initiation of episodes of SWRs. Fentanyl was most potent in producing these effects and morphine the least. Interestingly, although SWRs were reduced by relatively high concentrations (Ն100 nM) of all agonists, they were significantly enhanced by very low concentrations of morphine (5-10 nM). Morphine and DAMGO at moderate-to-high concentrations increased network excitability and reduced inhibition. Furthermore, DAMGO suppressed inhibition more readily than it increased excitation, whereas morphine suppressed inhibition only at high concentrations. These drug effects were reversed by the MOR antagonists naloxone and CTOP. CONCLUSIONS AND IMPLICATIONSWe found that the SWRs were significantly modulated by three MOR agonists and that the SWRs were very sensitive to subtle changes in the excitation/inhibition balance induced by MOR agonists. Such modulation might underlie the effects of these agonists on hippocampus-dependent memory. AbbreviationsICI, intra-cluster interval; IEI, inter-event interval; IEpI, inter-episode interval; MOR, m-opioid receptor; PPI, paired-pulse inhibition; PS, population spike; SWR, sharp wave ripple BJP British Journal of Pharmacology DOI:10.1111DOI:10. /j.1476DOI:10. -5381.2012 1146 British Journal of Pharmacology (2013) IntroductionEndogenous and clinically administered opioids act on many receptors (Waldhoer et al., 2004) and are involved in a wide variety of functions (Drolet et al., 2001) including hippocampus-dependent learning and memory (Wise, 1989;Meilandt et al., 2004;Bodnar, 2010;Kesner and Warthen, 2010;Dacher and Nugent, 2011). Nevertheless, the mechanisms by which opioids affect hippocampus-dependent memory appear to be highly complex and poorly understood.The critical involvement of the hippocampus in learning and memory (Eichenbaum, 2004;Squire et al., 2004) is underpinned by a number of different types of neuronal activity supporting distinct processes (Battaglia et al., 2011). For example, it is assumed that the encoding of new information that occurs during active behaviour is associated with q oscillation (Hasselmo, 2005) whereas memory consolidation takes place during inactivity (Alvarez and Squire, 1994;McGaugh, 2000). It is generally thought that memory consolidation entails the generation of irregular activity of sharp wave ripples...

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“…These data are consistent with preclinical studies showing that single intraperitoneal injection of either ethanol or amphetamine lead to increases in microdialysate b-endorphin concentrations taken from the rat nucleus accumbens 12,13 and the central nucleus of the amygdala. 14 However, the findings of Colasanti et al 11 failed to be replicated by another group using intravenous amphetamine administration; 15 therefore, the sensitivity of [ 11 C]carfentanil to EOP release after amphetamine challenge warrants further investigation. In addition to [ 11 C]carfentanil's sensitivity to EOP release, various preclinical [16][17][18] and clinical 5,8 paradigms suggest that [ 11 C]diprenorphine may also be susceptible to EOP release; however, the ability of amphetamine to reduce [ 11 C]diprenorphine binding has not yet been tested.…”

Section: Introductionmentioning

confidence: 99%

Imaging Endogenous Opioid Peptide Release with [¹¹C]Carfentanil and [³H]Diprenorphine: Influence of Agonist-Induced Internalization

Quelch

Katsouri

Nutt

et al. 2014

J Cereb Blood Flow Metab

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Understanding the cellular processes underpinning the changes in binding observed during positron emission tomography neurotransmitter release studies may aid translation of these methodologies to other neurotransmitter systems. We compared the sensitivities of opioid receptor radioligands, carfentanil, and diprenorphine, to amphetamine-induced endogenous opioid peptide (EOP) release and methadone administration in the rat. We also investigated whether agonist-induced internalization was involved in reductions in observed binding using subcellular fractionation and confocal microscopy. After radioligand administration, significant reductions in [ 11 C]carfentanil, but not [ 3 H]diprenorphine, uptake were observed after methadone and amphetamine pretreatment. Subcellular fractionation and in vitro radioligand binding studies showed that amphetamine pretreatment only decreased total [11 C]carfentanil binding. In vitro saturation binding studies conducted in buffers representative of the internalization pathway suggested that m-receptors are significantly less able to bind the radioligands in endosomal compared with extracellular compartments. Finally, a significant increase in m-receptor-early endosome co-localization in the hypothalamus was observed after amphetamine and methadone treatment using double-labeling confocal microscopy, with no changes in d-or k-receptor co-localization. These data indicate carfentanil may be superior to diprenorphine when imaging EOP release in vivo, and that alterations in the ability to bind internalized receptors may be a predictor of ligand sensitivity to endogenous neurotransmitter release.

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Effects of acute ethanol on opioid peptide release in the central amygdala: an in vivo microdialysis study

Abstract: Acute systemic ethanol administration induced a dose- and time-dependent increase in beta-endorphin and dynorphin A1-8 release at the level of the CeA, which may be involved in ethanol consumption.

Cited by 84 publications

References 54 publications

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Effects of μ‐opioid receptor modulation on the hippocampal network activity of sharp wave and ripples

Imaging Endogenous Opioid Peptide Release with [¹¹C]Carfentanil and [³H]Diprenorphine: Influence of Agonist-Induced Internalization

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Effects of acute ethanol on opioid peptide release in the central amygdala: an in vivo microdialysis study

Abstract: Acute systemic ethanol administration induced a dose- and time-dependent increase in beta-endorphin and dynorphin A1-8 release at the level of the CeA, which may be involved in ethanol consumption.

Cited by 84 publications

References 54 publications

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

κ-Opioid Receptors in the Central Amygdala Regulate Ethanol Actions at Presynaptic GABAergic Sites

Effects of μ‐opioid receptor modulation on the hippocampal network activity of sharp wave and ripples

Imaging Endogenous Opioid Peptide Release with [11C]Carfentanil and [3H]Diprenorphine: Influence of Agonist-Induced Internalization

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Imaging Endogenous Opioid Peptide Release with [¹¹C]Carfentanil and [³H]Diprenorphine: Influence of Agonist-Induced Internalization