Opioid peptide regulation of neurons in the bed nucleus of the stria terminalis: a microiontophoretic study

Dalsass, Mario; Siegel, Allan

doi:10.1016/0006-8993(90)90799-h

Cited by 12 publications

(6 citation statements)

References 21 publications

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“…Although electrophysiological evidence indicates that NMDA receptors are involved in excitatory postsynaptic signaling in the BNST (Egli and Winder, 2003), ultrastructural (Gracy and Pickel, 1995) and pharmacological (Forray et al, 1995) data suggest that this protein may also have an axonal expression in this brain region. With regard to μOR, stimulation of this receptor in the BNST has been shown to produce a complex set of electrophysiological responses, including primarily excitatory (Dalsass and Siegel, 1990), inhibitory (Sawada and Yamamoto, 1981), or mixed (Casada and Dafny, 1993) actions, consistent with fine structural reports that μOR is present in both pre- and postsynaptic sites in the BNST (Jaferi and Pickel, 2009). …”

Section: Introductionsupporting

confidence: 62%

“…These events may be relevant to μOR, which was found to be co-expressed with NR1 in BNST neurons. The dendritic distribution of μOR and NR1 in postsynaptic compartments of BNST neurons, including those receiving excitatory contacts, provides a subcellular basis for the ability of opioid agonists to modulate excitatory signaling (Dalsass and Siegel, 1990) and influence opioid-dependent plasticity in response to exposure to opioid exposure (Dumont et al, 2008) and drug procurement behavior (Dumont et al, 2005). …”

Section: Discussionmentioning

confidence: 99%

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The NMDA-NR1 receptor subunit and the mu-opioid receptor are expressed in somatodendritic compartments of central nucleus of the amygdala neurons projecting to the bed nucleus of the stria terminalis

Beckerman

Glass

2012

Experimental Neurology

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The pathway between the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST) is emerging as a critical mediator of stress-related affective processes. Evidence also indicates that exposure to drugs of abuse, like opioids, is associated with NMDA-type glutamate receptor-dependent plasticity in the CeA and BNST. However, there is little evidence that NMDA receptors are expressed in CeA neurons projecting to the BNST, or are required for opioid-induced BNST neural activation. Immunoelectron microscopy, tract tracing, and conditional gene deletion technology were used to investigate the synaptic organization of the NMDA receptor and the mu-opioid receptor (μOR) in the CeA-BNST pathway. By dual labeling electron microscopy, numerous CeA-BNST projection neurons expressed the NMDA-NR1 receptor subunit (NR1) or μOR. By triple labeling, it was also found that NR1 and μOR were co-expressed in some CeA-BNST projection neurons. Despite being colocalized in somato-dendritic compartments of CeA neurons, NR1 and μOR were rarely expressed in their axonal terminations in the BNST. Deleting the NR1 gene in CeA neurons resulted in a reduction of morphine-induced Fos protein labeling in the ventral BNST. In summary, NR1 and μOR are coexpressed in somatodendritic sites of CeA neurons, including those projecting to the BNST. In addition, expression of the NR1 gene in CeA neurons is required for morphine-induced BNST neural activation. Thus, postsynaptic NMDA receptors and μORs are positioned for the co-modulation of CeA projection neurons to the BNST, which may provide a synaptic substrate for stress-induced emotional processes critically involved in opioid addictive behaviors.

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Section: Introductionsupporting

confidence: 62%

Section: Discussionmentioning

confidence: 99%

The NMDA-NR1 receptor subunit and the mu-opioid receptor are expressed in somatodendritic compartments of central nucleus of the amygdala neurons projecting to the bed nucleus of the stria terminalis

Beckerman

Glass

2012

Experimental Neurology

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“…The observed effects could be explained by the action of morphine at two levels. Different lines of data support the possibility of a direct effect of morphine in vBNST (Casada and Dafny, 1990 ; Dalsass and Siegel, 1990). In this regard, large numbers of endomorphine‐1‐like immunoreactive fibers have been observed in BNST (Martin‐Schild et al., 1999).…”

Section: Ne Extracellular Levels In Bnst Of Morphine‐treated Ratsmentioning

confidence: 98%

“…Few studies have addressed the participation of the ventral bed nucleus of the stria terminalis (vBNST) in opiate actions (Dalsass and Siegel, 1990 ; Casada and Dafny, 1993). Different lines of data support the idea that this nucleus could be an anatomical substrate of opiate addiction and withdrawal.…”

mentioning

confidence: 99%

Chronic Morphine Treatment and Withdrawal Increase Extracellular Levels of Norepinephrine in the Rat Bed Nucleus of the Stria Terminalis

Fuentealba¹,

Forray²,

Gysling³

2000

Journal of Neurochemistry

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Extracellular levels of norepinephrine (NE) and glutamate (Glu) in the ventral bed nucleus of the stria terminalis (vBNST) of saline-and chronic morphine-treated rats, with or without withdrawal, were studied by means of the in vivo microdialysis technique in anesthetized rats. In addition, the tissue concentration of NE was studied at different rostrocaudal levels of the vBNST. Chronic morphine treatment significantly increased extracellular levels of NE, but not Glu, in vBNST. At 48 h after naloxone-induced morphine withdrawal there was a further significant increase in the extracellular levels of NE, but not Glu, in vBNST. The presence of UK 14304, an ␣ 2 -adrenergic agonist, induced a significant decrease in NE extracellular levels in all experimental groups. In contrast, UK 14304 induced a significant decrease in Glu extracellular levels only in saline-treated rats. The results also show that the vBNST presents a rostrocaudal gradient of NE and contains 9.4% of total brain NE. The increase in NE extracellular levels in vBNST induced by chronic morphine treatment and the further increase in NE levels 48 h after naloxone-induced morphine withdrawal suggest that NE in vBNST may be involved in the pharmacological effects of chronic morphine and withdrawal. Key Words: Norepinephrine -Ventral bed nucleus of the stria terminalis-Morphine-Naloxone-Withdrawal-Microdialysis.

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“…Based on its cytoarchitecture, chemoarchitecture, and projection patterns, the BNST ALG also possesses distinct neuronal subpopulations, however 70–90% can be categorized as medium sized spiny GABAergic neurons (McDonald, 1983; Sun and Cassell, 1993). Despite this apparent homology, neurons of this region exhibit heterogenous physiological responses to several neurotransmitters, including opiates (Casada and Dafny, 1993; Dalsass and Siegel, 1990), norepinephrine (Casada and Dafany, 1993), acetylcholine (Casada and Dafany, 1993), oxytocin (Ingram et al, 1990), and serotonin (Levita et al, 2004; Guo et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

A transcriptomic analysis of type I–III neurons in the bed nucleus of the stria terminalis

Hazra

Guo

Ryan

et al. 2011

Molecular and Cellular Neuroscience

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Opioid peptide regulation of neurons in the bed nucleus of the stria terminalis: a microiontophoretic study

Cited by 12 publications

References 21 publications

The NMDA-NR1 receptor subunit and the mu-opioid receptor are expressed in somatodendritic compartments of central nucleus of the amygdala neurons projecting to the bed nucleus of the stria terminalis

The NMDA-NR1 receptor subunit and the mu-opioid receptor are expressed in somatodendritic compartments of central nucleus of the amygdala neurons projecting to the bed nucleus of the stria terminalis

Chronic Morphine Treatment and Withdrawal Increase Extracellular Levels of Norepinephrine in the Rat Bed Nucleus of the Stria Terminalis

A transcriptomic analysis of type I–III neurons in the bed nucleus of the stria terminalis

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