Distribution of delta opioid receptor-expressing neurons in the mouse hippocampus

Erbs, Eric; Faget, Lauren; Scherrer, Grégory; Kessler, Pascal; Hentsch, Didier; Vonesch, J-L; Matifas, Audrey; Kieffer, Brigitte L.; Massotte, Dominique

doi:10.1016/j.neuroscience.2012.06.023

Cited by 52 publications

(54 citation statements)

References 39 publications

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“…Nr AB2251, Millipore, Billerica, MA, USA, dilution 1:2000) and goat anti-choline acetyltransferase (ChAT) (Cat. Nr AB144, Millipore, Billerica, MA, USA, dilution 1:400) polyclonal antibodies have been largely used in the literature and in our laboratory (Erbs et al, 2012). Rat anti-Substance P (SP) monoclonal antibody (Cat.…”

Section: Methodsmentioning

confidence: 99%

Expression of mu opioid receptor in dorsal diencephalic conduction system: New insights for the medial habenula

et al. 2014

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The habenular complex, encompassing medial (MHb) and lateral (LHb) divisions, is a highly conserved epithalamic structure involved in the dorsal diencephalic conduction system (DDC). These brain nuclei regulate information flow between the limbic forebrain and the mid- and hindbrain, integrating cognitive with emotional and sensory processes. The MHb is also one of the strongest expression sites for mu opioid receptors (MORs), which mediate analgesic and rewarding properties of opiates. At present however, anatomical distribution and function of these receptors have been poorly studied in MHb pathways. Here we took advantage of a newly generated MOR-mcherry knock-in mouse line to characterize MOR expression sites in the DDC. MOR-mcherry fluorescent signal is weak in the lateral habenula, but strong expression is visible in the medial habenula, fasciculus retroflexus and interpeduncular nucleus (IPN), indicating that MOR is mainly present in the MHb-IPN pathway. MOR-mcherry cell bodies are detected both in basolateral and apical parts of MHb, where the receptor co-localizes with cholinergic and Substance P (SP) neurons, respectively, representing two main MHb neuronal populations. MOR-mcherry is expressed in most MHb-SP neurons, and is present in only a subpopulation of MHb-cholinergic neurons. Intense diffuse fluorescence detected in lateral and rostral parts of the IPN further suggests that MOR-mcherry is transported to terminals of these SP and cholinergic neurons. Finally, MOR-mcherry is present in septal regions projecting to the MHb, and in neurons of the central and intermediate IPN. Together, this study describes MOR expression in several compartments of the MHb-IPN circuitry. The remarkably high MOR density in the MHb-IPN pathway suggests that these receptors are in a unique position to mediate analgesic, autonomic and reward responses.

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Section: Methodsmentioning

confidence: 99%

Expression of mu opioid receptor in dorsal diencephalic conduction system: New insights for the medial habenula

et al. 2014

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“…DORs are broadly expressed in the nervous system [14]. In the forebrain, a main site for the control of epileptic seizures [15], DORs are expressed in cortex and hippocampus with well-characterized expression in GABAergic neurons for hippocampus [16, 17]. …”

Section: Introductionmentioning

confidence: 99%

Delta opioid receptors expressed in forebrain GABAergic neurons are responsible for SNC80-induced seizures

Chung

Boehrer

Stéphan

et al. 2015

Behavioural Brain Research

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The delta opioid receptor (DOR) has raised much interest for the development of new therapeutic drugs, particularly to treat patients suffering from mood disorders and chronic pain. Unfortunately, the prototypal DOR agonist SNC80 induces mild epileptic seizures in rodents. Although recently developed agonists do not seem to show convulsant properties, mechanisms and neuronal circuits that support DOR-mediated epileptic seizures remain to be clarified. DORs are expressed throughout the nervous system. In this study we tested the hypothesis that SNC80-evoked seizures stem from DOR activity at the level of forebrain GABAergic transmission, whose inhibition is known to facilitate the development of epileptic seizures. We generated a conditional DOR knockout mouse line, targeting the receptor gene specifically in GABAergic neurons of the forebrain (Dlx-DOR). We measured effects of SNC80 (4.5, 9, 13.5 and 32 mg/kg), ARM390 (10, 30 and 60 mg/kg) or ADL5859 (30, 100 and 300 mg/kg) administration on electroencephalograms (EEGs) recorded in Dlx-DOR mice and their control littermates (Ctrl mice). SNC80 produced dose-dependent seizure events in Ctrl mice, but these effects were not detected in Dlx-DOR mice. As expected, ARM390 and ADL5859 did not trigger any detectable change in mice from both genotypes. These results demonstrate for the first time that SNC80-induced DOR activation induces epileptic seizures via direct inhibition of GABAergic forebrain neurons, and supports the notion of differential activities between first and second-generation DOR agonists.

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“…In the hippocampus, these receptors are mainly present in gamma-aminobutyric acid (GABA)ergic neurons of the DH, e.g. Ammon's horn and dentate gyrus [39], suggesting their involvement in neural plasticity. Moreover, it has recently been reported that Oprd1 2/2 mice display decreased ability to solve hippocampal-dependent tasks, e.g.…”

Section: Introductionmentioning

confidence: 99%

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

Yin

Meck

2014

Phil. Trans. R. Soc. B

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Mice with cytotoxic lesions of the dorsal hippocampus (DH) underestimated 15 s and 45 s target durations in a bi-peak procedure as evidenced by proportional leftward shifts of the peak functions that emerged during training as a result of decreases in both ‘start’ and ‘stop’ times. In contrast, mice with lesions of the ventral hippocampus (VH) displayed rightward shifts that were immediately present and were largely limited to increases in the ‘stop’ time for the 45 s target duration. Moreover, the effects of the DH lesions were congruent with the scalar property of interval timing in that the 15 s and 45 s functions superimposed when plotted on a relative timescale, whereas the effects of the VH lesions violated the scalar property. Mice with DH lesions also showed enhanced reversal learning in comparison to control and VH lesioned mice. These results are compared with the timing distortions observed in mice lacking δ -opioid receptors (Oprd1 −/− ) which were similar to mice with DH lesions. Taken together, these results suggest a balance between hippocampal–striatal interactions for interval timing and demonstrate possible functional dissociations along the septotemporal axis of the hippocampus in terms of motivation, timed response thresholds and encoding in temporal memory.

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Distribution of delta opioid receptor-expressing neurons in the mouse hippocampus

Cited by 52 publications

References 39 publications

Expression of mu opioid receptor in dorsal diencephalic conduction system: New insights for the medial habenula

Expression of mu opioid receptor in dorsal diencephalic conduction system: New insights for the medial habenula

Delta opioid receptors expressed in forebrain GABAergic neurons are responsible for SNC80-induced seizures

Comparison of interval timing behaviour in mice following dorsal or ventral hippocampal lesions with mice having δ -opioid receptor gene deletion

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