Olfactory receptor neurons express D2 dopamine receptors

Koster, Nancy L.; Norman, Andrew B.; Richtand, Neil M.; Nickell, William T.; Puché, Adam C.; Pixley, Sarah K.; Shipley, Michael T.

doi:10.1002/(sici)1096-9861(19990906)411:4<666::aid-cne10>3.0.co;2-s

Cited by 83 publications

(60 citation statements)

References 33 publications

(57 reference statements)

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“…Among the G protein-coupled receptors expressed in the olfactory bulb, D2R is highly and selectively expressed on the ON terminals (32). To determine whether Endo3 is co-expressed with presynaptic D2R in this region, we incubated olfactory bulbs with anti-Endo3 and anti-D2R antibodies, and we found that D2Rs were co-localized with Endo3 at the same glomerular synapses (Fig.…”

Section: Inhibition Of Transferrin Endocytosis By Endophilin 3-tomentioning

confidence: 91%

Inhibitory Role of Endophilin 3 in Receptor-mediated Endocytosis

Sugiura

Iwata

Matsuoka

et al. 2004

Journal of Biological Chemistry

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Endophilin 1 (Endo1) participates in synaptic vesicle biogenesis through interactions of its Src homology 3 domain with the polyphosphoinositide phosphatase Synaptojanin and the GTPase Dynamin. Endo1 has also been reported to affect endocytosis by converting membrane curvature via its lysophosphatidic acid acyltransferase activity. Here we report that a closely related isoform of Endo1, Endo3, inhibits clathrin-mediated endocytosis. Mutational analyses showed that the variable region of Endo3 is important in regulating transferrin endocytosis. In the brain, Endo3 is co-localized with dopamine D2 receptor in olfactory nerve terminals and inhibits its clathrin-mediated endocytosis in COS-7 cells. Furthermore, overexpression of Endo3 in an olfactory epithelium-derived cell line suppressed dopamine D2 receptor-mediated endocytosis and therefore accelerated its dopamine-induced differentiation. These results indicate that Endo3 may act as a negative regulator of clathrin-mediated endocytosis in brain neurons.

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Section: Inhibition Of Transferrin Endocytosis By Endophilin 3-tomentioning

confidence: 91%

Inhibitory Role of Endophilin 3 in Receptor-mediated Endocytosis

Sugiura

Iwata

Matsuoka

et al. 2004

Journal of Biological Chemistry

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“…Lesions of the olfactory nerve eliminate D2 receptor ligand binding in the theses layer. Olfactory receptor neurons express D2 receptor mRNA (Koster et al, 1998). In OB slice preparations, DA and selective D2 agonists block responses of olfactory bulb neurons to olfactory nerve stimulation (V. Aroniadou-Anderjaska and M. Shipley, unpublished observations).…”

Section: A Role For An Inducible Tyrosine Hydroxylase Enzymementioning

confidence: 94%

Odor-Induced, Activity-Dependent Transneuronal Gene InductionIn Vitro: Mediation by NMDA Receptors

Puché

Shipley

1999

J. Neurosci.

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Expression of tyrosine hydroxylase (TH) by juxtaglomerular (JG) neurons of the olfactory bulb (OB) requires innervation of the bulb by olfactory receptor neurons (ORNs). ORN lesion selectively downregulates TH in JG neurons. In reversible odor deprivation, TH expression is downregulated as the naris is closed and then upregulated upon naris reopening. The mechanism or mechanisms regulating this dependence are unknown. TH expression could be regulated by trophic factor release and/or synaptic activity from ORN terminals. We investigated TH expression in cocultures of dissociated postnatal rat OB cells and embryonic olfactory neuroepithelium (OE) slice explants. THpositive neurons in control dissociated OB cell cultures alone comprise only a small fraction of the total population of cells present in the culture. However, when OE slice explants are cocultured with dispersed OB cells, there is a mean 2.4-fold increase in the number of TH-positive neurons. ORNs in vivo use glutamate as a neurotransmitter. Broad spectrum excitatory amino acid antagonists (kyurenic acid) or selective antagonists of the NMDA receptor (APV) both prevent induction of TH expression in OE-OB cocultures. Furthermore, pulse application of NMDA stimulates TH expression in OB neurons in the absence of OE. In vitro, OB TH neurons express NMDA receptors, suggesting that NMDA stimulation is acting directly on TH neurons. Exposure of OE explants to natural odorants results in upregulation of TH, presumably through increased ORN activity, which could be blocked by APV. These findings indicate that odorant-stimulated glutamate release by ORN terminals regulates TH expression via NMDA receptors on JG dopaminergic neurons.

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“…In addition, ON terminals express GABA B receptors (Bonino et al 1999;Kratskin et al 2006;Priest and Puche 2004) Koster et al 1999;Maher and Westbrook 2008;Parrish-Aungst et al 2007;Wachowiak and Cohen 1999). Thus ON-evoked PPD can be due to at least two distinct presynaptic mechanisms: reduced vesicle availability and transmitter release due to the high release probability of ON terminals and presynaptic inhibition via activation of GABA B Rs and/or DA D 2 Rs on ON terminals.…”

Section: On-and Et-driven Pg Cells Differentially Regulate Phasic Andmentioning

confidence: 99%

Two GABAergic Intraglomerular Circuits Differentially Regulate Tonic and Phasic Presynaptic Inhibition of Olfactory Nerve Terminals

Shao

Puché²,

Kiyokage³

et al. 2009

Journal of Neurophysiology

106

218

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Olfactory nerve axons terminate in olfactory bulb glomeruli forming excitatory synapses onto the dendrites of mitral/tufted (M/T) and juxtaglomerular cells, including external tufted (ET) and periglomerular (PG) cells. PG cells are heterogeneous in neurochemical expression and synaptic organization. We used a line of mice expressing green fluorescent protein under the control of the glutamic acid decarboxylase 65-kDa gene (GAD65+) promoter to characterize a neurochemically identified subpopulation of PG cells by whole cell recording and subsequent morphological reconstruction. GAD65+ GABAergic PG cells form two functionally distinct populations: 33% are driven by monosynaptic olfactory nerve (ON) input (ON-driven PG cells), the remaining 67% receive their strongest drive from an ON→ET→PG circuit with no or weak monosynaptic ON input (ET-driven PG cells). In response to ON stimulation, ON-driven PG cells exhibit paired-pulse depression (PPD), which is partially reversed by GABAB receptor antagonists. The ON→ET→PG circuit exhibits phasic GABAB-R-independent PPD. ON input to both circuits is under tonic GABAB-R-dependent inhibition. We hypothesize that this tonic GABABR-dependent presynaptic inhibition of olfactory nerve terminals is due to autonomous bursting of ET cells in the ON→ET→PG circuit, which drives tonic spontaneous GABA release from ET-driven PG cells. Both circuits likely produce tonic and phasic postsynaptic inhibition of other intraglomerular targets. Thus olfactory bulb glomeruli contain at least two functionally distinct GABAergic circuits that may play different roles in olfactory coding.

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Olfactory receptor neurons express D2 dopamine receptors

Cited by 83 publications

References 33 publications

Inhibitory Role of Endophilin 3 in Receptor-mediated Endocytosis

Inhibitory Role of Endophilin 3 in Receptor-mediated Endocytosis

Odor-Induced, Activity-Dependent Transneuronal Gene InductionIn Vitro: Mediation by NMDA Receptors

Two GABAergic Intraglomerular Circuits Differentially Regulate Tonic and Phasic Presynaptic Inhibition of Olfactory Nerve Terminals

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