Dopaminergic modulation at the olfactory nerve synapse

Berkowicz, David; Trombley, Paul Q.

doi:10.1016/s0006-8993(99)02342-2

Cited by 98 publications

(89 citation statements)

References 41 publications

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“…On sensory afferents, D 2 -like receptors have been detected in mammals (Nickell et al, 1991;Coronas et al, 1997;Gutièrrez-Mecinas et al, 2005) but not in amphibians (Duchamp-Viret et al, 1997), suggesting that effects of DA on sensory input differ between species. In mammals and turtles, DA or agonists of D 2 -like receptors reduced MC responses to olfactory nerve stimulation via a presynaptic mechanism and decreased presynaptic calcium influx into sensory axon terminals (Hsia et al, 1999;Wachowiak and Cohen, 1999;Berkowicz and Trombley, 2000;Ennis et al, 2001;Maher and Westbrook, 2008). We therefore examined whether DA modulates transmitter release from sensory afferents also in zebrafish.…”

Section: Effects Of Da On Sensory Afferentsmentioning

confidence: 99%

“…DA modulates sensory input to MCs in mammals and reptiles by acting on presynaptic D 2 -like receptors (Hsia et al, 1999;Wachowiak and Cohen, 1999;Berkowicz and Trombley, 2000;Ennis et al, 2001;Maher and Westbrook, 2008) and has been suggested to directly regulate MC activity via D 2 -like receptors in amphibians (Duchamp-Viret et al, 1997). In addition, DA can modulate synaptic transmission between MCs and interneurons (Brünig et al, 1999;Davila et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

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Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

Bundschuh

Zhu²,

Schärer³

et al. 2012

J. Neurosci.

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In the olfactory bulb, the modulatory neurotransmitter dopamine (DA) is coexpressed with GABA by local interneurons, but its role in odor processing remains obscure. We examined functions of DA mediated by D 2 -like receptors in the olfactory bulb of adult zebrafish by pharmacology, whole-cell recordings, calcium imaging, and optogenetics. Bath application of DA had no detectable effect on odorantevoked sensory input. DA directly hyperpolarized mitral cells (

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Section: Effects Of Da On Sensory Afferentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

Bundschuh

Zhu²,

Schärer³

et al. 2012

J. Neurosci.

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“…These PG cells might provide localized inhibition to mitral/tufted cell dendrites or other nearby JG cells. Dopaminergic and GABAergic PG cells presynaptically inhibit ON terminals (Hsia et al, 1999;Wachowiak and Cohen, 1999;Aroniadou-Anderjaska et al, 2000;Berkowicz and Trombley, 2000;Ennis et al, 2001). Because at least 20% of PG cells receive monosynaptic ON input, it is possible that they mediate presynaptic inhibition of the ON.…”

Section: Juxtaglomerular Neurons and Glomerular Circuitrymentioning

confidence: 99%

External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

Hayar

Karnup

Ennis³

et al. 2004

J. Neurosci.

217

354

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“…Instead, GOA-1 appears to be activated in response to prolonged or strong odor stimuli. In the olfactory bulb, olfactory receptor neurons (ORNs) are thought to be presynaptically inhibited by GABA and dopamine released by juxtaglomerular cells, which receive excitatory glutamatergic input from ORNs in the glomeruli (47)(48)(49)(50). By analogy, interneurons located downstream of AWC neurons in C. elegans may release an inhibitory signal to repress activity of AWC neurons during olfactory adaptation, and this inhibitory signal may be transmitted by GOA-1 in AWC neurons.…”

Section: Factors That Act Downstream Of the Egl-30 Gq␣-dag Signalingmentioning

confidence: 99%

G _o α regulates olfactory adaptation by antagonizing G _q α-DAG signaling in Caenorhabditis elegans

Matsuki

Kunitomo

Iino

2006

Proc. Natl. Acad. Sci. U.S.A.

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The heterotrimeric G protein Go is abundantly expressed in the mammalian nervous system and modulates neural activities in response to various ligands. However, G o's functions in living animals are less well understood. Here, we demonstrate that GOA-1 G o␣ has a fundamental role in olfactory adaptation in Caenorhabditis elegans. Impairment of GOA-1 G o␣ function and excessive activation of EGL-30 G q␣ cause a defect in adaptation to AWC-sensed odorants. These pathways antagonistically modulate olfactory adaptation in AWC chemosensory neurons. Wild-type animals treated with phorbol esters and double-mutant animals of diacylglycerol (DAG) kinases, dgk-3; dgk-1, also have a defect in adaptation, suggesting that elevated DAG signals disrupt normal adaptation. Constitutively active GOA-1 can suppress the adaptation defect of dgk-3; dgk-1 double mutants, whereas it fails to suppress the adaptation defect of animals with constitutively active EGL-30, implying that GOA-1 acts upstream of EGL-30 in olfactory adaptation. Our results suggest that down-regulation of EGL-30 -DAG signaling by GOA-1 underlies olfactory adaptation and plasticity of chemotaxis.chemotaxis ͉ G protein T he olfactory sensory system can endow animals with abilities to detect food sources and mates and, in some cases, to avoid harmful chemicals and predators. Sensitivity to an odor stimulus can be appropriately adjusted by previous experience, allowing the sensory system to adapt to changeable environments. In mammals, olfactory adaptation (habituation) is known to occur throughout the odorant sensory pathway; for example, olfactory receptor neurons (1), secondary interneurons (2), and primary and higher-order olfactory cortices (3). These adaptation mechanisms appear to allow animals to increase the range of concentrations of odor that can be sensed and to discriminate among multiple odors.The nematode Caenorhabditis elegans has only 302 neurons, and a variety of behaviors have been observed. Of these, olfactory behavior is relatively well studied. Volatile odorants are mainly sensed by five pairs of sensory neurons, AWA, AWB, AWC, ADL, and ASH (4-6), of which AWA and AWC chemosensory neurons mediate attraction behavior (4). In this response, olfactory adaptation has also been observed (7). Animals lacking OSM-9 TRPV channel (7, 8), EGL-4 cGMPdependent protein kinase (9) or animals overexpressing ODR-1 guanylyl cyclase (10) exhibited defects in olfactory adaptation to AWC-sensed odorants. By contrast, animals with mutated tax-6, which encodes calcineurin, exhibited hyperadaptation (11), suggesting that Ca 2ϩ and cGMP signaling cascades participate in olfactory adaptation. Moreover, ARR-1 arrestin (12), TBX-2 T-box transcription factor (13), and the Ras-MAPK pathway (14) are also known to act in olfactory adaptation, illustrating that olfactory adaptation in C. elegans is modulated by complicated mechanisms consisting of multiple signaling cascades and control of gene expression.In general, neural activities are modulated by many types of ligands th...

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Dopaminergic modulation at the olfactory nerve synapse

Cited by 98 publications

References 41 publications

Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

G _o α regulates olfactory adaptation by antagonizing G _q α-DAG signaling in Caenorhabditis elegans

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Dopaminergic modulation at the olfactory nerve synapse

Cited by 98 publications

References 41 publications

Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

Dopaminergic Modulation of Mitral Cells and Odor Responses in the Zebrafish Olfactory Bulb

External Tufted Cells: A Major Excitatory Element That Coordinates Glomerular Activity

G o α regulates olfactory adaptation by antagonizing G q α-DAG signaling in Caenorhabditis elegans

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G _o α regulates olfactory adaptation by antagonizing G _q α-DAG signaling in Caenorhabditis elegans