Odorants differentially enhance phosphoinositide turnover and adenylyl cyclase in olfactory receptor neuronal cultures

Ronnett, Gabriele V.; Cho, Helen; Hester, Lynda D.; Wood, S F; Snyder, Solomon H.

doi:10.1523/jneurosci.13-04-01751.1993

Cited by 104 publications

(66 citation statements)

References 31 publications

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“…Acutely dissociated and long term in vitro preparations of rat ORNs respond to odorant stimulation (Pixley and Pun, 1990;Trombley and Westbrook, 1991;Ronnett et al, 1993). Preliminary evidence from our laboratory using calcium-and voltagesensitive dyes indicate that organotypic slice cultures of OE also respond vigorously to odorant application.…”

Section: Odorant Stimulation Of Orns Drives Th Expression In Coculturmentioning

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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Section: Odorant Stimulation Of Orns Drives Th Expression In Coculturmentioning

confidence: 94%

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

Puché

Shipley

1999

J. Neurosci.

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“…Two other compelling reasons make the study of Ca 2ϩ stores in ORNs necessary. First, odorants sometimes also cause formation of InsP 3 (Boekhoff et al 1990;Ronnett et al 1993). It has been proposed that InsP 3 mediates a second transduction mechanism by opening InsP 3 -gated channels (Boekhoff et al 1990;Schild et al 1995), but this proposal is at odds with experiments suggesting that odor transduction is mediated solely by the cAMP pathway (Belluscio et al 1998;Brunet et al 1996).…”

Section: Introductionmentioning

confidence: 99%

Amplification of Odor-Induced Ca²⁺ Transients by Store-Operated Ca²⁺ Release and Its Role in Olfactory Signal Transduction

Zufall

Leinders‐Zufall

Greer

2000

Journal of Neurophysiology

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release does not seem to be necessary for generation of an immediate electrophysiological response, nor does it contribute significantly to the Ca 2ϩ transients in the olfactory cilia. Rather, it is important for amplifying the magnitude and duration of Ca 2ϩ transients in the dendrite and soma and is thus necessary for the spread of an odorinduced Ca 2ϩ wave from the cilia to the soma. We show that this amplification process depends on Ca 2ϩ -induced Ca 2ϩ release. The results indicate that stimulation of ORNs with odorants can produce Ca 2ϩ mobilization from intracellular stores without an immediate effect on the receptor potential. Odor-induced, store-dependent Ca 2ϩ mobilization may be part of a feedback pathway by which information is transferred from the distal dendrite of an ORN to its soma.

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“…5). At least three second messengers have been identified to mediate or modulate peripheral olfactory signal transduction: IP3, cAMP, and cGMP Breer and Shepherd, 1993;Ronnett et al, 1993), and odorants of the same class can activate both the cAMP or IP3 pathways, which may also co-exist in the same cell (for a review, see Breer et al, 1994, and references within). The role of IP3 as a second messenger in olfaction was recently shown by several laboratories (Breer et al, 1990;Restrepo et al, 1993a;Honda et al, 1995).…”

Section: (I) Introductionmentioning

confidence: 99%

Chemosensory Function and Dysfunction

Spielman

1998

Critical Reviews in Oral Biology & Medicine

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Taste and smell are fundamental sensory systems essential in nutrition and food selection, for the hedonic and sensory experience of food, for efficient metabolism, and, in general, for the maintenance of a good quality of life. The gustatory and olfactory systems demonstrate a diversity of transduction mechanisms, and during the last decade, considerable progress has been made toward our understanding of the basic mechanisms of taste and smell. Understanding normal chemosensory function helps clarify the molecular events that underlie taste and smell disorders. At least 2,000,000 Americans suffer from chemosensory disorders-a number that is likely to grow as the aging segment of the population increases. Smell disorders are more frequent than taste disturbances, due to the vulnerability and anatomical distinctiveness of the olfactory system, and because a decline in olfactory function is part of the normal aging process. Common gustatory and olfactory complaints are due to a number of medications, to upper respiratory infections, to nasal and paranasal sinus diseases, and to damage to peripheral nerves supplying taste and smell. Most chemosensory complaints have an identifiable cause. Although diagnosis of taste and smell disorders has improved considerably over the last two decades, treatment of these disorders is still limited to conditions with discernible and reversible causes. Future research is needed for a better understanding of chemosensory mechanisms, establishing improved diagnostic procedures, and disseminating knowledge on chemosensory disorders among practitioners and the general public.

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Odorants differentially enhance phosphoinositide turnover and adenylyl cyclase in olfactory receptor neuronal cultures

Cited by 104 publications

References 31 publications

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

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

Amplification of Odor-Induced Ca²⁺ Transients by Store-Operated Ca²⁺ Release and Its Role in Olfactory Signal Transduction

Chemosensory Function and Dysfunction

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Odorants differentially enhance phosphoinositide turnover and adenylyl cyclase in olfactory receptor neuronal cultures

Cited by 104 publications

References 31 publications

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

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

Amplification of Odor-Induced Ca2+ Transients by Store-Operated Ca2+ Release and Its Role in Olfactory Signal Transduction

Chemosensory Function and Dysfunction

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Amplification of Odor-Induced Ca²⁺ Transients by Store-Operated Ca²⁺ Release and Its Role in Olfactory Signal Transduction