Neurotransmitters as developmental signals

Meier, Eddi; Hertz, Leif; Schousboe, Arne

doi:10.1016/0197-0186(91)90113-r

Cited by 269 publications

(150 citation statements)

References 147 publications

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“…The potential role of GABA in mediating these and other inhibitory interactions remains to be explored. Alternatively, GABA in taste buds may function as an excitatory transmitter (Fiumelli and Woodin, 2007) or as a neurotrophic substance (Meier et al, 1999). Unfortunately, GAD1-null mice do not live beyond birth (Asada et al, 1997), ruling out taste tests on postnatal animals lacking GABAergic mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Tomchik¹,

Berg²,

Kim³

et al. 2007

J. Neurosci.

221

270

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A longstanding question in taste research concerns taste coding and, in particular, how broadly are individual taste bud cells tuned to taste qualities (sweet, bitter, umami, salty, and sour). Taste bud cells express G-protein-coupled receptors for sweet, bitter, or umami tastes but not in combination. However, responses to multiple taste qualities have been recorded in individual taste cells. We and others have shown previously there are two classes of taste bud cells directly involved in gustatory signaling: "receptor" (type II) cells that detect and transduce sweet, bitter, and umami compounds, and "presynaptic" (type III) cells. We hypothesize that receptor cells transmit their signals to presynaptic cells. This communication between taste cells could represent a potential convergence of taste information in the taste bud, resulting in taste cells that would respond broadly to multiple taste stimuli. We tested this hypothesis using calcium imaging in a lingual slice preparation. Here, we show that receptor cells are indeed narrowly tuned: 82% responded to only one taste stimulus. In contrast, presynaptic cells are broadly tuned: 83% responded to two or more different taste qualities. Receptor cells responded to bitter, sweet, or umami stimuli but rarely to sour or salty stimuli. Presynaptic cells responded to all taste qualities, including sour and salty. These data further elaborate functional differences between receptor cells and presynaptic cells, provide strong evidence for communication within the taste bud, and resolve the paradox of broad taste cell tuning despite mutually exclusive receptor expression.

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Section: Discussionmentioning

confidence: 99%

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Tomchik¹,

Berg²,

Kim³

et al. 2007

J. Neurosci.

221

270

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“…18 However, the routine administration of dBcAMP is intended to replace differentiating noradrenergic signals, which the cultured cells do not receive because they are harvested before locus coeruleus fibres reach the neopallium, and it makes the cultured astrocytes much more similar to their in vivo counterparts. 34 In the cells treated with dBcAMP, the level of expression of the 5-HT 2B receptor was increased, 5 but the treatment had no effect on expression of ADAR2 and GluK2 (B. Li and L. Peng, unpublished results, 2010). Nevertheless, it remains a goal to confirm key aspects of this study in vivo with subsequent fluorescence-activated cell sorting to obtain freshly isolated astrocytes and neurons.…”

Section: Limitationsmentioning

confidence: 99%

“…From day 3, the serum concentration was reduced to 10%, and after the age of 2 weeks, 0.25 mM dibutyryl cyclic adenosine monophosphate (dBcAMP) was included in the medium. Such cultures are known to be morphologically and functionally differentiated, 34 to express many characteristics of astrocytes in vivo 32 and to be highly enriched (> 95 purity) in glial fibrillary acidic protein (GFAP)-and glutamine synthetase-expressing astrocytes, with the main contaminating cells being macro phages (< 5%) and neurons and oligodendrocytes being absent. 35 …”

Section: Cell Culturesmentioning

confidence: 99%

Fluoxetine affects GluK2 editing, glutamate-evoked Ca²⁺ influx and extracellular signal-regulated kinase phosphorylation in mouse astrocytes

Zhang

et al. 2011

jpn

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. Background:We sought to study the effects of chronic exposure to fluoxetine -a selective serotonin reuptake inhibitor (SSRI) and specific 5-HT 2B receptor agonist in astrocytes -on the expression of kainate receptors (GluK1-5) in cultured astrocytes and in intact brains in mice and on GluK2 editing by adenosine deaminase acting on RNA (ADAR), as well as the ensuing effects of fluoxetine on glutamate-mediated Ca 2+ influx and extracellular signal-regulated kinase (ERK) 1/2 phosphorylation in astrocytes. Methods: We performed reverse transcription-polymerase chain reaction (PCR) to assess mRNA expression. We analyzed RNA editing with amplification refractory mutation system PCR and complementary DNA sequencing. Protein expression and ERK phosphorylation were assessed using Western blots. We studied gene silencing with specific small interfering RNAs (siRNA), and we studied intracellular Ca 2+ using fluorometry. Results: All GluK subunits were present in the brain in vivo, and GluK2-5 subunits were present in cultured astrocytes. Fluoxetine upregulated GluK2 and ADAR2. Enhanced GluK2 editing by fluoxetine abolished glutamate-mediated increases in intra cellular Ca 2+ and ERK 1/2 phosphorylation. Enhanced editing of GluK2 was prevented by siRNA against the 5-HT 2B receptor or ADAR2. Limitations: Limitations of our study include the use of an in vitro system, but our cultured cells in many respects behave like in vivo astrocytes. Conclusion: Fluoxetine alters astrocytic glutamatergic function.

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“…These cultures are highly enriched in astrocytes (>95% purity of glial fibrillary acidic protein-(GFAP-) and glutamine synthetase-expressing astrocytes) (Hertz et al 1985). Addition of dBcAMP leads to a morphological and functional differentiation as evidenced by the extension of cell processes and increases in several metabolic and functional activities characteristic of astrocytes in situ (Meier et al 1991); in addition this treatment promotes Ca 2+ flux through voltage-dependent channels (Hertz et al 1989). …”

Section: Cell Culturesmentioning

confidence: 99%

Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine

Bai

Song

et al. 2017

Psychopharmacology

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Here we present the data indicating that chronic treatment with fluoxetine regulates Cav-1/PTEN/PI3K/AKT/GSK-3β signalling pathway and glycogen content in primary cultures of astrocytes with bi-phasic concentration dependence. At lower concentrations fluoxetine down-regulates gene expression of Cav-1, decreases membrane content of PTEN, increases activity of PI3K/AKT, and elevates GSK-3β phosphorylation thus suppressing its activity. At higher concentrations fluoxetine acts in an inverse fashion. As expected, fluoxetine at lower concentrations increased while at higher concentrations decreased glycogen content in astrocytes. Our findings indicate that bi-phasic regulation of glycogen content via Cav-1/PTEN/AKT/GSK-3β pathway by fluoxetine may be responsible for both therapeutic and side effects of the drug.

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Neurotransmitters as developmental signals

Cited by 269 publications

References 147 publications

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Fluoxetine affects GluK2 editing, glutamate-evoked Ca²⁺ influx and extracellular signal-regulated kinase phosphorylation in mouse astrocytes

Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine

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Neurotransmitters as developmental signals

Cited by 269 publications

References 147 publications

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Breadth of Tuning and Taste Coding in Mammalian Taste Buds

Fluoxetine affects GluK2 editing, glutamate-evoked Ca2+ influx and extracellular signal-regulated kinase phosphorylation in mouse astrocytes

Bi-phasic regulation of glycogen content in astrocytes via Cav-1/PTEN/PI3K/AKT/GSK-3β pathway by fluoxetine

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Fluoxetine affects GluK2 editing, glutamate-evoked Ca²⁺ influx and extracellular signal-regulated kinase phosphorylation in mouse astrocytes