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Subthreshold glutamate release from mitral cell dendrites.

ABSTRACT: The dendrites of a number of neuron types function as presynaptic structures, releasing transmitter after action potentials and dendritic spikes. In this regard, dendrites can function like axons, producing discrete outputs after suprathreshold electrical events. However, as the major site of synaptic inputs, dendrites experience ongoing subthreshold fluctuations in membrane potential, raising the question of whether these subthreshold changes can cause changes in transmitter release. Here, we show that mitral cells of the accessory olfactory bulb release glutamate from their dendrites in response to both subthreshold and suprathreshold stimuli. Whereas subthreshold output was typically low under control conditions, it could be enhanced several fold by pharmacological or endogenous activation of group I metabotropic glutamate receptors. These results indicate that presynaptic dendrites can support two distinct forms of output, and can dynamically regulate how electrical activity is coupled to transmitter release.

SUBMITTER: Castro JB

PROVIDER: S-EPMC2709214 | biostudies-literature | 2009 May

REPOSITORIES: biostudies-literature

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Subthreshold glutamate release from mitral cell dendrites.

Castro Jason B JB Urban Nathaniel N NN

The Journal of neuroscience : the official journal of the Society for Neuroscience 20090501 21

The dendrites of a number of neuron types function as presynaptic structures, releasing transmitter after action potentials and dendritic spikes. In this regard, dendrites can function like axons, producing discrete outputs after suprathreshold electrical events. However, as the major site of synaptic inputs, dendrites experience ongoing subthreshold fluctuations in membrane potential, raising the question of whether these subthreshold changes can cause changes in transmitter release. Here, we s ...[more]

PMID: 19474329

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Project description:Epileptic seizures are frequent in patients with glioblastoma, and anticonvulsive treatment is often necessary. While clinical guidelines recommend all approved anticonvulsants, so far it is still unclear which of the available drugs is the best therapeutic option for treating glioma-associated seizures, also in view of possible anti-tumorigenic effects. In our study, we employed four patient-derived low-passage cell lines of glioblastoma and three cell lines of brain metastases, and challenged these cultures with four anticonvulsants with different mechanisms of action: levetiracetam, valproic acid, carbamazepine and perampanel. Cell proliferation was determined by bromodeoxyuridine incorporation. To further analyze the effects of perampanel, apoptosis induction was measured by caspase 3/7 activation. Glutamate release was quantified and glucose uptake was determined using 18F-fluorodeoxyglucose. Real-time polymerase chain reaction was employed to assess the expression of genes associated with glutamate release and uptake in brain tumor cells. Of the four anticonvulsants, only perampanel showed systematic inhibitory effects on cell proliferation, whereas all other anticonvulsants failed to inhibit glioma and metastasis cell growth in vitro. Metastasis cells were much more resistant to perampanel than glioblastoma cell lines. Glucose uptake was attenuated in all glioblastoma cells after perampanel exposure, whereas cell death via apoptosis was not induced. Extracellular glutamate levels were found to be significantly higher in glioblastoma cell lines as compared to metastasis cell lines, but could be reduced by perampanel exposure. Incubation with perampanel up-regulated glutamine synthetase expression in glioblastoma cells, whereas treatment with valproic acid and levetiracetam downregulated excitatory amino acid transporter-2 expression. Overall, our data suggest that perampanel acts as an anticonvulsive drug and additionally mediated anti-tumorigenic effects.

Dataset Information

Subthreshold glutamate release from mitral cell dendrites.

Publications

Subthreshold glutamate release from mitral cell dendrites.

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