51. Glutamate Co-Release by Monoamine Neurons
- Author
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Jose Alfredo Mendez, Gregory Dal Bo, and Louis-Eric Trudeau
- Subjects
Glutamate receptor ,Biology ,chemistry.chemical_compound ,Norepinephrine ,Glutamatergic ,Monoamine neurotransmitter ,medicine.anatomical_structure ,nervous system ,Axon terminal ,chemistry ,Dopamine ,medicine ,Axon ,Neurotransmitter ,Neuroscience ,medicine.drug - Abstract
A wide range of indirect data obtained during the last two decades has suggested that monoamine neurons may co-release neurotransmitters. Ultrastructural investigations have consistently reported that these neurons, including dopamine, serotonin and norepinephrine neurons establish both junctional (i.e. synaptic) and non-junctional (i.e. non-synaptic) axon terminals. The hypothesis that some of these terminals can mediate synaptic glutamate release has received strong support from cell culture studies as well as indirect support from electrophysiological recordings obtained in slice preparations and in intact animals. The molecular identification of vesicular glutamate transporters (VGluTs) in recent years has provided a new impetus and a new strategy to confirm the glutamatergic phenotype of neurons. A number of recent results now confirm that while many serotonin neurons express VGluT3, a subset of norepinephrine and dopamine neurons express VGluT2, thus supporting the hypothesis of glutamate co-transmission. The possibility that the neurotransmitter repertoire of central monoamine neurons may be plastic during development and in the context of activity-dependent neuronal plasticity or disease is now a major direction of current research.
- Published
- 2008