Abstract

Glutamate is the most common neurotransmitter in both the central and the peripheral nervous system. Glutamate is present in all types of neurons in sensory ganglia, and is released not only from their peripheral and central axon terminals but also from their cell bodies. Consistently, these neurons express ionotropic and metabotropic receptors, as well as other molecules involved in the synthesis, transport and release of the neurotransmitter. Primary sensory neurons are the first neurons in the sensory channels, which receive information from the periphery, and are thus key players in the sensory transduction and in the transmission of this information to higher centers in the pathway. These neurons are tightly enclosed by satellite glial cells, which also express several ionotropic and metabotropic glutamate receptors, and display increases in intracellular calcium accompanying the release of glutamate. One of the main interests in our group has been the study of the implication of the peripheral nervous system in sensory-dependent plasticity. Recently, we have provided novel evidence in favor of morphological changes in first- and second-order neurons of the trigeminal system after sustained alterations of the sensory input. Moreover, these anatomical changes are paralleled by several molecular changes, among which those related to glutamatergic neurotransmission are particularly relevant. In this review, we will describe the state of the art of the glutamatergic system in sensory ganglia and its involvement in input-dependent plasticity, a fundamental ground for advancing our knowledge of the neural mechanisms of learning and adaptation, reaction to injury, and chronic pain.

Highlights

  • Glutamate is the most abundant excitatory neurotransmitter in both the central and the peripheral nervous systems, at least in vertebrates

  • It was shown in the barrel cortex that deprivation responses are mediated by the induction of Long Term Depression (LTD) in intracortical excitatory synapses established in pyramidal neurons between layers IV and II–III [11]

  • Growing evidence highlights the importance of intraganglionic glutamate system in peripheral neuropathies, and SGCs should be taken into account for understanding the mechanisms of glutamatergic signaling, under physiological conditions, and for designing new therapies aimed at dealing with peripheral nervous system (PNS) disorders

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Summary

Introduction

Glutamate is the most abundant excitatory neurotransmitter in both the central and the peripheral nervous systems, at least in vertebrates. A large body of data has been gathered on the involvement of the glutamatergic system in these phenomena in the cortex It was shown in the barrel cortex that deprivation responses are mediated by the induction of Long Term Depression (LTD) in intracortical excitatory synapses established in pyramidal neurons between layers IV and II–III [11]. This fraction varied across studies, ranging from 30% in rat and monkey DRG [28] to 35% in rats, mostly in small neurons [29], up to 65% in cats DRG [30] These neurons express molecules involved in glutamate signaling including proteins involved in its synthesis, transport and release [25,31,32], and others directly related to glutamatergic neurotransmission, such as ionotropic and metabotropic receptors [33,34,35,36,37,38]

Kainate
Metabotropic Receptors
Group I
Group III
Vesicular Glutamate Transporters
Satellite Glial Cells
Schwann Cells
The Glutamatergic System Reacts to Innocuous Manipulation of the Input
Findings
Concluding Note
Full Text
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