Abstract
In the sensory ganglion, just as in the CNS, neurotransmitter and gliotransmitters have profound effects on pain behavior. Current evidence indicates that ATP, CGRP and TNF-alpha are serving as neuro/glio neurotransmitters within the sensory ganglion. In this enclosed area where there are no synapses, transmitters are released in a narrow gap, the size of a synaptic cleft, separating sensory neurons from satellite cells. We have now evidence that glutamate is released within the ganglion. Initially, we found that silencing the glutamate transporter GLAST in the ganglion leads to an increase in pain behavior in a reversible manner.
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