Abstract
Despite the absence of synaptic contacts, cross-excitation of neurons in sensory ganglia during signal transmission is considered to be chemically mediated and appears increased in chronic pain states. In this study, we modulated neurotransmitter release in sensory neurons by direct application of type A botulinum neurotoxin (BoNT/A) to sensory ganglia in an animal model of neuropathic pain and evaluated the effect of this treatment on nocifensive. Unilateral sciatic nerve entrapment (SNE) reduced the ipsilateral hindpaw withdrawal threshold to mechanical stimulation and reduced hindpaw withdrawal latency to thermal stimulation. Direct application of BoNT/A to the ipsilateral L4 dorsal root ganglion (DRG) was localized in the cell bodies of the DRG and reversed the SNE-induced decreases in withdrawal thresholds within 2 days of BoNT/A administration. Results from this study suggest that neurotransmitter release within sensory ganglia is involved in the regulation of pain-related signal transmission.
Highlights
Peripheral nerve injury induces neuropathic pain states and hyperexcitability of neurons within sensory ganglia [1]
The main findings of this study were as follows: (i) sciatic nerve entrapment (SNE) decreased the hindpaw withdrawal threshold to mechanical stimulation and withdrawal latency to thermal stimulation, and direct application of
Peripheral nerve injury increases excitability of primary sensory neurons; this increase is widely considered to contribute to the behavioral symptoms of neuropathic pain [24,25]
Summary
Peripheral nerve injury induces neuropathic pain states and hyperexcitability of neurons within sensory ganglia [1]. P, calcitonin gene-related peptide (CGRP), and adenosine triphosphate (ATP), are released from the somata of neurons within sensory ganglia in vivo and in vitro [7,8,9,10,11], and that substance P [12] and ATP [13] excite neurons within sensory ganglia. We showed that ganglionic neurotransmitter release increases in inflammatory and neuropathic pain states [8,14]. This suggests that neuropathy-induced increases in transmitter release from neuronal somata within sensory ganglia may result in increased cross-excitation of neighboring neurons, thereby increasing transmission of pain-related signals. Blockade of neurotransmitter release within sensory ganglia should reduce neuropathic pain symptoms
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