These authors contributed equally to this work.
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Endomorphin-2 is released from newborn rat primary sensory neurons in a frequency- and calcium-dependent manner
Article first published online: 28 JUN 2008
DOI: 10.1111/j.1460-9568.2008.06238.x
© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
Additional Information
How to Cite
Scanlin, H. L., Carroll, E. A., Jenkins, V. K. and Balkowiec, A. (2008), Endomorphin-2 is released from newborn rat primary sensory neurons in a frequency- and calcium-dependent manner. European Journal of Neuroscience, 27: 2629–2642. doi: 10.1111/j.1460-9568.2008.06238.x
Publication History
- Issue published online: 28 JUN 2008
- Article first published online: 28 JUN 2008
- Received 21 November 2007, revised 31 March 2008, accepted 2 April 2008
- Abstract
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Keywords:
- activity-dependent release;
- dorsal root ganglion;
- nodose-petrosal;
- opiates
Abstract
Recent evidence indicates that endomorphins, endogenous mu-opioid receptor (MOR) agonists, modulate synaptic transmission in both somatic and visceral sensory pathways. Here we show that endomorphin-2 (END-2) is expressed in newborn rat dorsal root ganglion (DRG) and nodose-petrosal ganglion complex (NPG) neurons, and rarely co-localizes with brain-derived neurotrophic factor (BDNF). In order to examine activity-dependent release of END-2 from neurons, we established a model using dispersed cultures of DRG and NPG cells activated by patterned electrical field stimulation. To detect release of END-2, we developed a novel rapid capture enzyme-linked immunosorbent assay (ELISA), in which END-2 capture antibody was added to neuronal cultures shortly before their electrical stimulation. The conventional assay was effective at reliably detecting END-2 only when the cells were stimulated in the presence of CTAP, a MOR-selective antagonist. This suggests that the strength of the novel assay is related primarily to rapid capture of released END-2 before it binds to endogenous MORs. Using the rapid capture ELISA, we found that stimulation protocols known to induce plastic changes at sensory synapses were highly effective at releasing END-2. Removal of extracellular calcium or blocking voltage-activated calcium channels significantly reduced the release. Together, our data provide the first evidence that END-2 is expressed by newborn DRG neurons of all sizes found in this age group, and can be released from these, as well as from NPG neurons, in an activity-dependent manner. These results point to END-2 as a likely mediator of activity-dependent plasticity in sensory pathways.