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Endomorphin‐2 is released from newborn rat primary sensory neurons in a frequency‐ and calcium‐dependent manner
Author(s) -
Scanlin Heather L.,
Carroll Elizabeth A.,
Jenkins Victoria K.,
Balkowiec Agnieszka
Publication year - 2008
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2008.06238.x
Subject(s) - sensory system , neuroscience , calcium , primary (astronomy) , calcium imaging , biology , psychology , medicine , physics , astronomy
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.