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Expression of Ca V 2.2 and Splice Variants of Ca V 2.1 in Oxytocin‐ and Vasopressin‐Releasing Supraoptic Neurones
Author(s) -
Wang D.,
Fisher T. E.
Publication year - 2014
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/jne.12127
Subject(s) - oxytocin , vasopressin , immunocytochemistry , medicine , axon , endocrinology , neuropeptide , chemistry , biology , microbiology and biotechnology , receptor
The magnocellular neurosecretory cells ( MNC s) release vasopressin ( VP ) and oxytocin ( OT ) from their axon terminals into the circulation and from their somata and dendrites to exert paracrine effects on other MNC s. MNC s express several types of voltage‐gated C a 2+ channels, including C a V 2.1 and C a V 2.2. These two channels types are similar in structure and function in other cells, but although influx of C a 2+ through C a V 2.2 triggers the release of both OT and VP into the circulation, C a V 2.1 is involved in stimulating the release of VP but not OT . Release of OT from MNC somata is also triggered by C a V 2.2 but not C a V 2.1. These observations could be explained by differences in the level of expression of C a V 2.1 in VP and OT MNC s or by differences in the way that the two channels interact with the exocytotic apparatus. We used immunohistochemistry to confirm earlier work suggesting that MNC s express variants of C a V 2.1 lacking portions of an internal loop that enables the channels to interact with synaptic proteins. We used an antibody that would recognise both the full‐length C a V 2.1 and the deletion variants to show that OT MNC s express fewer C a V 2.1 channels than do VP MNC s in both somata and axon terminals. We used the reverse transcriptase ‐ polymerase chain reaction and immunocytochemistry to test whether MNC s express similar deletion variants of C a V 2.2 and were unable to find any evidence to support this. Our data suggest that the different roles that C a V 2.1 and C a V 2.2 play in MNC secretion may be a result of the different levels of expression of C a V 2.1 in VP and OT MNC s, as well as the expression in MNC s of deletion variants of C a V 2.1 that do not interact with exocytotic proteins and therefore may be less likely to mediate exocytotic release.