Abstract
Magnocellular neurons of the supraoptic nucleus (SON) secrete oxytocin and vasopressin from axon terminals in the neurohypophysis, but they also release large amounts of peptide from their somata and dendrites, and this can be regulated both by activity-dependent Ca2+ influx and by mobilization of intracellular Ca2+. This somato-dendritic release can also be primed by agents that mobilise intracellular Ca2+, meaning that the extent to which it is activity-dependent, is physiologically labile. We investigated the role of different Ca2+ channels in somato-dendritic release; blocking N-type channels reduced depolarisation-induced oxytocin release from SONs in vitro from adult and post-natal day 8 (PND-8) rats, blocking L-type only had effect in PND-8 rats, while blocking other channel types had no significant effect. When oxytocin release was primed by prior exposure to thapsigargin, both N- and L-type channel blockers reduced release, while P/Q and R-type blockers were ineffective. Using confocal microscopy, we found immunoreactivity for Cav1.2 and 1.3 channel subunits (which both form L-type channels), 2.1 (P/Q type), 2.2 (N-type) and 2.3 (R-type) in the somata and dendrites of both oxytocin and vasopressin neurons, and the intensity of the immunofluorescence signal for different subunits differed between PND-8, adult and lactating rats. Using patch-clamp electrophysiology, the N-type Ca2+ current density increased after thapsigargin treatment, but did not alter the voltage sensitivity of the channel. These results suggest that the expression, location or availability of N-type Ca2+ channels is altered when required for high rates of somato-dendritic peptide release.
Highlights
Many neurons release a wide variety of signalling molecules from their soma and dendrites to autoregulate their activity, communicate with adjacent neurons and glia, and modulate afferent nerve ending activity [1,2,3,4].In magnocellular neurons of the supraoptic (SON) and paraventricular nuclei, oxytocin and vasopressin are released from somata and dendrites, with important consequences [5,6]
Explants of the supraoptic nucleus (SON) responded to two repeated depolarisations (S1 and S2: 50 mM K+) with similar amounts of oxytocin release (Fig. 1A,B; controls are shown in black lines)
We found that in vitro depolarisationinduced oxytocin secretion from adult SONs depends on Ca2+ influx via N-type channels
Summary
Many neurons release a wide variety of signalling molecules from their soma and dendrites to autoregulate their activity, communicate with adjacent neurons and glia, and modulate afferent nerve ending activity [1,2,3,4]. Like the release of conventional neurotransmitters, oxytocin and vasopressin secretion from axon terminals in the neurohypophysis depends on depolarisation-evoked Ca2+ entry through highvoltage-activated Ca2+ channels. By thapsigargin or cyclopiazonic acid, and is seen as a late emerging and prolonged potentiation of depolarisation evoked peptide release [20,22]. We hypothesised that this might be achieved in part by a change in Ca2+ entry via voltage operated Ca2+ channels. We have used fluorescence immunocytochemistry to describe the a1-subunits distribution in oxytocin and vasopressin neurons and to determine changes in subunit expression at times of high dendritic release (lactation and postnatal day 8 (PND-8)) and after thapsigargin-induced priming
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