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The Involvement of Actin, Calcium Channels and Exocytosis Proteins in Somato-Dendritic Oxytocin and Vasopressin Release

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The Involvement of Actin, Calcium Channels and Exocytosis Proteins in Somato-Dendritic Oxytocin and Vasopressin Release

Vicky Tobin et al. Front Physiol.

Abstract

Hypothalamic magnocellular neurons release vasopressin and oxytocin not only from their axon terminals into the blood, but also from their somata and dendrites into the extracellular space of the brain, and this can be regulated independently. Differential release of neurotransmitters from different compartments of a single neuron requires subtle regulatory mechanisms. Somato-dendritic, but not axon terminal release can be modulated by changes in intracellular calcium concentration [(Ca(2+))] by release of calcium from intracellular stores, resulting in priming of dendritic pools for activity-dependent release. This review focuses on our current understanding of the mechanisms of priming and the roles of actin remodeling, voltage-operated calcium channels (VOCCs) and SNARE proteins in the regulation somato-dendritic and axon terminal peptide release.

Keywords: exocytosis; hypothalamus; neuropeptides; oxytocin; pituitary; vasopressin.

Figures

Figure 1
Figure 1
Vasopressin and oxytocin are synthesized by a few thousand large (magnocellular) neurons (vasopressin cells are immunostained with fluorescent green and oxytocin cells with fluorescent red) whose cell bodies are located mainly in the supraoptic (A) and paraventricular (not shown) nuclei of the hypothalamus. (B) The vasopressin immunostaining is punctate and represents individual or aggregates of large dense-cored vesicles. In the dendrite thickenings the vesicles are particularly abundant. Strong punctuate staining of VAMP2 (red labeling) was seen around the vasopressin and oxytocin (not shown) somata and dendrites, however there was no co-localization with the peptide suggesting labeling of pre-synaptic terminals. (C) Large dense-core vesicles in an electron microscopic section of a dendrite appear as dark, round, membrane-bound organelles (black dots). Scale bars show (A) 100, (B) 10, and (C) 1μm respectively.
Figure 2
Figure 2
Comparison of peptides release from somata-dendrites (A) and axon terminals (B) of magnocellular neurons. Depolarization induced calcium entry via voltage-operated calcium channels (VOCCs) stimulates peptide release from large dense-cored vesicles (LDCVs). In the somata-dendrites this requires the depolymerization of F-actin to G-actin. The stimulation of G-protein coupled receptors, such as the oxytocin receptor (OTR), stimulates the mobilization of calcium from intracellular stores and an increase in both the number of LDCVs and N-type channels at the plasma membrane which primes release for subsequent activity-dependent release. In contrast, release from axon terminal appears more simple; LDCV movement utilizes actin depolymerization, but release does not depend upon it. Although some members of the SNARE family are detectable by immunocytochemistry in both compartments, there appears to be a lack of VAMP, SNAP-25 and synaptotagmin-1 in the somata-dendrites, with their function perhaps being replaced by other SNARE proteins.

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