Dendritic osmosensors modulate activity-induced calcium influx in oxytocinergic magnocellular neurons of the mouse PVN

Abstract

Hypothalamic oxytocinergic magnocellular neurons have a fascinating ability to release peptide from both their axon terminals and from their dendrites. Existing data indicates that the relationship between somatic activity and dendritic release is not constant, but the mechanisms through which this relationship can be modulated are not completely understood. Here we use a combination of electrical and optical recording techniques to quantify activity-induced calcium influx in proximal vs. distal dendrites of oxytocinergic magnocellular neurons located in the paraventricular nucleus of the hypothalamus (OT-MCNs). Results reveal that the dendrites of OT-MCNs are weak conductors of somatic voltage changes, however activity-induced dendritic calcium influx can be robustly regulated by both osmosensitive and non-osmosensitive ion channels located along the dendritic membrane. Overall, this study reveals that dendritic conductivity is a dynamic and endogenously regulated feature of OT-MCNs that is likely to have substantial functional impact on central oxytocin release.

Shared and divergent contribution of vitamin A and oxytocin to the aetiology of autism spectrum disorder

“…Although elevated steroid hormone levels and steroidogenic activity have reportedly been associated with autism [62] , [65] , and steroid hormones and VA metabolites can regulate early brain development by binding to homologous nuclear receptors [67] , how VA is involved in steroid-mediated processes and affects ASD phenotypes warrants further exploration. In contrast, potential biomarkers associated with oxytocin only were enriched in the calcium-related functions, which strongly affect central oxytocin release [68] and are associated with ASD-like behaviours [69] . Among the shared VA and oxytocin-related genes, mitogen-activated protein kinase 3 ( MAPK3 ) was the top one gene associated with ASD pathology.…”

The ventral CA2 region of the hippocampus and its differential contributions to social memory and social aggression

“…The following drugs were bath-applied at the following concentrations: SR 95531 (1 µM, Tocris, #1262), CGP 55845 (2 µM,Tocris, #1248). Data analysis was performed using custom software written in OriginC 50 (OriginLab Corporation, Northampton, MA) and PRISM (Graphpad) 50 .…”

https://fz.kiev.ua/index.php?abs=2034

“…These neurons in vertebrates originate from the wall of the third ventricle, migrate and transform from bipolar into the cells with reach dendrite tree and bifurcated axon that allows extra pituitary release of OT, in the forebrain in particular [11]. OT release from axonal terminals within the posterior pituitary delivers the peptide into the bloodstream and release from the neuron dendrites contributes to the brain pool of this peptide [12]. OT being delivered in the latter way dramatically increases the local concentration of OT comparatively to the serum level and this elevation together with the localization of OT-releasing nuclei near the third cerebral ventricle facilitates the brain distribution of OT.…”

“…Ca 2+ channels are found to be critical for the differential release of OT and for the control of firing patterns of the OT-releasing SON neurons [13]. Dendritic release of the OT requires Ca 2+ entry that may be modulated by GABAA receptors on dendrites [12]. Various signals act via different amounts of this calcium.…”