Ct. Wotjak et al., Forced swimming stimulates the expression of vasopressin and oxytocin in magnocellular neurons of the rat hypothalamic paraventricular nucleus, EUR J NEURO, 13(12), 2001, pp. 2273-2281
Previous studies have shown that a 10-min forced swimming session triggers
the release of both vasopressin and oxytocin into the extracellular fluid o
f the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) in rat
s. At the same time oxytocin, but not vasopressin, was released from the ax
on terminals into the blood. Here we combined forced swimming with in situ
hybridization to investigate whether (i) the stressor-induced release of va
sopressin and oxytocin within the PVN originates from parvo- or magnocellul
ar neurons of the nucleus, and (ii) central release with or without concomi
tant peripheral secretion is followed by changes in the synthesis of vasopr
essin and/or oxytocin. Adult male Wistar rats were killed 2, 4 or 8 h after
a 10-min forced swimming session and their brains processed for in situ hy
bridization using S-35-labelled oligonucleotide probes. As measured on phot
o-emulsion-coated slides, cellular vasopressin mRNA concentration increased
in magnocellular PVN neurons 2 and 4 h after swimming (P < 0.05). Similarl
y, oxytocin mRNA concentration was significantly increased in magnocellular
neurons of the PVN at 2 and 8 h (P < 0.05). We failed to observe significa
nt effects on vasopressin and oxytocin mRNA levels in the parvocellular PVN
and in the SON. Taken together with results from previous studies, our dat
a suggest that magnocellular neurons are the predominant source of vasopres
sin and oxytocin released within PVN in response to forced swimming. Furthe
rmore, in the case of vasopressin, central release in the absence of periph
eral secretion is followed by increased mRNA levels, implying a refill of d
epleted somato-dendritic vasopressin stores. Within the SON, however, mRNA
levels are poor indicators of the secretory activity of magnocellular neuro
ns during stress.