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    • The present in vitro experiments confirm

    2022-05-12

    The present in vitro experiments confirm previous suppositions (Ciosek, Gałecka, 2011, Izdebska, Ciosek, 2010) that Gal modulates AVP and OT release by acting at every level of the hypothalamo-neurohypophysial system. In fact, both 10−10 M and 10−8 M Gal diminished basal release of AVP and OT from the isolated NH and Hth–NH explants. In the case of OT release from the Hth–NH explant, Gal exerts the strongest inhibitory impact in the concentration of 10−10 M. This effect seems to be incidental as our earlier reports (Ciosek, Drobnik, 2013, Izdebska, Ciosek, 2010) did not show the differences in the activity of both Gal concentrations. The present results confirm those of in vitro studies by Gálfi et al, 2002, Gálfi et al, 2003 and Nagyéri et al. (2009) who observed that Gal inhibits AVP release from the incubated neurohypophysial tissue. Moreover, the present results show that Gal has the same inhibitory effect on AVP release when added into the medium enriched with excess potassium ions. However, this effect of Gal on OT release was not marked during the incubation of the NH or Hth–NH complex in the K+-enriched medium. On the basis of these results it may be supposed that Gal acts as an inhibitory neuromodulator of AVP and OT secretion affecting the axon terminals in the neurohypophysis and modifying the processes related to transport and release of both neurohormones at the level of the hypothalamo-neurohypophysial system. It is possible that the influence of Gal did not depend on the tested concentration during the incubation, and that Gal is an endogenous factor disturbing the release of AVP and OT. The second objective of our study was to evaluate the potential influence of GALP on AVP and OT release from the hypothalamo-neurohypophysial system in vitro. An in vivo experiment conducted by Onaka et al. (2005) indicates that GALP may play an important role in the release of AVP and OT from the neurohypophysis. After intracerebroventricular administration of GALP (2 nmol), plasma concentrations of both hormones were significantly increased as compared with values in the saline-injected control rats. Plasma hormone concentrations after GALP returned to the level of saline-injected control rats within 30–60 min (Onaka et al., 2005). In turn, the Fidaxomicin mg of GALP mRNA in the posterior pituitary was markedly increased in rats after dehydration or salt loading, manipulations that stimulate the secretion of AVP and OT (Suzuki et al., 2010). In streptozotocin-induced diabetic rats, which are in a hyperosmotic state with elevated plasma AVP levels, GALP mRNA levels were increased approximately 20-fold in the neural lobe as compared to control (Shen and Gundlach, 2004). GALP expression was unaffected in the ARC during these states. The expression of GALP mRNA in the neural lobe of the pituitary is also induced by another condition associated with activation of magnocellular neurones, lactation (Cunningham et al., 2004). On the other hand, Dungan-Lemko et al. (2008) reported that congenital deficiency of GALP does not interfere with normal lactation in mice. The precise nature of the actions of GALP on vasopressinergic and oxytocinergic neurons is still not quite clear. Our results are consistent with those of previous in vivo studies. They demonstrate that both 10−9 and 10−10 M GALP distinctly stimulate basal and K+ ion-stimulated AVP release from the neurohypophysis as well as the hypothalamo-neurohypophysial explant. An important role in this neurosecretory control may be played by GALP-containing neurohypophysial astrocytes (pituicytes). Under normal physiological conditions, astrocytes act as a physical and chemical barrier, limiting neuron–neuron interactions, as well as the diffusion of neurotransmitters in the extracellular space (Rosso, Mienville, 2009, Stern, Filosa, 2013). These changes can be also produced in vitro in neurohypophysial explants (Hatton et al., 1984). The likely synthesis/release of GALP by these specialized astrocytes and its transcriptional regulation by osmotic challenges strongly suggests a role for this novel peptide in the regulation of pituicyte morphology. The results for OT achieved in the present study were not so clear. GALP at concentrations of 10−9 M and 10−10 M stimulated basal release of OT from the isolated NH and Hth–NH explants. GALP-stimulated OT release was not abolished by the galanin receptor antagonist, galantide. However, GALP was also found to exert an inhibitory effect on OT release when added into a medium enriched with potassium ions. It is hard to comment on this significant difference between the reactions of OT-ergic neurons to GALP. The possibility that GALP exerts an indirect influence on the function of the hypothalamo-neurohypophysial system via activation of NPY neurons should be considered (Larsen et al, 1994, Seth et al, 2003).