Abstract
The involvement of nitric oxide (NO) in the modulation of teleost osmoresponsive circuits is suggested by the facts that NO synthase enzymes are expressed in the neurosecretory systems and may be regulated by osmotic stimuli. The present paper is an overview on the research suggesting a role for NO in the central modulation of hormone release in the hypothalamo-neurohypophysial and the caudal neurosecretory systems of teleosts during the osmotic stress response. Active NOS enzymes are constitutively expressed by the magnocellular and parvocellular hypophysiotropic neurons and the caudal neurosecretory neurons of teleosts. Moreover, their expression may be regulated in response to the osmotic challenge. Available data suggests that the regulatory role of NO appeared early during vertebrate phylogeny and the neuroendocrine modulation by NO is conservative. Nonetheless, NO seems to have opposite effects in fish compared to mammals. Indeed, NO exerts excitatory effects on the electrical activity of the caudal neurosecretory neurons, influencing the amount of peptides released from the urophysis, while it inhibits hormone release from the magnocellular neurons in mammals.
Highlights
Nitric oxide is a gaseous messenger that is endogenously produced in cells and tissues of all major groups of organisms and acts in a variety of biological processes
The distribution of nos1 transcripts in the brain of the adult zebrafish was compared to NADPH diaphorase (NADPHd) activity and Nos2-ir and these results suggested the expression of additional Nos1 enzymes in teleosts [39]
Active NO synthases (NOSs) enzymes are constitutively expressed by both neurosecretory hypophysiotropic and caudal neurons and their expression may be regulated in response to the osmotic challenge
Summary
Nitric oxide is a gaseous messenger that is endogenously produced in cells and tissues of all major groups of organisms and acts in a variety of biological processes. The effects of central nitrergic systems on the hydromineral imbalance are controversial, overall studies show a modulatory role for NO in the release of both AVP and OXT In both PVN and SON of the rat hypothalamus, the expression of NOS1 is up-regulated after chronic salt loading [14,15] or water deprivation [16] and NO has as an inhibitory role on AVP and OXT secretion. All the available data agree that NO acts as a modulator in the homeostatic balance and sympathetic activity of the hypothalamus of mammals [17] Both electrophysiological and neuroendocrine evidence confirmed that NO inhibits the activity of magnocellular neurons in the SON and PVN nuclei of the hypothalamus influencing the release of AVP and OXT from the neurohypophysis. The present paper is a review on the research data demonstrating the modulatory role of NO in the HNS and the caudal neurosecretory system (CNSS), the two neuroendocrine systems controlling osmoregulation in teleosts
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