Symposium: NEUROPLASTIC CHANGES EXERTED BY BRAIN NEUROCHEMICAL SYSTEMS, HORMONES, AND GENES IN NEURAL DEVELOPMENT AND FLUID AND CARDIOVASCULAR BALANCE

GODINO A.

Foz Iguazú

Congreso; 1st PanAmerican Congress of Physiological Sciences (PanAm-2014), which theme is ?Physiology without borders?.; 2014

At present, a great amount of research is being carried out to evaluate how the adult phenotype is a consequence of environmental signals that can be operating on genes during perinatal development (like critical periods of intrauterine life or early postnatal stage ) or even during adulthood as has been demonstrated in the induction-delay-expression experimental paradigm. Permanent changes in the homeostatic regulation of fluid and electrolyte systems for example could lead to increased risk factors for certain increasingly prevalent diseases in our society, such as hypertension. However, this phenomenon, that is known as perinatal programming or neuroplasticity (during adulthood), and involves the participation of different neuromodulators like estrogen, serotonin, vasopressin and the brain renin-angiotensin-Aldosterone system among others, may modify the efficiency of future responses to stimuli based on previous experience. In this symposium we analyzed several models of neuroplasticitity and for example, the sensitization of sodium appetite (ie, the ingestion of salty substances), thirst (water drinking), and blood pressure regulation that are mainly associated with altered activity of the brain renin-angiotensin-Aldo system. In particular I spoke about the serotonergic system involvement in the modulation of electrolyte homeostasis. In our studies we demonstrated that body sodium status modulates the central serotonergic circuit involved in hydroelectrolyte homeostasis. In this way, sodium depletion and sodium overload, decreases and increases respectively the brain serotonergic cells activity. These changes in serotonergic neural activity and serotonergic mechanisms are involved in the manifestation of sodium appetite behavior, promoting fluid homeostasis reestablishment when balance is altered.