Lactate inhibited sodium intake in dehydrated rats.

Recent studies have suggested that glial cells, especially astrocytes, are involved in balanced hydromineral modulation. In response to increased extracellular Na+ concentration, astrocytic Nax channels are activated, promoting lactate production and release. Furthermore, previous in vitro studies have suggested that lactate and hypertonic Na + solution activate SFO GABAergic neurons involved in the salt-appetite central pathways. Here, we evaluated the role of lactate in dehydration-induced sodium and water intake. To this end, intracerebroventricular microinjection (icv) of l-lactate or α-cyano-4-hydroxycinnamic acid (α-CHCA, MCT lactate transporter inhibitor) was performed in rats subjected to 48 h of water deprivation (WD) and 1 h of partial rehydration after 48 h of WD (WD-PR). The rehydration protocol was used to distinguish the mechanisms of thirst and sodium appetite induced by WD. Then, water and sodium (0.3 M NaCl) intake were evaluated for 2 h. Our results showed that central α-CHCA induced an increase in sodium preference in WD rats. Furthermore, central lactate increased water intake but reduced sodium intake in WD-PR animals. In contrast, central lactate transporter inhibition did not change water or sodium intake in WD-PR rats. Our results suggest that lactate is involved in inhibitory mechanisms that induce sodium intake avoidance in dehydrated rats.

PhysioArt: a teaching tool to motivate students to learn physiology.

Learning physiology is challenging for students. The nature of the discipline, which includes many complex mechanisms, makes the subject complicated. Furthermore, the length of the textbooks and the usual multiple-choice tests, which prioritize memorizing instead of understanding, tend to discourage the students. Therefore, different pedagogical strategies have been adopted to motivate and facilitate the learning of physiology. In this sense, many pedagogical strategies have been using art as a tool to motivate and induce students to self-learn. Besides, art as a pedagogical tool has also been shown to be important in developing self-assurance, self-pride, as well as the development of critical-thinking skills in the students. Here, we incorporate a new practice of self-directed teaching and learning, which involves artwork interpretation in a physiological context. This extra-classroom activity integrating art and physiology (The PhysioArt Project) improved students'engagement, increasing their interest in the discipline by providing a more creative, pleasurable, and enthusiastic atmosphere for enjoying and learning physiology, which also has contributed to the development of creativity, critical thinking, and students' self-assurance. Interestingly, the benefits elicited by The PhysioArt Project activities have also helped us to enhance the student-professor relationship, inducing a more humanized education.

Central interaction between nitric oxide, lactate and glial cells to modulate water and sodium intake in rats.

The "astrocyte-to-neuron lactate shuttle" (ANLS) mechanism is part of the central inhibitory pathway to modulate sodium intake. An interaction between the GABAergic neurons and nitric oxide (NO) in the subfornical organ (SFO) in salt-appetite inhibition has been suggested. In addition, NO is a key molecule involved in astrocytic energy metabolism and lactate production. In the present study, we hypothesized there is an interaction between astrocytic lactate and central NO to negatively modulate water and sodium intake through the ANLS mechanism. The results showed that central Nω-nitro-L-arginine methyl ester (L-NAME, NO-synthase inhibition) induced an increase in water and sodium intake. These responses were attenuated by previous central microinjection of fluorocitrate (FCt, a reversible glial inhibitor). Interestingly, L-NAME-induced water and sodium intake were also decreased by previous microinjection of lactate but did not change after inhibition of the ANLS mechanism by α-cyano 4-hydroxycinnamic acid (α-CHCA), an inhibitor of the MCT lactate transporter. Our results suggest a central interaction between NO, glial cells, and lactate to modulate water and sodium intake.