It is known that hypercapnia as well as hypoxia

It is known that hypercapnia, as well as hypoxia, can result in a decrease in body temperature, but the mechanisms involved are not very well known (Barros and Branco, 1998; Saiki and Mortola, 1996). One clobetasol price mg is that when there is an acute hypercapnic exposure, acidosis plays an inhibitory role in metabolism, increases heat loss due to vasodilation of the blood vessels of the skin, and changes the concentrations of serotonin and norepinephrine in the hypothalamus, causing a decrease in body temperature (Schaefer et al., 1975). However, in rats, the temperature drop during hypercapnia is not as common as it is with hypoxia, as it seems to depend on the level of hypercapnia employed and the intensity of hyperventilation. We observed, in the control group, that hypercapnia did not alter the body temperature of the animals as observed in previous studies (Biancardi et al., 2008; de Carvalho et al., 2010) however, the group treated with LY341495, but not with MCPG, had a notable decrease in body temperature, both in the light phase and in the dark phase. There are three possible explanations for this result: First, since the injection of LY341495 into the LH/PFA caused intense hyperventilation, this may have caused a great loss of heat, resulting in hypothermia. Second, the observed effects on body temperature with the microinjection of LY341495 but not MCPG could be due to the specificity of LY341495 compound, which is highly selective for metabotropic receptors of groups II and III. MCPG, on the other hand, affects all groups of the glutamate metabotropic receptors - Group I, consisting of mGluR1 and mGluR5, Group II and Group III (Schoepp et al., 1999). While Group I exerts excitatory effects via IP3/Ca2+ signal transduction, Groups II/III have inhibitory effects via inhibitory G-protein activation (Niswender and Conn, 2010). Another reasonable hypothesis that deserves investigation is the possibility that the observed decreased body temperature could be a result of the effect of LY341495 on melanin concentrating hormone (MCH) neurons, since MCH-expressing neurons are intermingled with orexinergic neurons in the LH/PFA, and are reported to affect energy balance and to lower body temperature (Glick et al., 2009). We analyzed the relationship between and Tb during hypercapnia in the LY341495 groups, to confirm that the increase of the CO2 response, with the antagonism of the Group II/III mGluRs, did not occur as a result of the fall of Tb in these groups. As observed in Fig. 6, the increase in the ventilatory response to CO2 occurred from the onset of hypercapnia when the temperature drop was not maximal yet. In addition, as the animals continue to decrease body temperature, the ventilatory response remains essentially the same, which suggests that the effect of Group II/III mGluRs antagonist on the ventilatory response to CO2 is not dependent on its effect on body temperature.
Conflict of interest
Introduction The hypothalamus is a brain region involved in distinct physiological functions including hydroelectrolytic regulation of body fluids (Antunes-Rodrigues et al., 2004). The adjustment of salt-intake behavior and neurohypophysial hormone release in response to variations in blood osmolarity are controlled by distinct hypothalamic nuclei (Antunes-Rodrigues et al., 2004; Johnson and Thunhorst, 1997; Mckinley et al., 2004). The hypothalamus is considered to be a specialized sensory apparatus of the brain through which minor variations of plasma osmolarity can be detected. In fact, the hypothalamus works as an “osmosensor” in the brain exerting a central control on the blood plasma osmolarity (see Verbalis, 2010). It is well documented that minor variations in hypothalamic osmolarity trigger neuronal activation and hormonal release in distinct hypothalamic nuclei. However, it is not fully clear how glial cells housed in the hypothalamus respond to hyperosmolarity.