RESUMO
Aim: To verify the involvement of transient receptor potential vanilloid 4 (TRPV4) in the process of progesterone induced body temperature rise in female rats during their sexual cycle. Methods: The body temperature and progesterone concentration at different stages of the normal female rats' sexual cycle were measured. The ovariectomized rats were given different doses of progesterone and their body temperature were measured. Female rats were administered with RN-1734, a specific antagonist of TRPV4 in the preoptic-anterior hypothalamus area (PO/AH) at the metestrus to observe the change of rats body temperature. Furthermore, RN 1734 was injected into the PO/AH area of ovariectomized rats which were preinjected with progesterone. The effect of progesterone on the body temperature of rats and the fluctuation of body temperature after blocking TRPV4 were observed. Results: There was a positive correlation between body temperature and progesterone doses in female rats at different stages of estrus cycle. In ovariectomized rats, different doses of progesterone were administered, indicating a dose-dependent increase in body temperature. RN- 1734 was injected to PO/AH 2 hours before the maximum body temperature on normal metestrus rats. It was observed that the increase range of body temperature decreased significantly after RN-1734 injection. This study also showed that RN-1734 significantly reduced the increase range of body temperature in ovariectomized rats administered with progesterone. Conclusions: The specific antagonist TRPV4 injected into the thermoregulation center could reduce the increase of body temperature in metestrus of normal rats, suggesting that TRPV4 may be involved in the process of the increase of rat body temperature induced by progesterone.
RESUMO
The amygdala, dorsal periaqueductal gray (dPAG), and medial hypothalamus have long been recognized to comprise a neural system responsible for the generation and elaboration of unconditioned fear in the brain. This neural substrate is well known to be under tonic inhibitory control exerted by ã-aminobutyric acid (GABA) mechanisms. Some evidence also suggests that these structures integrate conditioned fear. A recent study using the fear-potentiated startle paradigm showed that GABAergic mechanisms in the anterior hypothalamic nucleus (AHN) and dorsomedial part of the ventromedial hypothalamic nucleus (VMHDM) regulate conditioned fear. The present study examined the extent to which GABAergic mechanisms in these brain regions are involved in conditioned fear by measuring freezing in response to a light used as a conditioned stimulus (CS). The GABA A receptor agonist muscimol and the GABA-synthesizing enzyme glutamic acid decarboxylase inhibitor semicarbazide were used as an enhancer and inhibitor of GABA mechanisms, respectively. Muscimol and semicarbazide were injected into the AHN or VMHDM of rats before fear conditioning. Muscimol injections into the AHN and VMHDM significantly reduced conditioned freezing, whereas inhibition of GABA transmission increased this conditioned response in the AHN. The present study further supports the hypothesis that GABAergic mechanisms in the AHN and VMHDM exert inhibitory control on the neural substrates of conditioned fear in the hypothalamus.