Navegando por Autor "Lima, Paulo Marcelo de Andrade"
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Item Abdominal TRPV1 channel desensitization enhances stress-induced hyperthermia during social stress in rats.(2023) Reis, Thayane Oliveira; Noronha, Sylvana Izaura Salyba Rendeiro de; Lima, Paulo Marcelo de Andrade; Abreu, Aline Rezende Ribeiro de; Mesquita, Laura Batista Tavares; Ferreira, Fernanda Isabel; Silva, Fernanda Cacilda dos Santos; Chianca Júnior, Deoclécio Alves; Menezes, Rodrigo Cunha Alvim deAims: In rats, stress-induced hyperthermia caused by social interaction depends on brown adipose tissue (BAT) thermogenesis and peripheral vasoconstriction. However, the peripheral mechanisms responsible for regulating the level of hyperthermia during social stress are still unknown. The transient receptor potential vanilloid 1 (TRPV1) subfamily, expressed in sensory and visceral neurons, can serve as a thermoreceptor. Here, we tested the hypothesis that the abdominal TRPV1 is essential in regulating stress-induced hyperthermia during social stress. Main methods: Male Wistar rats received an intraperitoneal injection of Resiniferatoxin (RTX) - an ultra-potent capsaicin analog, (i.e., to desensitize the TRPV1 channels) or vehicle. Seven days later, we evaluated the effects of abdominal TRPV1 channels desensitization on core body temperature (CBT), brown adipose tissue (BAT) temperature, tail skin temperature, and heart rate (HR) of rats subjected to a social stress protocol. Key findings: We found abdominal TRPV1 desensitization increased CBT and BAT temperature but did not change tail skin temperature and HR during rest. However, under social stress, we found that abdominal TRPV1 desensitization heightened the increase in CBT and BAT caused by stress. Also, it abolished the increase in tail skin temperature that occurs during and after social stress. TRPV1 desensitization also delayed the HR recovery after the exposure to the social stress. Significance: These results show that abdominal TRPV1 channels desensitization heightens stress-induced hyperthermia, causing heat dissipation during and after social stress, enabling optimal thermal control during social encounters.Item Association of high-fat diet with neuroinflammation, anxiety-like defensive behavioral responses, and altered thermoregulatory responses in male rats.(2019) Noronha, Sylvana Izaura Salyba Rendeiro de; Lima, Paulo Marcelo de Andrade; Campos, Glenda Siqueira Viggiano; Chírico, Máira Tereza Talma; Abreu, Aline Rezende Ribeiro de; Figueiredo, Amanda Braga de; Silva, Fernanda Cacilda dos Santos; Chianca Júnior, Deoclécio Alves; Lowry, Christopher; Menezes, Rodrigo Cunha Alvim deOverweight and obesity are a worldwide pandemic affecting billions of people. These conditions have been associated with a chronic low-grade inflammatory state that is recognized as a risk factor for a range of somatic diseases as well as neurodevelopmental disorders, anxiety disorders, trauma- and stressor-related disorders, and affective disorders. We previously reported that the ingestion of a high-fat diet (HFD; 45% fat kcal/g) for nine weeks was capable of inducing obesity in rats in association with increased reactivity to stress and increased anxiety-related defensive behavior. In this study, we conducted a nine-week diet protocol to induce obesity in rats, followed by investigation of anxiety-related defensive behavioral responses using the elevated T-maze (ETM), numbers of FOS-immunoreactive cells after exposure of rats to the avoidance or escape task of the ETM, and neuroinflammatory cytokine expression in hypothalamic and amygdaloid nuclei. In addition, we investigated stress-induced cutaneous thermoregulatory responses during exposure to an open-field (OF). Here we demonstrated that nine weeks of HFD intake induced obesity, in association with increased abdominal fat pad weight, increased anxiety-related defensive behavioral responses, and increased proinflammatory cytokines in hypothalamic and amygdaloid nuclei. In addition, HFD exposure altered avoidance- or escape task-induced FOSimmunoreactivity within brain structures involved in control of neuroendocrine, autonomic, and behavioral responses to aversive stimuli, including the basolateral amygdala (BLA) and dorsomedial (DMH), paraventricular (PVN) and ventromedial (VMH) hypothalamic nuclei. Furthermore, rats exposed to HFD, relative to control dietfed rats, responded with increased tail skin temperature at baseline and throughout exposure to an open-field apparatus. These data are consistent with the hypothesis that HFD induces neuroinflammation, alters excitability of brain nuclei controlling neuroendocrine, autonomic, and behavioral responses to stressful stimuli, and enhances stress reactivity and anxiety-like defensive behavioral responses.Item Estrogen receptor β activation within dorsal raphe nucleus reverses anxiety-like behavior induced by food restriction in female rats.(2018) Campos, Glenda Siqueira Viggiano; Noronha, Sylvana Izaura Salyba Rendeiro de; Souza, Aline Maria Arlindo de; Lima, Paulo Marcelo de Andrade; Abreu, Aline Rezende Ribeiro de; Chianca Júnior, Deoclécio Alves; Menezes, Rodrigo Cunha Alvim deSevere food restriction (FR), as observed in disorders like anorexia nervosa, has been associated to the reduction of estrogen levels, which in turn could lead to anxiety development. Estrogen receptors, mainly ERβ type, are commonly found in the dorsal raphe nucleus (DRN) neurons, an important nucleus related to anxiety modulation and the primary source of serotonin (5-HT) in the brain. Taking together, these findings suggest an involvement of estrogen in anxiety modulation during food restriction, possibly mediated by ERβ activation in serotonergic DRN neurons. Thus, the present study investigated the relationship between food restriction and anxiety-like behavior, and the involvement of DRN and ERβ on the modulation of anxiety-like behaviors in animals subjected to FR. For that, female Fischer rats were grouped in control group, with free access to food, or a FR group, which received 40% of control intake during 14 days. Animals were randomly treated with 17β-estradiol (E2), DPN (ERβ selective agonist), or their respective vehicles, PBS and DMSO. Behavioral tests were performed on Elevated T-Maze (ETM) and Open Field (OF). Our results suggest that FR probably reduced the estrogen levels, since the remained in the non-ovulatory cycle phases, and their uterine weight was lower when compared to control group. The FR rats showed increased inhibitory avoidance latency in theETM indicating that FR is associated with the development of an anxiety-like state. The injections of both E2 and DPN into DRN of FR animals had an anxiolytic effect. Those data suggest thatanxiety-like behavior induced by FR could be mediated by a reduction of ERβ activation in the DRN neurons, probably due to decreased estrogen levels.Item The role of peripheral transient receptor potential vanilloid 1 channels in stress-induced hyperthermia in rats subjected to an anxiogenic environment.(2022) Lima, Paulo Marcelo de Andrade; Reis, Thayane Oliveira; Wanner, Samuel Penna; Chianca Júnior, Deoclécio Alves; Menezes, Rodrigo Cunha Alvim deAnxiety resulting from psychogenic stimuli elicit stress-induced hyperthermia in rats, often called “psychogenic fever”, which is part of a coordinated response to situations seen as novel or distressing. Brain transient receptor potential vanilloid 1 (TRPV1) channels modulate both thermoregulation and animal behavior; however, the role of peripheral TRPV1 channels in regulating these responses during exposure to an anxiogenic environment has not been determined. Thus, the present study aimed to investigate the involvement of abdominal TRPV1 channels in stress-induced hyperthermia and behavior in rats subjected to an unconditioned anxiety test. Desensitized rats (peripheral desensitization of TRPV1 channels with resiniferatoxin; RTX) and their respective controls were subjected to a 15-min open field (OF) test. The core body temperature (Tcore), tail skin temperature (Tskin), and rats’ movements inside the arena were recorded. The OF test induced a similar increase in Tcore in both groups throughout the exposure time; however, at the recovery period, the RTX-treated rats had a slower reduction in Tcore due to lower tail skin heat loss. Tskin decreased significantly in both groups during exposure to OF but, during recovery, the RTX-treated rats showed impaired skin vasodilation. Also, RTX-treated rats entered fewer times and spent less time in the OF center square, suggesting an anxiety-related behavior. Our findings indicate that, under stressful conditions, peripheral TRPV1 channels modulate thermoregulatory and behavioral responses. The TRPV1 desensitization induces a more prolonged hyperthermic response due to lower cutaneous heat dissipation, alongside a more evident anxiety-like behavior in rats subjected to the OF apparatus.