Central administration of aminooxyacetate, an inhibitor of H2S production, affects thermoregulatory but not cardiovascular and ventilatory responses to hypercapnia in spontaneously hypertensive rats.

Hydrogen sulfide (HS) is classically known for its toxic effects. More recently HS has been documented as a neuromodulator. Here we investigated the central effects of aminooxyacetate (AOA; inhibitor of the HS-synthesizing enzyme cystathionine β-synthase, CBS) on cardiovascular, respiratory and thermoregulatory responses to hypercapnia in spontaneously hypertensive rats (SHR).

Anxiolytic-like effect of hydrogen sulfide (HS) in rats exposed and re-exposed to the elevated plus-maze and open field tests.

Hydrogen sulfide (HS), an endogenous gaseous mediator, modulates many physiological functions in mammals but evidence of its involvement in emotional and behavioral aspects is currently scarce. We hypothesized that this gas plays a modulatory role in behavioral parameters in rats submitted to tests (for 5min) in the open field (OF) and elevated plus-maze (EPM - test and retest). Male Wistar rats (200-250g) were intraperitoneally injected with saline or NaS (a HS donor; 4, 8 and 12mg/kg) either once or for 8days, and submitted to the OF test or to the EPM test and retest.

Involvement of endogenous central hydrogen sulfide (HS) in hypoxia-induced hypothermia in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) display autonomic imbalance and abnormal body temperature (Tb) adjustments. Hydrogen sulfide (HS) modulates hypoxia-induced hypothermia, but its role in SHR thermoregulation is unknown. We tested the hypothesis that SHR display peculiar thermoregulatory response to hypoxia and that endogenous HS overproduced in the caudal nucleus of the solitary tract (NTS) of SHR modulates this response.

Involvement of endogenous hydrogen sulfide (H2S) in the rostral ventrolateral medulla (RVLM) in hypoxia-induced hypothermia.

Hypoxia evokes a regulated decrease in deep body temperature (Tb). Hydrogen sulfide (H2S), a signaling molecule that belongs to the gasotransmitter family, has been demonstrated to participate in several brain-mediated responses. Rostral ventrolateral medulla (RVLM) is a brainstem region involved in thermoregulation.

Endogenous hydrogen sulfide in the rostral ventrolateral medulla/Bötzinger complex downregulates ventilatory responses to hypoxia.

Hydrogen sulfide (H2S) is now recognized as a new gaseous transmitter involved in several brain-mediated responses. The rostral ventrolateral medulla (RVLM)/Bötzinger complex is a region in the brainstem that is involved in cardiovascular and respiratory functions. Recently, it has been shown that exogenous H2S in the RVLM modulates autonomic function and thus blood pressure.

Role of hydrogen sulfide in the formalin-induced orofacial pain in rats.

Hydrogen sulfide (H2S) is a gasotransmitter synthesized in peripheral tissues by the enzyme cystathionine gamma-lyase (CSE). This gas has been documented to be involved in a wide variety of processes including inflammation and nociception. The aim of the present study was to investigate the role of the peripheral H2S pathway in nociceptive response to the orofacial formalin experimental model of pain.

Activation of corticotropin-releasing factor receptors from the basolateral or central amygdala increases the tonic immobility response in guinea pigs: an innate fear behavior.

The tonic immobility (TI) behavior is an innate response associated with extreme threat situations such as a predator attack. Several studies have provided evidence suggesting an important role for corticotropin-releasing factor (CRF) in the regulation of the endocrine system, defensive behaviors and behavioral responses to stress. TI has been shown to be positively correlated with the basal plasma levels of corticosterone.

GABAergic antagonist blocks the reduction of tonic immobility behavior induced by activation of 5-HT2 receptors in the basolateral nucleus of the amygdala in guinea pigs.

Tonic immobility (TI) is a temporary state of profound motor inhibition induced by situations that generate intense fear, with the objective of protecting an animal from attacks by predators. A preliminary study by our group demonstrated that microinjection into the basolateral nucleus of the amygdala (BLA) of an agonist to 5-HT(1A) and 5-HT(2) receptors promoted a decrease in TI duration. In the current study, the effects of GABAergic stimulation of the BLA and the possible interaction between GABA(A) and 5-HT(2) receptors on TI modulation were investigated.