Abstract
Hydrogen sulfide (H2S) is a novel neurotransmitter that has been shown to influence cardiovascular functions as well and corticotrophin hormone (CRH) secretion. Since the paraventricular nucleus of the hypothalamus (PVN) is a central relay center for autonomic and endocrine functions, we sought to investigate the effects of H2S on the neuronal population of the PVN. Whole cell current clamp recordings were acquired from the PVN neurons and sodium hydrosulfide hydrate (NaHS) was bath applied at various concentrations (0.1, 1, 10, and 50 mM). NaHS (1, 10, and 50 mM) elicited a concentration-response relationship from the majority of recorded neurons, with almost exclusively depolarizing effects following administration. Cells responded and recovered from NaHS administration quickly and the effects were repeatable. Input differences from baseline and during the NaHS-induced depolarization uncovered a biphasic response, implicating both a potassium and non-selective cation conductance. The results from the neuronal population of the PVN shed light on the possible physiological role that H2S has in autonomic and endocrine function.
Highlights
Hydrogen sulfide (H2S) is produced endogenously in mammals in a variety of different cells types from the brain, blood, skin, liver, and kidney [1]
The majority (n = 52, 80%) of neurons were responsive, with (96%) of responsive cells depolarizing, which was characterized by a rapid rise in membrane potential immediately after neurons and sodium hydrosulfide hydrate (NaHS) entered the bath, followed by maintenance of the effects for the duration of donor application, and a rapid recovery to baseline membrane potential associated of replacement of bath solution with artificial cerebrospinal fluid (aCSF) (Fig. 1)
We examined the effects of hydrogen sulfide on paraventricular nucleus of the hypothalamus (PVN) neurons differentially classified according to their electrophysiological fingerprints as magnocellular neurons (MNC), preautonomic neurons (PA) or NE
Summary
Hydrogen sulfide (H2S) is produced endogenously in mammals in a variety of different cells types from the brain, blood, skin, liver, and kidney [1]. While not all aspects of endogenous H2S production are well understood, physiological sources of H2S include its production by enzymatic action, as well as release in response to physiological stimuli from stored pools in the cytosol and/or mitochondria [9] These three enzymes have been suggested to be differentially distributed throughout the body, with CBS being highly expressed in brain tissue [3,10], CSE in the liver, kidney, thoracic aorta, ileum, gastrointestinal tract, portal vein and uterus [11], and 3MST localized to the mitochondria [12]. While the physiological sources of H2S remain poorly understood, there are a few mechanism suggested in the literature
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