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HSD2 neurons
HSD2 neurons are a small group of neurons in the brainstem which are uniquely sensitive to the mineralocorticosteroid hormone aldosterone, through expression of HSD11B2. They are located within the caudal medulla oblongata, in the nucleus of the solitary tract (NTS). HSD2 neurons are activated during a prolonged deficit in body sodium or fluid volume, as occurs after dietary sodium deprivation or during frank hypovolemia. They are also activated by supraphysiologic stimulation of the mineralocorticoid receptor. They are inactivated when salt is ingested.〔 To date, HSD2 neurons have been identified and studied only in rats and mice.
== Basic characteristics ==
The term "HSD2 neurons" is used in the scientific literature to refer to a subpopulation of neurons in the NTS which express both the mineralocorticoid receptor (MR) and 11-beta-hydroxysteroid dehydrogenase type 2 (HSD2).〔 HSD2 is an enzyme that metabolizes cortisol and other glucocorticosteroids, which typically prevent aldosterone from binding to the mineralocorticoid receptor. This pre-receptor mechanism for modifying hormone binding is necessary for cellular sensitivity to aldosterone because, under physiologic conditions, cortisol circulates at 100-1000 times higher concentrations than aldosterone. As both cortisol and aldosterone bind the mineralocorticoid receptor with equal affinity, cortisol effectively crowds out aldosterone in cells without abundant HSD2. In cells with HSD2, however, aldosterone has increased access to the MR, such that increases and decreases in the circulating concentration of this hormone will produce a change in receptor activity. In HSD2 neurons (and all other cells that express both HSD2 and MR), aldosterone binds to MR and translocates it from the cytoplasm to the nucleus, causing transcriptional changes. Unlike aldosterone-sensitive cells in epithelial tissues (e.g. in the kidney), the physiologic effects of aldosterone-MR activation in HSD2 neurons are unknown. It has been suggested, but not proven, that aldosterone promotes the firing activity of these neurons. Aldosterone is not necessary for HSD2 neuron activation because this can be evoked by sodium deprivation even in rats without adrenal glands,〔 which are the exclusive source of circulating aldosterone.
HSD2 neurons express the transcription factor Phox2b. This means that HSD2 neurons probably release the excitatory transmitter glutamate onto their synaptic target neurons, as all Phox2b-expressing neurons in the NTS express the vescicular glutamate transporter VGlut2. HSD2 neurons do not produce a wide array of other proteins that typify most other subtypes of NTS neurons, including tyrosine hydroxylase, choline acetyltransferase, nitric oxide synthase, cholecystokinin, neurotensin, neuropeptide FF, substance P, somatostatin, inhibin-β, glucagon-like peptide-1, corticotropin-releasing hormone, dynorphin, calretinin, and calbindin. A small number of HSD2 neurons (less than 2%) may express the neuropeptide galanin.〔 Their lack of expression of the aforementioned markers suggests that HSD2 neurons form a unique subpopulation within the NTS. To date, there is no information available about the electrophysiologic characteristics of these neurons.
抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』
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