The nucleus tractus solitarii (NTS) is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity. Phenotypically-characterized NTS neurons have been implicated in the differential regulation of blood pressure (BP). Here, we investigated whether phenylethanolamine N-methyltransferase (PNMT)-expressing NTS (NTS^PNMT) neurons contribute to the control of BP. We demonstrate that photostimulation of NTS^PNMT neurons has variable effects on BP. A depressor response was produced during optogenetic stimulation of NTS^PNMT neurons projecting to the paraventricular nucleus of the hypothalamus, lateral parabrachial nucleus, and caudal ventrolateral medulla. Conversely, photostimulation of NTS^PNMT neurons projecting to the rostral ventrolateral medulla produced a robust pressor response and bradycardia. In addition, genetic ablation of both NTS^PNMT neurons and those projecting to the rostral ventrolateral medulla impaired the arterial baroreflex. Overall, we revealed the neuronal phenotype- and circuit-specific mechanisms underlying the contribution of NTS^PNMT neurons to the regulation of BP.
Solitary Nucleus/metabolism* ; Blood Pressure/physiology* ; Phenylethanolamine N-Methyltransferase/metabolism* ; Neurons/metabolism* ; Paraventricular Hypothalamic Nucleus/metabolism*

Olfaction and food intake are interrelated and regulated. In the process of feeding, the metabolic signals in the body and the feeding signals produced by food stimulation are first sensed by the arcuate nucleus of hypothalamus and the nucleus tractus solitarius of brain stem, and then these neurons project to the paraventricular nucleus of hypothalamus. The paraventricular nucleus transmits the signals to other brain regions related to feeding and regulates feeding behavior. In this process, olfactory signals can be transmitted to hypothalamus through olfactory bulb and olfactory cortex to regulate feeding behavior. At the same time, gastrointestinal hormones (ghrelin, insulin, leptin, etc.) and some neurotransmitters (acetylcholine, norepinephrine, serotonin, endocannabinoid, etc.) produced in the process of feeding act on the olfactory system to regulate olfactory function, which in turn affects the feeding itself. This review summaries the research progress of the interaction between olfaction and food intake and its internal mechanism from the aspects of neuronal and hormonal regulation.
Arcuate Nucleus of Hypothalamus/metabolism* ; Feeding Behavior/physiology* ; Hypothalamus ; Paraventricular Hypothalamic Nucleus ; Smell

AIMTo investigate the effect of paraventricular nucleus (PVN) stimulation and the c-fos expression within PVN and nucleus tractus solitarius (NTS) of the rat following gastric ischemia/reperfusion injury (GI/RI).

METHODSThe rat celiac artery was clamped for thirty minutes and reperfused for sixty minutes, using Fos immunohistochemical method (ABC method) examined the c-fos expression within PVN and NTS.

RESULTS(1) Both electrical and chemical stimulation of the PVN obviously attenuated the GI/ RI. (2) Bilateral electrolytic lesion of NTS could eliminate the protective effect of electrical stimulation of the PVN. (3) The Fos-like immunoreactive neurons were increased in bilateral PVN and NTS by GI/RI.

CONCLUSIONThe function of PVN and NTS could be affected by the GI/RI noxious stimulation. PVN, NTS were involved in the regulation of GI/RI.

Animals ; Gastric Mucosa ; pathology ; Male ; Paraventricular Hypothalamic Nucleus ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; metabolism ; Solitary Nucleus ; metabolism ; Stomach ; blood supply

Mongolian gerbil has been as an model animal for studing the neurological diseases such as stroke and epilepsy because of the congenital incompleteries in Willis circle, as well as the investigation of water metabolism because of the long time-survival in the condition of water-deprived desert condition, compared with other animal species. In order to accomplish this research, first of all another divided the laboratory animals 5 groups of which each group include the 5 animals. In this study of the long term water deprived condition author investigatied the vasopressinergic and oxytocinergic magnocellular neurons of the hypothalamus by using a quantitative immunohistochemistry, measured the plasma osmolalities at the time of sacrifice of indivisual animals, and the body weights every day during water-deprived. The results obtained in this study were summarized as followings: 1. The body weights and decreasing rates of the body weight in water-deprived animal groups were continuosly decreased. 2. The plasma osmolalities were increased from the 5th water-deprived day, after then the gradually increase reached nearly its equilibrium state at the 10th water-deprived day. 3. Vasopressin and oxytocin immunoreactive cells were mainly observed in PVN, SON and a few in the lateral magnocellular area of hypothalamus. 4. The number of VP immunoreactive cells in paraventricular and supraoptic nucleus were abruptly decreas-ed until the 5th day in the supraoptic nucleus in number and until the 10th day in the paraventricular nucleus of water-deprived. 5. The OT secreting cells were severely decreased on the 5th water deprived day in paraventricular and supraoptic nucleus, after than these cells were very slowly decreased until to the 38th water deprived day.
Animals ; Animals, Laboratory ; Body Weight ; Circle of Willis ; Epilepsy ; Gerbillinae* ; Hypothalamus* ; Immunohistochemistry ; Metabolism ; Neurons* ; Osmolar Concentration ; Oxytocin ; Paraventricular Hypothalamic Nucleus ; Plasma ; Stroke ; Supraoptic Nucleus ; Vasopressins

It is well established that increased excitability of the presympathetic neurons in the hypothalamic paraventricular nucleus (PVN) during hypertension leads to heightened sympathetic outflow and hypertension. However, the mechanism underlying the overactivation of PVN presympathetic neurons remains unclear. This study aimed to investigate the role of endogenous corticotropin-releasing factor (CRF) on the excitability of presympathetic neurons in PVN using Western blot, arterial blood pressure (ABP) and renal sympathetic nerve activity (RSNA) recording, CRISPR/Cas9 technique and patch-clamp technique. The results showed that CRF protein expression in PVN was significantly upregulated in spontaneously hypertensive rats (SHRs) compared with normotensive Wistar-Kyoto (WKY) rats. Besides, PVN administration of exogenous CRF significantly increased RSNA, heart rate and ABP in WKY rats. In contrast, knockdown of upregulated CRF in PVN of SHRs inhibited CRF expression, led to membrane potential hyperpolarization, and decreased the frequency of current-evoked firings of PVN presympathetic neurons, which were reversed by incubation of exogenous CRF. Perfusion of rat brain slices with artificial cerebrospinal fluid containing CRF receptor 1 (CRFR1) blocker, NBI-35965, or CRF receptor 2 (CRFR2) blocker, Antisauvagine-30, showed that blocking CRFR1, but not CRFR2, hyperpolarized the membrane potential and inhibited the current-evoked firing of PVN presympathetic neurons in SHRs. However, blocking CRFR1 or CRFR2 did not affect the membrane potential and current-evoked firing of presympathetic neurons in WKY rats. Overall, these findings indicate that increased endogenous CRF release from PVN CRF neurons enhances the excitability of presympathetic neurons via activation of CRFR1 in SHRs.
Rats ; Animals ; Rats, Inbred SHR ; Paraventricular Hypothalamic Nucleus/physiology* ; Receptors, Corticotropin-Releasing Hormone/metabolism* ; Rats, Inbred WKY ; Corticotropin-Releasing Hormone/metabolism* ; Neurons/physiology* ; Hypertension ; Sympathetic Nervous System

Organotypic slice cultures have been developed as an alternative to acute brain slices because the neuronal viability and synaptic connectivity in these cultures can be preserved well for a prolonged period of time. This study evaluated a stationary organotypic slice culture developed for the hypothalamic paraventricular nucleus (PVN) of rat. The results showed that the slice cultures maintain the typical shape of the nucleus, the immunocytochemical signals for oxytocin, vasopressin, and corticotropin-releasing hormone, and the electrophysiological properties of PVN neurons for up to 3 weeks in vitro. The PVN neurons in the culture expressed the green fluorescent protein gene that had been delivered by the adenoviral vectors. The results indicate that the cultured slices preserve the properties of the PVN neurons, and can be used in longterm studies on these neurons in vitro.
Adenoviridae ; Animals ; Cell Culture Techniques/*methods ; Corticotropin-Releasing Hormone/metabolism ; Electrophysiology ; Genetic Vectors ; Green Fluorescent Proteins/metabolism ; Immunohistochemistry ; Neurons/*cytology/metabolism ; Oxazines ; Oxytocin/metabolism ; Paraventricular Hypothalamic Nucleus/*anatomy & histology/cytology/metabolism ; Rats ; Vasopressins/metabolism

OBJECTIVETo investigate the effect of maternal deprivation on the activity of hypothalamo-pituitary-adrenal (HPA) axis, acute stress response and the sex hormone receptors expression in hypothalamic paraventricular nucleus (PVN) in female rats.

METHODSMaternal deprivation model was induced in female Sprague-Dawley (SD) rats. Foot shock was given at different stages of estrus cycle during the adulthood. Plasma estradiol, testosterone and adrenocorticotropin (ACTH) levels were determined by radioimmunoassay; and plasma corticosterone level was measured by enzyme linked immunosorbent assay. The expression of androgen receptor (AR) and estrogen receptor (ER-β) in the hypothalamic PVN was detected by immunohistochemistry.

RESULTSDecreased plasma ACTH and corticosterone levels were found in the proestrus of female rats with maternal deprivation (P=0.012 and P=0.019, respectively). A significant down-regulation (P=0.008) of PVN-AR, but not PVN-ER-β expression was found in female rats with maternal deprivation.

CONCLUSIONMaternal deprivation may reduce the HPA axis activity in female SD rats, which is closely correlated with the fluctuation of the circulating sex hormones. The androgen in the hypothalamus seems to play a more important role than the estrogen in this procedure.

Adrenocorticotropic Hormone ; blood ; Animals ; Corticosterone ; blood ; Estradiol ; blood ; Female ; Hypothalamo-Hypophyseal System ; physiopathology ; Maternal Deprivation ; Paraventricular Hypothalamic Nucleus ; metabolism ; Pituitary-Adrenal System ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Receptors, Androgen ; metabolism ; Receptors, Estrogen ; metabolism ; Stress, Physiological ; Testosterone ; blood

AIMTo investigate the possible involvement of gamma-aminobutyric acid (GABA) in the paraventricular nucleus (PVN) in cardiovascular responses induced by central salt loading.

METHODSDirect perfusion into PVN region with hypertonic saline (0.6 mol/L) was performed in conscious rats by using an in vivo brain microdialysis technique. Then, the extracellular concentration of GABA in the PVN region was measured by microdialysis and high performance liquid chromatography (HPLC) techniques, and the blood pressure (BP) and heart rate (HR) were with recorded simultaneously. Bicuculline (an antagonist of GABAA receptor) or saclofen (an antagonist of GABAB receptor) were coperfused hypertonic saline into PVN region, then the cardiovascular responses were examined.

RESULTS(1) The local perfusion of 0.6 mol/L saline elicited significant increases on BP and HR (P < 0.01). In addition, perfusion of 0.6 mol/L saline increased the extracellular GABA levels in the PVN region, which reached 561.96% +/- 173.96% (P < 0.05) of the basal level. (2) Bicuculline or salcofen significantly attenuated the in-response of BP (P < 0.01, respectively), whereas the antagonists did not influence the response of HR induced by hypertonic saline.

CONCLUSIONLocal perfusion of hypertonic saline in the PVN region elicits a local release of GABA, which may act via GABA(A) and GABA(B) receptors to produce pressor response.

Animals ; Blood Pressure ; drug effects ; physiology ; Male ; Microdialysis ; methods ; Paraventricular Hypothalamic Nucleus ; metabolism ; physiology ; Pressoreceptors ; drug effects ; Rats ; Rats, Wistar ; Saline Solution, Hypertonic ; administration & dosage ; pharmacology ; gamma-Aminobutyric Acid ; metabolism

This study was conducted to define the molecular mechanism of fasting-induced down-regulation of neuronal nitric oxide synthase (nNOS) expression in the hypothalamic paraventricular nucleus (PVN). Rats were adrenalectomized (ADX), and then either underwent food deprivation or received varying doses of dexamethasone for 48 h. The brain tissues were processed for NADPH-diaphorase (NADPH-d) staining, a histochemical marker of nNOS enzyme activity. Both the ADX and the sham operated rats showed a significant weight loss after 48 h of food deprivation. Food deprivation decreased the number of NADPH-d containing cells in the PVN of sham rats, however, not in the ADX rats. Dexamethasone dose- dependently decreased NADPH-d cells in the PVN of ADX rats. The effect of ADX or dexamethasone was limited to the parvocellular subdivision of PVN. These results suggest that the adrenal glucocorticoids may down-regulate nNOS expression in the PVN during food deprivation.
*Adrenalectomy ; Animals ; Biological Markers ; Dexamethasone/blood/pharmacology ; Down-Regulation/physiology ; Fasting/*physiology ; Food Deprivation/physiology ; Glucocorticoids/blood/pharmacology ; Male ; NADPH Dehydrogenase/*metabolism ; Nitric-Oxide Synthase/*metabolism ; Paraventricular Hypothalamic Nucleus/*enzymology ; Rats ; Rats, Sprague-Dawley ; Support, Non-U.S. Gov't

In this study, we examined if glucocorticoids are required for the fasting-induced decrease of neuronal nitric oxide synthase (nNOS) in the magnocellular division of the paraventricular nucleus (PVN). Rats were adrenalectomized, subjected to 48 h of food deprivation with/without dexamethasone (5 mg/ kg, 4 subcutaneous injections with 12 h intervals), and the brain slices were processed for NADPH-diaphorase (NADPH- d) staining, a histochemical marker for nNOS in neuronal cells. In food deprived adrenalectomized rats, but not in free fed intact rats, dexamethasone significantly decreased NADPH-d staining in the magnocellular PVN. We previously reported that food deprivation decreases nNOS in the magnocellular PVN of intact rats. Thus, the present results together with our previous report suggest that although glucocorticoids are required for fasting-induced nNOS down-regulation in the magnocellular PVN, glucocorticoids may not be directly involved and some other molecular signals produced by food deprivation may play a pivotal role over glucocorticoid in the regulatory pathway for nNOS expression in this brain region.
Adrenalectomy ; Animals ; Dexamethasone/pharmacology ; Down-Regulation ; Fasting/*metabolism ; Male ; NADPH Dehydrogenase/*analysis ; Nitric-Oxide Synthase/genetics ; Paraventricular Hypothalamic Nucleus/*enzymology ; Peptides/physiology ; Rats ; Rats, Sprague-Dawley ; Research Support, Non-U.S. Gov't ; Weight Gain