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Journal articles on the topic 'Paraventricular nucleus'

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Published: 4 June 2021

Last updated: 25 April 2022

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1

Badoer, Emilio. "Role of the hypothalamic PVN in the regulation of renal sympathetic nerve activity and blood flow during hyperthermia and in heart failure." American Journal of Physiology-Renal Physiology 298, no. 4 (April 2010): F839—F846. http://dx.doi.org/10.1152/ajprenal.00734.2009.

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The hypothalamic paraventricular nucleus is a key integrative area in the brain involved in influencing sympathetic nerve activity and in the release of hormones or releasing factors that contribute to regulating body fluid homeostasis and endocrine function. The endocrine and hormonal regulatory function of the paraventricular nucleus is well studied, but the regulation of sympathetic nerve activity and blood flow by this region is less clear. Here we review the critical role of the paraventricular nucleus in regulating renal blood blow during hyperthermia and the evidence pointing to an important pathophysiological role of the paraventricular nucleus in the elevated renal sympathetic nerve activity that is a characteristic of heart failure.

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2

Fraser, Kurt M., and Patricia H. Janak. "Stressing the other paraventricular nucleus." Nature Neuroscience 21, no. 7 (June 25, 2018): 901–2. http://dx.doi.org/10.1038/s41593-018-0178-1.

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3

Uribe, Rosa Maria, Patricia Joseph-Bravo, and Jean-Louis Charli. "Pups removal enhances thyrotropin-releasing hormone mRNA in the hypothalamic paraventricular nucleus." European Journal of Endocrinology 133, no. 3 (September 1995): 354–60. http://dx.doi.org/10.1530/eje.0.1330354.

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Uribe RM, Joseph-Bravo P, Charli J-L. Pups removal enhances thyrotropin-releasing hormone mRNA in the hypothalamic paraventricular nucleus. Eur J Endocrinol 1–60. ISSN 0804–4643 Previous studies have shown that lactation and suckling alter thyrotropin-releasing hormone (TRH) biosynthesis in hypothalamic paraventricular neurons. The amounts of paraventricular TRH mRNA and mediobasal hypothalamus (MBH) TRH were determined following removal of the pups to examine whether paraventricular TRH neuron activity is altered during the transition from lactation to estrous cycle. Paraventricular TRH mRNA and MBH TRH levels were determined by Northern blot analysis and radioimmunoassay, respectively. We had shown previously that after an 8-h withdrawal of the pups at mid-lactation the MBH TRH and paraventricular TRH mRNA levels are not modified. This condition was compared to one where pups were removed for 56 h, finding a significant decrease (46%, p < 0.005) of MBH TRH and a significant increase (156%, p < 0.02) of paraventricular TRH mRNA. The effect observed in the paraventricular TRH mRNA was correlated negatively with the serum corticosterone levels, a potential negative regulator of paraventricular TRH mRNA. The results were similar if a 1-h suckling period was introduced 8 h after withdrawal of the pups to induce a transient increase of corticosterone levels. The pattern of TRH mRNA was specific to the paraventricular nucleus because there was no enhancement in the preoptic area-anterior hypothalamus. In summary, our data suggest that TRH biosynthesis in paraventricular neurons is slowly adjusted after withdrawal of the pups, possibly to prepare TRH neurons to the new secretory demands of the estrous cycle. JL Charli, Instituto de Biotecnologia, UNAM, AP 510-3, Cuernavaca, Mor. 62271, México

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4

Pyner, Susan. "The paraventricular nucleus and heart failure." Experimental Physiology 99, no. 2 (January 6, 2014): 332–39. http://dx.doi.org/10.1113/expphysiol.2013.072678.

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5

Adams, E. "The paraventricular nucleus modulates immune function." Journal of Neuroimmunology 16, no. 1 (September 1987): 11. http://dx.doi.org/10.1016/0165-5728(87)90144-5.

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6

Yamaguchi, Ken'ichi, Hitoshi Hama, Kazuo Watanabe, and Chieko Adachi. "Effect of dopamine injection into the anteroventral third ventricular region and the paraventricular nucleus on vasopressin secretion in conscious rats." Acta Endocrinologica 127, no. 5 (November 1992): 420–24. http://dx.doi.org/10.1530/acta.0.1270420.

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To investigate the role of dopamine receptors situated in the paraventricular nucleus and the anteroventral third ventricular region in regulating vasopressin release, responses of plasma AVP and its controlling factors to injections of dopamine into these regions and the lateral cerebral ventricle were examined in conscious rats. The injections of 156 nmol (30 μg) dopamine into the cerebral ventricle produced transient rises in plasma AVP 5 min later. When the dose of dopamine was reduced to 26 nmol (5 μg), the increase in plasma AVP was not provoked any more. However, injections of 26 nmol dopamine into the paraventricular nucleus greatly augmented plasma AVP 5 and 15 min later. This dose of dopamine was without effect on plasma AVP when injected into the anteroventral third ventricular region, including the organum vasculosum lamina terminalis, median preoptic nucleus, medial preoptic area and the periventricular preoptic nucleus. These dopamine administrations in the cerebral ventricle, paraventricular nucleus and the anteroventral third ventricular region did not significantly change AVP-controlling factors such as plasma osmolality, sodium and arterial pressure. On the basis of these results, we conclude that dopamine receptors in the paraventricular nucleus may function to facilitate AVP secretion, whereas those in the anteroventral third ventricular region may not play an important role in the regulation of AVP release.

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7

Csáki, Ágnes, Katalin Köves, Zsolt Boldogkői, Dóra Tombácz, and Zsuzsanna E. Tóth. "The Same Magnocellular Neurons Send Axon Collaterals to the Posterior Pituitary and Retina or to the Posterior Pituitary and Autonomic Preganglionic Centers of the Eye in Rats." NeuroSci 2, no. 1 (January 20, 2021): 27–44. http://dx.doi.org/10.3390/neurosci2010002.

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In rats, some parvocellular paraventricular neurons project to spinal autonomic centers. Using the virus tracing technique, we have demonstrated that some magnocellular paraventricular neurons, but not supraoptic neurons, also project to autonomic preganglionic centers of the mammary gland, gingiva, or lip. A part of these neurons has shown oxytocin immunoreactivity. In the present experiment, we have examined whether the same magnocellular neuron that sends fibers to the retina or autonomic preganglionic centers of the eye also projects to the posterior pituitary. Double neurotropic viral labeling and oxytocin immunohistochemistry were used. After inoculation of the posterior pituitary and the eye with viruses, spreading in a retrograde direction and expressing different fluorescence proteins, we looked for double-labeled neurons in paraventricular and supraoptic nuclei. Double-labeled neurons were observed in non-sympathectomized and cervical-sympathectomized animals. Some double-labeled neurons contained oxytocin. After the optic nerve was cut, the labeling did not appear in the supraoptic nucleus; however, it could still be observed in the paraventricular nucleus. In the paraventricular nucleus, the double-labeled cells may be the origin of centrifugal visual fibers or autonomic premotor neurons. In the supraoptic nucleus, all double-labeled neurons are cells of origin of centrifugal visual fibers.

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8

Castren, E., and J. M. Saavedra. "Lack of vasopressin increases hypothalamic atrial natriuretic peptide binding sites." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 1 (July 1, 1989): R168—R173. http://dx.doi.org/10.1152/ajpregu.1989.257.1.r168.

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Atrial natriuretic peptide (ANP) binding sites were measured by quantitative autoradiography in the supraoptic and paraventricular nuclei and in the subfornical organ of hypophysectomized, adrenalectomized, and genetically vasopressin-deficient (Brattleboro) rats. Hypophysectomized and Brattleboro rats had significantly higher numbers of ANP binding sites in the supraoptic nucleus and in the magnocellular subdivision of the paraventricular nucleus than their respective controls. ANP binding density was also increased in the parvocellular subdivision of the paraventricular nucleus in hypophysectomized rats and in the subfornical organ of homozygous Brattleboro rats. When homozygous Brattleboro rats were treated with vasopressin, the density of ANP binding sites was restored to control level in the subfornical organ but not in the supraoptic or paraventricular nuclei. Adrenalectomy did not influence ANP binding in the brain areas studied. Increased ANP binding density in Brattleboro rats and after hypophysectomy in the nuclei in which vasopressin neurons are located suggest that ANP binding sites may represent physiologically active receptors and may mediate the inhibitory action of ANP on vasopressin secretion.

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9

Ceccatelli, Sandra, and Catello Orazzo. "Effect of different types of stressors on peptide messenger ribonucleic acids in the hypothalamic paraventricular nucleus." Acta Endocrinologica 128, no. 6 (June 1993): 485–92. http://dx.doi.org/10.1530/acta.0.1280485.

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Using in situ hybridization we have studied the effects of different types of stressors, such as ether, immobilization, cold and swimming, on the expression of several peptide messenger ribonucleic acids (mRNAs) in the hypothalamic paraventricular nucleus of adult male rats. Paraventricular nucleus sections were hybridized using synthetic oligonucleotide probes complementary to mRNA for corticotropin-releasing hormone, neurotensin, enkephalin and thyrotropin-releasing hormone. A clear upregulation of neurotensin mRNA was seen after ether and, to a lesser extent, after immobilization stress, whereas after the two other stressors neurotensin mRNA was undetectable, as in control rats. An increase in enkephalin mRNA was observed in a selective region of the dorsal part of the medioparvocellular subdivision of the paraventricular nucleus only after ether and immobilization stress. No significant changes were seen in corticotropin-releasing hormone and thyrotropin-releasing hormone mRNA levels in any of the experimental paradigms. The present results show selective changes for various peptide mRNAs in the paraventricular nucleus after various types of stress. Significant effects could be demonstrated only on neurotensin and enkephalin mRNA after ether and immobilization stress. This suggests that adaptive changes in the rate of synthesis, processing and transport of the peptide may develop over a longer period of time.

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10

Babovic, Sinisa, Dejan Ivanov, Ljilja Mijatov-Ukropina, Takashi Toyonaga, Ivan Dimitrijevic, and Milena Djordjevic. "Cytoarchitecture of the human paraventricular hypothalamic nucleus." Medical review 62, no. 9-10 (2009): 417–20. http://dx.doi.org/10.2298/mpns0910417b.

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Introduction. The significance of this research in terms of structure and biochemical processes in PVN contributes to further understanding of vital physiological processes from delivery and stress to delicate chemical processes that keep the hypothalamo-hypophysial axis in balance. Conclusion. Comparative studies of the human hypothalamus with the hypothalamus of other mammals enable further research, especially pharmacological and physiological ones. These are made possible with the aid of highly sophisticated equipment for examination of neurophysiological features of the brain.

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11

Koutcherov, Yuri, Juergen K. Mai, Ken W. S. Ashwell, and George Paxinos. "Organization of the human paraventricular hypothalamic nucleus." Journal of Comparative Neurology 423, no. 2 (2000): 299–318. http://dx.doi.org/10.1002/1096-9861(20000724)423:2<299::aid-cne8>3.0.co;2-a.

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12

Morin, L. P., and J. Blanchard. "Organization of the hamster paraventricular hypothalamic nucleus." Journal of Comparative Neurology 332, no. 3 (June 15, 1993): 341–57. http://dx.doi.org/10.1002/cne.903320307.

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13

Smith, P. M., and A. V. Ferguson. "Paraventricular nucleus efferents influence area postrema neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 2 (February 1, 1996): R342—R347. http://dx.doi.org/10.1152/ajpregu.1996.270.2.r342.

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Extracellular single-unit recordings were obtained from area postrema neurons (AP), and peristimulus histograms were used to determine the effects of paraventricular nucleus (PVN) stimulation on these cells from anesthetized Sprague-Dawley rats. Of 91 AP cells tested, 30.8% responded to PVN stimulation with a short-latency (28.2 +/- 3.3 ms, mean +/- SE), short-duration (49.3 +/- 8.0 ms) excitation, whereas 8.6% were inhibited. In animals that had stimulation sites outside of PVN (non-PVN), only 4 of the 72 AP cells tested (5.6%) were influenced by stimulation. These excitatory effects of PVN stimulation on AP neurons were unaffected by V1-receptor blockade. Of 93 nucleus of the solitary tract (NTS) cells tested, 38.9% responded to PVN stimulation with a short-latency (18.5 +/- 2.4 ms), short-duration (48.8 +/- 9.6 ms) excitation and 22.2% with short-latency (20.75 +/- 4.1 ms), long-duration (204.4 +/- 44.9 ms) inhibitions. In contrast, non-PVN stimulation sites influenced only 19% of NTS neurons tested, all of which were excited. These data demonstrate that activation of PVN neurons elicits excitatory effects on the majority of AP neurons influenced. They further emphasize the potential significance of descending hypothalamic inputs in controlling neuronal activity in this circumventricular organ.

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14

Powis, Jeff E., Jaideep S. Bains, and Alastair V. Ferguson. "Leptin depolarizes rat hypothalamic paraventricular nucleus neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 5 (May 1, 1998): R1468—R1472. http://dx.doi.org/10.1152/ajpregu.1998.274.5.r1468.

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Leptin, the protein product of the ob/ obgene, is thought to have a central site of action, presumably within the hypothalamus, through which it regulates feeding behavior. The paraventricular nucleus (PVN) is one structure that has been implicated in regulating feeding behavior. Using patch-clamp recording techniques, this study examines the direct membrane effects of leptin on neurons in a coronal PVN slice. Bath application of the physiologically active leptin fragment (amino acids 22–56) elicited dose-related depolarizations in 82% of the type I cells tested ( n = 17) and 67% of the type II cells tested ( n = 9). By contrast, the physiologically inactive leptin fragment (amino acids 57–92) had no discernible effect on membrane potential ( n = 7). The effects of this peptide were unaffected following synaptic isolation of the cells by bath application of the sodium channel blocker tetrodotoxin ( n = 5). Voltage clamp recordings in six cells demonstrated that leptin increased a nonspecific cation conductance with a reversal potential near −30 mV. These findings suggest that neurons in PVN may play an important role in the central neuronal circuitry involved in the physiological response to leptin.

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15

Shirasaka, Tetsuro, Satoshi Miyahara, Takato Kunitake, Qing-Hua Jin, Kazuo Kato, Mayumi Takasaki, and Hiroshi Kannan. "Orexin depolarizes rat hypothalamic paraventricular nucleus neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 4 (October 1, 2001): R1114—R1118. http://dx.doi.org/10.1152/ajpregu.2001.281.4.r1114.

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Orexins, also called hypocretins, are newly discovered hypothalamic peptides that are thought to be involved in various physiological functions. In spite of the fact that orexin receptors, especially orexin receptor 2, are abundant in the hypothalamic paraventricular nucleus (PVN), the effects of orexins on PVN neurons remain unknown. Using a whole cell patch-clamp recording technique, we investigated the effects of orexin-B on PVN neurons of rat brain slices. Bath application of orexin-B (0.01–1.0 μM) depolarized 80.8% of type 1 ( n = 26) and 79.2% of type 2 neurons tested ( n = 24) in the PVN in a concentration-dependent manner. The effects of orexin-B persisted in the presence of TTX (1 μM), indicating that these depolarizing effects were generated postsynaptically. Addition of Cd2+(1 mM) to artificial cerebrospinal fluid containing TTX (1 μM) significantly reduced the depolarizing effect in type 2 neurons. These results suggest that orexin-B has excitatory effects on the PVN neurons mediated via a depolarization of the membrane potential.

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16

Ferri, C. C., and A. V. Ferguson. "Interleukin-1β Depolarizes Paraventricular Nucleus Parvocellular Neurones." Journal of Neuroendocrinology 15, no. 2 (January 17, 2003): 126–33. http://dx.doi.org/10.1046/j.1365-2826.2003.00870.x.

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17

Pérez-Delgado, M., Garcia Garcia, E. Carmona-Calero, H. Pérez-González, A. Castañeyra-Perdomo, and R. Ferres-Torres. "Alcohol Effects on Paraventricular Hypothalamic Nucleus Morphometry." Cells Tissues Organs 153, no. 4 (1995): 282–89. http://dx.doi.org/10.1159/000147729.

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18

Benarroch, Eduardo E. "Paraventricular nucleus, stress response, and cardiovascular disease." Clinical Autonomic Research 15, no. 4 (August 2005): 254–63. http://dx.doi.org/10.1007/s10286-005-0290-7.

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19

Ahmari, Niousha, Monica M. Santisteban, Douglas R. Miller, Natalie M. Geis, Riley Larkin, Ty Redler, Heather Denson, et al. "Elevated bone marrow sympathetic drive precedes systemic inflammation in angiotensin II hypertension." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 2 (August 1, 2019): H279—H289. http://dx.doi.org/10.1152/ajpheart.00510.2018.

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Increased sympathetic nervous system activity is a hallmark of hypertension (HTN), and it is implicated in altered immune system responses in its pathophysiology. However, the precise mechanisms of neural-immune interaction in HTN remain elusive. We have previously shown an association between elevated sympathetic drive to the bone marrow (BM) and activated BM immune cells in rodent models of HTN. Moreover, microglial-dependent neuroinflammation is also seen in rodent models of HTN. However, the cause-effect relationship between central and systemic inflammatory responses and the sympathetic drive remains unknown. These observations led us to hypothesize that increase in the femoral BM sympathetic nerve activity (fSNA) initiates a cascade of events leading to increase in blood pressure (BP). Here, we investigated the temporal relationship between the BM sympathetic drive, activation of the central and peripheral immune system, and increase in BP in the events leading to established HTN. The present study demonstrates that central infusion of angiotensin II (ANG II) induces early microglial activation in the paraventricular nucleus of hypothalamus, which preceded increase in the fSNA. In turn, activation of fSNA correlated with the timing of increased production and release of CD4+.IL17+ T cells and other proinflammatory cells into circulation and elevation in BP, whereas infiltration of CD4+ cells to the paraventricular nucleus marked establishment of ANG II HTN. This study identifies cellular and molecular mechanisms involved in neural-immune interactions in early and established stages of rodent ANG II HTN. NEW & NOTEWORTHY Early microglia activation in paraventricular nucleus precedes sympathetic activation of the bone marrow. This leads to increased bone marrow immune cells and their release into circulation and an increase in blood pressure. Infiltration of CD4+ T cells into paraventricular nucleus paraventricular nucleus marks late hypertension.

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20

Martin, Douglas S., and Joseph R. Haywood. "Reduced GABA inhibition of sympathetic function in renal-wrapped hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 5 (November 1, 1998): R1523—R1529. http://dx.doi.org/10.1152/ajpregu.1998.275.5.r1523.

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Animals with bilateral cannulas in the paraventricular nucleus were made hypertensive by a one-kidney, figure eight renal wrap procedure or sham operated. Femoral artery and vein catheters were inserted for arterial pressure measurement and plasma catecholamine determination. After recovery and 4 days after hypertension surgery, bicuculline methiodide or muscimol was microinjected into the paraventricular nucleus. In some rats, nitroprusside was infused intravenously to reflexly stimulate the sympathetic nervous system. In control rats, bicuculline increased blood pressure, heart rate, and plasma norepinephrine and epinephrine concentrations. In contrast, in hypertensive rats blood pressure did not change while the heart rate response was maintained. Plasma norepinephrine and epinephrine responses were reduced 75 and 68%, respectively. Muscimol injections decreased arterial pressure in the hypertensive rats. Heart rate responses to nitroprusside were similar in the two groups of rats, while the plasma catecholamine responses were attenuated in the hypertensive animals. These data suggest that GABA function in the paraventricular nucleus is reduced in renal wrap hypertension.

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21

Kawano, J. "Suprachiasmatic nucleus projections to the paraventricular thalamic nucleus of the rat." Thalamus & Related Systems 1, no. 3 (November 2001): 197–202. http://dx.doi.org/10.1016/s1472-9288(01)00019-x.

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22

Kawano, June, KarlE Krout, and ArhurD Loewy. "Suprachiasmatic nucleus projections to the paraventricular thalamic nucleus of the rat." Thalamus and Related Systems 1, no. 03 (November 2001): 197. http://dx.doi.org/10.1017/s147292880100019x.

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23

Ciriello, John, and Michael B. Gutman. "Functional identification of central pressor pathways originating in the subfornical organ." Canadian Journal of Physiology and Pharmacology 69, no. 7 (July 1, 1991): 1035–45. http://dx.doi.org/10.1139/y91-154.

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The functional projections from pressor sites in the subfornical organ (SFO) were identified using the 2-deoxyglucose (2-DG) autoradiographic method in urethane-anesthetized, sinoaortic-denervated rats. Autoradiographs of brain and spinal cord sections taken from rats whose SFO was continuously stimulated electrically for 45 min with stereotaxically placed monopolar electrodes (150 μA, 1.5-ms pulse duration, 15 Hz) following injection of tritiated 2-DG were compared with control rats that received intravenous infusions of pressor doses of phenylephrine to mimic the increase in arterial pressure observed during SFO stimulation. Comparisons were also made to autoradiographs from rats in which the ventral fornical commissure (CFV), just dorsal to the SFO, was electrically stimulated. The pressor responses during either electrical stimulation of the SFO or intravenous infusion of phenylephrine were similar in magnitude. On the other hand, stimulation of the CFV did not elicit a significant pressor response. Electrical stimulation of the SFO increased 2-DG uptake, in comparison to the phenylephrine-infused rats, in the nucleus triangularis, septofimbrial nucleus, lateral septal nucleus, nucleus accumbens, bed nucleus of the stria terminalis, dorsal and ventral nucleus medianus (median preoptic nucleus), paraventricular nucleus of the thalamus, hippocampus, supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus of the hypothalamus, and the intermediolateral nucleus of and central autonomic area of the thoracic spinal cord. In contrast, in rats whose CFV was stimulated, these nuclei did not demonstrate changes in 2-DG uptake compared with control animals that received pressor doses of phenylephrine. These data have demonstrated some of the components of the neural circuitry likely involved in mediating the pressor responses to stimulation of the SFO and the corrective responses to activation of the SFO by disturbances to circulatory and fluid balance homeostasis.Key words: cardiovascular reflex pathways, drinking, median preoptic nucleus, osmoreceptors, paraventricular nucleus of the hypothalamus, supraoptic nucleus.

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24

Purvis, C. C., and M. J. Duncan. "Discrete thalamic lesions attenuate winter adaptations and increase body weight." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 273, no. 1 (July 1, 1997): R226—R235. http://dx.doi.org/10.1152/ajpregu.1997.273.1.r226.

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The midline thalamus (e.g., the paraventricular thalamic nuclei and the reuniens nucleus) of Siberian hamsters and other mammals has been reported to contain specific binding sites for melatonin, a hormone that is essential for photoperiodically induced winter adaptations such as reproductive quiescence, loss of body weight, daily torpor, and the winter molt. The first experiment investigated whether the midline thalamus is necessary for these winter adaptations. Adult Siberian hamsters received discrete neurotoxic lesions of the paraventricular thalamic nuclei or the reuniens nucleus while under pentobarbital sodium-induced anesthesia. After recovery, the hamsters were monitored for winter adaptations while they were exposed to short photoperiods (10 h light/day) for 12 wk at 22 degrees C then for 60 days at 7 degrees C. Lesions of the reuniens nucleus, but not of the paraventricular thalamic nuclei, significantly inhibited short photoperiod-induced loss of body weight and tended to increase food consumption and decrease daily torpor. The second experiment showed that lesions of the reuniens nucleus increased body weight gain compared with that in controls during exposure to long photoperiods at 22 degrees C for 16 wk. In summary, these findings show that the reuniens nucleus is an important site for regulation of body weight and suggest that lesions of the reuniens nucleus may attenuate winter metabolic adaptations by causing an increase in body weight.

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25

Priou, Anne, Charles Oliver, and Michel Grino. "In situ hybridization of arginine vasopressin (AVP) heteronuclear ribonucleic acid reveals increased AVP gene transcription in the rat hypothalamic paraventricular nucleus in response to emotional stress." Acta Endocrinologica 128, no. 5 (May 1993): 466–72. http://dx.doi.org/10.1530/acta.0.1280466.

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The regulation of anterior pituitary adrenocorticotropin hormone (ACTH) secretion during stress involves several hypothalamic neurohormones, including arginine vasopressin (AVP). In situ hybridization techniques have been used to study the regulation of neuropeptide messenger ribonucleic acids in the hypothalamus. Owing to the relatively slow time course of the changes in cytoplasmic messenger ribonucleic acid concentrations, rapid alterations in the level of neuropeptide gene transcription could not be detected. Because of its rapid processing, the nuclear level of the heteronuclear ribonucleic acid should reflect the rate of its synthesis, namely the transcription of the gene. We have used in situ hybridization with a probe complementary to a portion of an intronic sequence of the rat AVP gene to study rapid changes in the level of AVP gene transcription during emotional stress. The specificity of our technique was demonstrated by the localization of the hybridization signals in the paraventricular nucleus, the supraoptic nucleus and the suprachiasmatic nucleus, and was confirmed by the nuclear localization of the labeling. Isolation and exposure of male rats to a novel environment induced an activation of the pituitary-adrenal axis and an increase in AVP heteronuclear ribonucleic acid concentrations in the paraventricular nucleus 2 h after the onset of the stress, suggesting that an increased AVP gene transcription may play a role in the activation of the pituitary-adrenal axis in response to emotional stress.

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26

Sandyk, Reuven, and Stanley R. Kay. "Paraventricular Nucleus-Pineal Interaction: Relevance to Tardive Dyskinesia." International Journal of Neuroscience 62, no. 3-4 (January 1991): 269–72. http://dx.doi.org/10.3109/00207459108999778.

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27

Herman, James P., Jeffrey G. Tasker, Dana R. Ziegler, and William E. Cullinan. "Local circuit regulation of paraventricular nucleus stress integration." Pharmacology Biochemistry and Behavior 71, no. 3 (March 2002): 457–68. http://dx.doi.org/10.1016/s0091-3057(01)00681-5.

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28

Geerling, Joel C., Jung-Won Shin, Peter C. Chimenti, and Arthur D. Loewy. "Paraventricular hypothalamic nucleus: Axonal projections to the brainstem." Journal of Comparative Neurology 518, no. 9 (May 1, 2010): 1460–99. http://dx.doi.org/10.1002/cne.22283.

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29

Uroz, Victoria, Lucía Prensa, and José Manuel Giménez-Amaya. "Chemical anatomy of the human paraventricular thalamic nucleus." Synapse 51, no. 3 (November 18, 2003): 173–85. http://dx.doi.org/10.1002/syn.10298.

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30

van Wamelen, Daniel J., N. Ahmad Aziz, Jasper J. Anink, Raymund A. C. Roos, and Dick F. Swaab. "Paraventricular Nucleus Neuropeptide Expression in Huntington's Disease Patients." Brain Pathology 22, no. 5 (February 16, 2012): 654–61. http://dx.doi.org/10.1111/j.1750-3639.2012.00565.x.

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31

Coote, J. H., J. Gardner, S. Gladwell, E. Sermasi, R. Ranson, K. Motawei, and S. Pyner. "THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS AND BLOOD PRESSURE CONTROL." Fundamental & Clinical Pharmacology 11, S1 (December 1997): 26s—30s. http://dx.doi.org/10.1111/j.1472-8206.1997.tb00870.x.

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32

Leibowitz, Sarah F., Sonia Diaz, and Donna Tempel. "Norepinephrine in the paraventricular nucleus stimulates corticosterone release." Brain Research 496, no. 1-2 (September 1989): 219–27. http://dx.doi.org/10.1016/0006-8993(89)91069-x.

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33

Saphier, David, and Feldman Shaul. "Electrophysiology of limbic forebrain and paraventricular nucleus connections." Brain Research Bulletin 17, no. 6 (December 1986): 743–50. http://dx.doi.org/10.1016/0361-9230(86)90085-7.

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34

Feldman, Shaul, Nissim Conforti, and Eldad Melamed. "Paraventricular nucleus serotonin mediates neurally stimulated adrenocortical secretion." Brain Research Bulletin 18, no. 2 (February 1987): 165–68. http://dx.doi.org/10.1016/0361-9230(87)90186-9.

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35

Kiss, Jozsef Zoltan. "Dynamism of chemoarchitecture in the hypothalamic paraventricular nucleus." Brain Research Bulletin 20, no. 6 (June 1988): 699–708. http://dx.doi.org/10.1016/0361-9230(88)90080-9.

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36

Guevara-Aguilar, R., L. L. Jimenez-Montufar, D. E. Garcia-Diaz, M. J. Wayner, and D. L. Armstrong. "Olfactory and visceral projections to the paraventricular nucleus." Brain Research Bulletin 20, no. 6 (June 1988): 799–801. http://dx.doi.org/10.1016/0361-9230(88)90094-9.

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37

Saphier, D., and S. Feldman. "Effects of neural stimuli on paraventricular nucleus neurones." Brain Research Bulletin 14, no. 5 (May 1985): 401–7. http://dx.doi.org/10.1016/0361-9230(85)90016-4.

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38

Gotoh, E., K. Murakami, T. D. Bahnson, and W. F. Ganong. "Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 253, no. 1 (July 1, 1987): R179—R185. http://dx.doi.org/10.1152/ajpregu.1987.253.1.r179.

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To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

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39

Darlington, Daniel N., Martin R. Schiller, Richard E. Mains, and Betty A. Eipper. "Expression of RESP18 in Peptidergic and Catecholaminergic Neurons." Journal of Histochemistry & Cytochemistry 45, no. 9 (September 1997): 1265–77. http://dx.doi.org/10.1177/002215549704500910.

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We examined the expression of regulated endocrine-specific protein of 18-kD (RESP18) in selected peptidergic and catecholaminergic neurons of adult rat brain. In the hypothalamic paraventricular, supraoptic, and accessory nuclei, RESP18 mRNA was highly expressed in neurons immunostained for oxytocin and vasopressin. RESP18 mRNA was also highly expressed in paraventricular nucleus neurons immunostained for corticotropin-releasing hormone, thyrotropin-releasing hormone, and somatostatin. RESP18 mRNA was expressed in POMC cells of the arcuate nucleus, in neuropeptide Y cells of the dorsal teg-mental nucleus, lateral reticular nucleus, and hippocampus, and in brainstem catechola-minergic neurons. RESP18 mRNA expression was high in all paraventricular and arcuate neurons, but RESP18 protein was detectable in the perikarya of a subset of these neurons, suggesting an important post-transcriptional component to the regulation of RESP18 expression. RESP18 antisera immunostained perikarya but not axon fibers or terminals. Sub-cellular fractionation of homogenates of several hypothalamic nuclei identified RESP18 protein in fractions enriched in endoplasmic reticulum. The presence of 22- and 24-kD RESP18 isoforms in the neural lobe of the pituitary indicated that some RESP18 protein exited the endoplasmic reticulum. The post-transcriptional regulation of RESP18 expression and localization of RESP18 protein primarily to the endoplasmic reticulum suggests that RESP18 plays a regulatory role in peptidergic neurons.

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Schaechter, Judith D., and Alfredo A. Sadun. "A second hypothalamic nucleus receiving retinal input in man: the paraventricular nucleus." Brain Research 340, no. 2 (August 1985): 243–50. http://dx.doi.org/10.1016/0006-8993(85)90920-5.

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41

Hori, N., N. Yuyama, and K. Tamura. "Biting Suppresses Stress-induced Expression of Corticotropin-releasing Factor (CRF) in the Rat Hypothalamus." Journal of Dental Research 83, no. 2 (February 2004): 124–28. http://dx.doi.org/10.1177/154405910408300208.

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Corticotropin-releasing factor (CRF) expressed in the hypothalamus plays an important role in mediating behavioral responses to stressors. Restraining the body of an animal has been shown to activate and induce an enhanced expression of CRF in paraventricular neurons of the rat hypothalamus. Since aggressive biting behavior is known to suppress stress-induced noradrenaline secretion in the central nervous system and the formation of gastric ulcers, we investigated the effect of biting on restraint-induced CRF expression in the rat hypothalamus. The number of CRF-expressing neurons in the paraventricular nucleus increased significantly after short time restraint (30 or 60 min) followed by a 180-minute post-restraint period. Biting of a wooden stick during the restraint stress significantly suppressed the restraint-induced enhancement of CRF expression in the paraventricular nucleus. These observations suggest a possible anti-stress effect of biting and an important role of para-functional masticatory activity in coping with stressful events.

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42

Singh, Purnima, Shubha Ranjan Dutta, Chi Young Song, SaeRam Oh, Frank J. Gonzalez, and Kafait U. Malik. "Brain Testosterone-CYP1B1 (Cytochrome P450 1B1) Generated Metabolite 6β-Hydroxytestosterone Promotes Neurogenic Hypertension and Inflammation." Hypertension 76, no. 3 (September 2020): 1006–18. http://dx.doi.org/10.1161/hypertensionaha.120.15567.

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Previously, we showed that peripheral administration of 6β-hydroxytestosterone, a CYP1B1 (cytochrome P450 1B1)-generated metabolite of testosterone, promotes angiotensin II-induced hypertension in male mice. However, the site of action and the underlying mechanism by which 6β-hydroxytestosterone contributes to angiotensin II-induced hypertension is not known. Angiotensin II increases blood pressure by its central action, and CYP1B1 is expressed in the brain. This study was conducted to determine whether testosterone-CYP1B1 generated metabolite 6β-hydroxytestosterone locally in the brain promotes the effect of systemic angiotensin II to produce hypertension in male mice. Central CYP1B1 knockdown in wild-type ( Cyp1b1 +/+ ) mice by intracerebroventricular-adenovirus-GFP (green fluorescence protein)-CYP1B1-short hairpin (sh)RNA attenuated, whereas reconstitution of CYP1B1 by adenovirus-GFP-CYP1B1-DNA in the paraventricular nucleus but not in subfornical organ in Cyp1b1 −/− mice restored angiotensin II-induced increase in systolic blood pressure measured by tail-cuff. Intracerebroventricular-testosterone in orchidectomized (Orchi)- Cyp1b1 +/+ but not in Orchi- Cyp1b1 −/− , and intracerebroventricular-6β-hydroxytestosterone in the Orchi- Cyp1b1 −/− mice restored the angiotensin II-induced: (1) increase in mean arterial pressure measured by radiotelemetry, and autonomic imbalance; (2) reactive oxygen species production in the subfornical organ and paraventricular nucleus; (3) activation of microglia and astrocyte, and neuroinflammation in the paraventricular nucleus. The effect of intracerebroventricular-6β-hydroxytestosterone to restore the angiotensin II-induced increase in mean arterial pressure and autonomic imbalance in Orchi- Cyp1b1 −/− mice was inhibited by intracerebroventricular-small interfering (si)RNA-androgen receptor (AR) and GPRC6A (G protein-coupled receptor C6A). These data suggest that testosterone-CYP1B1-generated metabolite 6β-hydroxytestosterone, most likely in the paraventricular nucleus via AR and GPRC6A, contributes to angiotensin II-induced hypertension and neuroinflammation in male mice.

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Simon, James K., and John Ciriello. "Contribution of afferent renal nerves to the metabolic activity of central structures involved in the control of the circulation." Canadian Journal of Physiology and Pharmacology 67, no. 9 (September 1, 1989): 1130–39. http://dx.doi.org/10.1139/y89-180.

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Afferent renal nerves (ARN) are thought to be an important link in the pathogenesis of hypertension because of their influence on neuronal circuits involved in the control of arterial pressure and body fluid homeostasis. However, the central neural pathways involved in mediating ARN information have not been completely elucidated. In the present study, regions of the brainstem and forebrain, whose metabolic activity was altered after renal denervation, were functionally identified using hexokinase histochemistry in the rat. No differences in arterial pressure or heart rate were observed in either the 3-day or 13-day ARN-transected (tARN) animals compared with the respective sham ARN-transected (sARN) groups. Significant increases in the hexokinase reaction product were seen in the parvocellular component of the paraventricular nucleus of the hypothalamus, the supraoptic nucleus, the arcuate nucleus, the subfornical organ, the median preoptic nucleus, and the medial nucleus of the amygdala in both the 3-day and 13-day tARN animals. The bed nucleus of the stria terminalis was observed to have a significant decrease in hexokinase activity in the tARN groups, as were the caudal and medial aspects of the nucleus of the solitary tract. In the 3-day tARN group only, a significant decrease in hexokinase activity was observed in the region of the brainstem containing the A5 cell group, compared with sARN animals. The magnocellular component of the paraventricular nucleus of the hypothalamus and the lateral hypothalmus was seen to have increased hexokinase activity in the 13-day tARN animals only. These results have demonstrated that removal of ARN input alters the activity of brainstem and forebrain structures that have previously been implicated in the control of the cardiovascular system and body fluid balance. These data suggest that changes in the tonic input from renal receptors to these central structures could contribute to the development and (or) maintenance of hypertension.Key words: hypertension, renal nerves, fluid balance, paraventricular nucleus of the hypothalamus, subfornical organ, nucleus of the solitary tract, cardiovascular reflex pathways.

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44

Salter-Venzon, Dawna, and Alan G. Watts. "The role of hypothalamic ingestive behavior controllers in generating dehydration anorexia: a Fos mapping study." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 4 (October 2008): R1009—R1019. http://dx.doi.org/10.1152/ajpregu.90425.2008.

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Giving rats 2.5% saline to drink for 3–5 days simply and reliably generates anorexia. Despite having the neurochemical and hormonal markers of negative energy balance, dehydrated anorexic rats show a marked suppression of spontaneous food intake, as well as the feeding that is usually stimulated by overnight starvation or a 2-deoxy-d-glucose (2DG) challenge. These observations are consistent with a dehydration-dependent inhibition of the core circuitry that controls feeding. We hypothesize that this inhibition is directed at those neurons in the paraventricular nucleus and lateral hypothalamic area that constitute the hypothalamic “behavior controller” for feeding rather than their afferent inputs from the arcuate nucleus or hindbrain that convey critical feeding-related sensory information. To test this hypothesis, we mapped and quantified the Fos-immunoreactive response to 2DG in control and dehydrated rats drinking 2.5% saline. Our rationale was that regions showing an attenuated Fos response to 2DG in dehydrated animals would be strong candidates as the targets of dehydration-induced suppression of 2DG feeding. We found that the Fos response to combined dehydration and 2DG was attenuated only in the lateral hypothalamic area, with dehydration alone increasing Fos in the lateral part of the paraventricular nucleus. In the arcuate nucleus and those regions of the hindbrain that provide afferent inputs critical for the feeding response to 2DG, the Fos response to 2DG was unaffected by dehydration. Therefore, dehydration appears to target the lateral hypothalamic area and possibly the lateral part of the paraventricular nucleus to suppress the feeding response to 2DG.

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45

Melis, Maria Rosaria, and Antonio Argiolas. "Erectile Function and Sexual Behavior: A Review of the Role of Nitric Oxide in the Central Nervous System." Biomolecules 11, no. 12 (December 11, 2021): 1866. http://dx.doi.org/10.3390/biom11121866.

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Nitric oxide (NO), the neuromodulator/neurotransmitter formed from l-arginine by neuronal, endothelial and inducible NO synthases, is involved in numerous functions across the body, from the control of arterial blood pressure to penile erection, and at central level from energy homeostasis regulation to memory, learning and sexual behavior. The aim of this work is to review earlier studies showing that NO plays a role in erectile function and sexual behavior in the hypothalamus and its paraventricular nucleus and the medial preoptic area, and integrate these findings with those of recent studies on this matter. This revisitation shows that NO influences erectile function and sexual behavior in males and females by acting not only in the paraventricular nucleus and medial preoptic area but also in extrahypothalamic brain areas, often with different mechanisms. Most importantly, since these areas are strictly interconnected with the paraventricular nucleus and medial preoptic area, send to and receive neural projections from the spinal cord, in which sexual communication between brain and genital apparatus takes place, this review reveals that central NO participates in concert with neurotransmitters/neuropeptides to a neural circuit controlling both the consummatory (penile erection, copulation, lordosis) and appetitive components (sexual motivation, arousal, reward) of sexual behavior.

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46

Bubser, Michael, and Ariel Y. Deutch. "Thalamic paraventricular nucleus neurons collateralize to innervate the prefrontal cortex and nucleus accumbens." Brain Research 787, no. 2 (March 1998): 304–10. http://dx.doi.org/10.1016/s0006-8993(97)01373-5.

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47

Honkaniemi, Jari, Tommi Kainu, Sandra Ceccatelli, Leena Rechardt, Tomas Hökfelt, and Markku Pelto-Huikko. "Fos and jun in rat central amygdaloid nucleus and paraventricular nucleus after stress." NeuroReport 3, no. 10 (October 1992): 849–52. http://dx.doi.org/10.1097/00001756-199210000-00007.

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48

Sato-Suzuki, Ikuko, Ichiro Kita, Mitsugu Oguri, and Hideho Arita. "O2 sensitivity in the paraventricular nucleus and yawning response." Neuroscience Research 31 (January 1998): S251. http://dx.doi.org/10.1016/s0168-0102(98)82124-x.

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49

Chang, Ya-Ting, Wei-Hsin Chen, Hsi-Chien Shih, Ming-Yuan Min, Bai-Chuang Shyu, and Chien-Chang Chen. "Anterior nucleus of paraventricular thalamus mediates chronic mechanical hyperalgesia." PAIN 160, no. 5 (May 2019): 1208–23. http://dx.doi.org/10.1097/j.pain.0000000000001497.

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50

Kvochina, Lyudmyla, Eileen M. Hasser, and Cheryl M. Heesch. "Pregnancy decreases GABAergic inhibition of the hypothalamic paraventricular nucleus." Physiology & Behavior 97, no. 2 (May 2009): 171–79. http://dx.doi.org/10.1016/j.physbeh.2009.02.018.

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