Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein–vasopressin fusion gene

Chu, Chun-Ping; Kato, Kazuo; Jin, Qinhan; Qiu, De-Lai; Yu, Nengwang; Oiso, Yutaka; Kannan, Hiroshi

doi:10.1016/j.neures.2005.06.011

Cited by 6 publications

(5 citation statements)

References 36 publications

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“…In this protocol, 0.25 m m V1a receptor antagonist was infused into the NTS at 0.25 μl h −1 . This dose was only 1/250th of previous studies in which the same antagonist, OPC‐21268, was infused into the lateral ventricle (Chu et al 2005; Kato et al 2009), and the infusion volume per hour was 1/800th of cerebrospinal fluid volume (Simchon et al 1999), suggesting that the effect of the antagonist was localized in the NTS and surrounding area. Therefore, our results from the V1a antagonist infusion suggest that V1a receptors in the NTS are involved in mediating baroreflex suppression in response to cerebral activation.…”

Section: Discussionmentioning

confidence: 79%

Voluntary locomotion linked with cerebral activation is mediated by vasopressin V1a receptors in free‐moving mice

Masuki¹,

Sumiyoshi²,

Koshimizu

et al. 2013

The Journal of Physiology

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Key points• Arterial blood pressure rises at the onset of voluntary locomotion, which is probably advantageous for increasing blood flow to contracting muscles without delay.• We previously reported in free-moving mice that the feedback control of arterial blood pressure through peripheral baroreceptors, which was dominant at rest, was suppressed during activation of the cerebral cortex; however, no neurotransmitter for the mechanisms has been identified.• Central suppression of the feedback control of arterial blood pressure at the onset of voluntary locomotion was abolished in vasopressin V1a receptor-deficient mice and by local infusion of a V1a receptor antagonist into the brainstem area, termed the nucleus tractus solitarii, of control mice.• Thus, central vasopressin might play an important role as a neurotransmitter in the pressor response at the onset of voluntary locomotion.Abstract We previously reported that cerebral activation suppressed baroreflex control of heart rate (HR) at the onset of voluntary locomotion. In the present study, we examined whether vasopressin V1a receptors in the brain were involved in these responses by using free-moving V1a receptor knockout (KO, n = 8), wild-type mice locally infused with a V1a receptor antagonist into the nucleus tractus solitarii (BLK, n = 8) and control mice (CNT, n = 8). Baroreflex sensitivity ( HR/ MAP) was determined from HR response ( HR) to a spontaneous change in mean arterial pressure ( MAP) every 4 s during the total resting period, which was ∼8.7 h, of the 12 h measuring period in the three groups. HR/ MAP was determined during the periods when the cross-correlation function (R(t)) between HR and MAP was significant (P < 0.05). Cerebral activity was determined from the power density ratio of θ to δ wave band (θ/δ) on the electroencephalogram every 4 s. Spontaneous changes in θ/δ were significantly correlated with R(t) during 62 ± 3% of the total resting period in CNT (P < 0.05), but only 38 ± 4% in KO and 47 ± 2% in BLK (vs. CNT, both P < 0.001). When R(t) and HR/ MAP were divided into six bins according to the level of θ/δ, both were positively correlated with θ/δ in CNT (both P < 0.001), while neither was correlated in KO or BLK (all P > 0.05). Moreover, the probability that mice started to move after an increase in θ/δ was 24 ± 4% in KO and 24 ± 6% in BLK, markedly lower than 61 ± 5% in CNT (both P < 0.001), with no suppression of the baroreflex control of HR. Abbreviations AVP, arginine vasopressin; CBF, cerebral blood flow; CNT, control; EEG, electroencephalogram; HR, heart rate; MAP, mean arterial pressure; NTS, nucleus tractus solitarii; REM, rapid eye movement; R(t), cross-correlation function between spontaneous changes in HR and MAP; V1a BLK, V1a receptor blockade; V1a KO, V1a receptor knockout; WT, wild-type; Z R (t) , transformed R(t); HR/ MAP, HR response to the spontaneous change in MAP; θ/δ, the power density ratio of θ to δ wave band in EEG.

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Section: Discussionmentioning

confidence: 79%

Voluntary locomotion linked with cerebral activation is mediated by vasopressin V1a receptors in free‐moving mice

Masuki¹,

Sumiyoshi²,

Koshimizu

et al. 2013

The Journal of Physiology

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“…To determine whether this coupling could also be engaged by endogenous ATP, we challenged the PVN with a hyperosmotic stimulus. A large bulk of evidence in the literature supports the fact that a hyperosmotic challenge results in the activation of both magnocellular and parvocellular PVN neuronal populations (e.g., increased c-Fos expression) (Chu et al 2005;Sharp et al 1991). Moreover, a hyperosmotic challenge was also shown to increase PVN neuronal excitability and evoke a PVN-mediated sympathoexcitatory response and, consequently, an elevation in blood pressure (Antunes et al 2006;Chen and Toney 2001;Chu et al 2010;Son et al 2013).…”

Section: Discussionmentioning

confidence: 93%

ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptor-mediated currents

Ferreira‐Neto

Antunes

Stern

2015

Journal of Neurophysiology

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Ferreira-Neto HC, Antunes VR, Stern JE. ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptormediated currents. J Neurophysiol 114: 159 -169, 2015. First published April 22, 2015 doi:10.1152/jn.01011.2014.-We have previously shown that ATP within the paraventricular nucleus (PVN) induces an increase in sympathetic activity, an effect attenuated by the antagonism of P2 and/or glutamatergic receptors. Here, we evaluated precise cellular mechanisms underlying the ATP-glutamate interaction in the PVN and assessed whether this receptor coupling contributed to osmotically driven sympathetic PVN neuronal activity. Whole-cell patch-clamp recordings obtained from PVN-rostral ventrolateral medulla neurons showed that ATP (100 M, 1 min, bath applied) induced an increase in firing rate (89%), an effect blocked by kynurenic acid (1 mM) or 4-[[4-Formyl-5-hydroxy-6-methyl-3-[(phosphonooxy)methyl]-2-pyridinyl]azo]-1,3-benzenedisulfonic acid tetrasodium salt (PPADS) (10 M). Whereas ATP did not affect glutamate synaptic function, ␣-amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) receptor-mediated currents evoked by focal application of AMPA (50 M, n ϭ 13) were increased in magnitude by ATP (AMPA amplitude: 33%, AMPA area: 52%). ATP potentiation of AMPA currents was blocked by PPADS (n ϭ 12) and by chelation of intracellular Ca 2ϩ (BAPTA, n ϭ 10). Finally, a hyperosmotic stimulus (mannitol 1%, ϩ55 mosM, n ϭ 8) potentiated evoked AMPA currents (53%), an effect blocked by PPADS (n ϭ 6). Taken together, our data support a functional stimulatory coupling between P2 and AMPA receptors (likely of extrasynaptic location) in PVN sympathetic neurons, which is engaged in response to an acute hyperosmotic stimulus, which might contribute in turn to osmotically driven sympathoexcitatory responses by the PVN.ATP; ␣-amino-3-hydroxy-5-methylisoxazole propionic acid; paraventricular nucleus; rostral ventrolateral medulla; hyperosmolarity BODY FLUID HOMEOSTASIS is tightly regulated by the integration of renal, cardiovascular, and neuroendocrine systems (Share and Claybaugh 1972). An increase in plasma osmolality induces several responses including an increase in sympathetic activity, blood pressure elevation, and the release of neurohormones, such as vasopressin and angiotensin II (Bealer 2000;Hatzinikolaou et al. 1980Hatzinikolaou et al. , 1981Stocker and Toney 2005;Weiss et al. 1996). Part of these responses are mediated through activation of the hypothalamic paraventricular nucleus (PVN) driven by the circumventricular organs in which central osmoreceptors are located (Antunes-Rodrigues et al. 2004;Stocker et al. 2008). The PVN is composed of magnocellular and parvocellular neurons. Magnocellular neurons synthesize and release vasopressin and oxytocin systemically from the posterior pituitary, whereas parvocellular neurons project to premotor sympathoexcitatory neurons located either in the rostral ventrolateral medulla (RVLM) and/or intermediolateral cell column of the spinal cord.Several neurotransmitters in t...

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“…Representative immunohistochemical data from these animals are presented in Figs. 3-6 with quantitative analysis of c-Fos expression summarized in Table 1. cerebroventricular administration of HS (21,66,76,97). The expected hormone release from terminals of magnocellular neurons in the pituitary resulted in elevated plasma levels of oxytocin and vasopressin correspondent with the prolonged rise in plasma osmolality, indicative of a role in restoring salt-water balance (9,114).…”

Section: Osmotic Stimulation Inhibits Glial and Perivascularvascular mentioning

confidence: 97%

Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus

Summy-Long

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Summy-Long JY, Hu S. Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus. Am J Physiol Regul Integr Comp Physiol 297: R1532-R1545, 2009. First published September 16, 2009 doi:10.1152/ajpregu.00340.2009.-During the brain's innate immune response microglia, astroglia and ependymal cells resolve/repair damaged tissue and control infection. Released interleukin-1␤ (IL-1␤) reaching cerebroventricles stimulates circumventricular organs (CVOs; subfornical organ, SFO; organum vasculosum lamina terminalis, OVLT), the median preoptic nucleus (MePO), and magnocellular and parvocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei. Hypertonic saline (HS) also activates these osmosensory CVOs and neuroendocrine systems, but, in contrast to IL-1␤, inhibits the peripheral immune response. To examine whether the brain's innate immune response is attenuated by osmotic stimulation, sterile acidic perfusion fluid was microdialyzed (2 l/ min) in the SON area of conscious rats for 6 h with sterile HS (1.5 M NaCl) injected subcutaneously (15 ml/kg) at 5 h. ϩ ; amoeboid/hypertrophied; IL-1␤ ϩ ) in the adjacent SON and bilaterally in perivascular areas of the PVN, periventricular hypothalamus and ependyma, coincident with c-Fos expression in ependymal cells and COX-2 in the vasculature. These microglial responses were attenuated by HS, coincident with activating parvocellular and magnocellular neuroendocrine systems and elevating circulating IL-1␤, oxytocin, and vasopressin. Acidosis-induced cellular injury from microdialysis activated the brain's innate immune response by a mechanism inhibited by peripheral osmotic stimulation. hypertonic saline; interleukin-1␤; acidosis; magnocellular neurons; c-Fos MICRODIALYSIS OF BRAIN NUCLEAR sites is used widely to monitor endogenous neural activity (28) and, more selectively, the central release of oxytocin and vasopressin from dendrites and somas of magnocellular neurons in the supraoptic nucleus (SON) spatially separated from their axon terminals in the neural lobe (68,73). Using this method in conscious rats, we found previously that basal release of interleukin-1␤ (IL-1␤) into dialysates (121) of the SON area increased in response to osmotic stimulation (106). Originally, the present immunohistochemical study was designed to identify local cellular sources of the cytokine (IL-1␤ ϩ ) and its biologic targets expressing the IL-1 type 1 receptor (IL-1R; 101) and having cyclooxygenase (COX-2) (65) or c-Fos induced by the cytokine (32, 60, 62). Our attention, however, widened to include the brain's innate immune response when our microdialysis studies showed activation of microglia in the SON (106).Like other tissues, an innate immune system in the brain responds to injury, protecting against infection and repairing damage in an effort to restore function (74, 87). Largely excluded from circulating blood cells and the peripheral immune system, the brain relies on glia and epend...

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Enhanced cardiovascular alteration and Fos expression induced by central salt loading in a conscious rat transgenic for the metallothionein–vasopressin fusion gene

Cited by 6 publications

References 36 publications

Voluntary locomotion linked with cerebral activation is mediated by vasopressin V1a receptors in free‐moving mice

Voluntary locomotion linked with cerebral activation is mediated by vasopressin V1a receptors in free‐moving mice

ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptor-mediated currents

Peripheral osmotic stimulation inhibits the brain's innate immune response to microdialysis of acidic perfusion fluid adjacent to supraoptic nucleus

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