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1 RVLM neurons unaffected by either CO(2) or BP were light
2 RVLM sympathoexcitatory neurons may be intrinsically pH-
5 20 ms pulses at 10 mW) was used to activate RVLM neurons that had been transduced by both vectors.
9 actin anesthetized female rats, the CVLM and RVLM were functionally defined by pressor and depressor
11 systemically (plasma) and centrally (NTS and RVLM) and reduced hypothalamic PGE(2) production, which
12 y via synaptic contacts in the RTN, NTS, and RVLM and provides significant anatomical evidence to sup
13 of LLTS, four brainstem (SP5, NAb, NTS, and RVLM) and two forebrain sites (PVN and SFO) were examine
14 increased receptor expression in the PVH and RVLM is the mechanism by which Ang II in the brain helps
15 p85alpha/p110delta expression in the PVN and RVLM is associated with increased PI3-kinase activity in
18 spite studies showing a relationship between RVLM-C1 and sympathetic activity in HF, no studies have
20 uadrants, i.e., left and right sides of both RVLM and CVLM in sham operated rats and in rats with a t
21 uadrants, i.e., left and right sides of both RVLM and CVLM in sham-operated rats (n = 10) and in rats
24 clamp recordings were made from bulbospinal RVLM neurons (n = 31) in brainstem slices prepared from
25 h clamp recordings from isolated bulbospinal RVLM neurons, 17beta-estradiol dose-dependently reduced
29 l ventrolateral medullary catecholaminergic (RVLM-CA) neurons e.g., by hypoxia is thought to increase
30 l ventrolateral medullary catecholaminergic (RVLM-CA) neurons use glutamate as a transmitter in the d
31 art failure (HF) is characterized by chronic RVLM-C1 activation, increased sympathetic activity and i
32 n the ipsilateral side but not contralateral RVLM, and to both RVLM quadrants in sham-operated rats.
34 arse commissural projection to contralateral RVLM was observed, and pericellular arbors were present
35 ic BP response were fully maintained despite RVLM pretreatment with the angiotensin II type 1 recepto
37 rs in RVLM, including its rostral extension (RVLM(RE) ), both of which contain bulbospinal catecholam
39 rats, we confirmed that the projection from RVLM catecholaminergic neurons to the orexinergic neuron
40 Ultrastructurally, mCherry terminals from RVLM-CA neurons in DbetaH(Cre/0) mice made predominantly
42 gic and glutamatergic inputs into identified RVLM-projecting neurons of the hypothalamic paraventricu
43 gnificantly lower (i.e., higher affinity) in RVLM and CVLM (164+/-38 and 178+/-27 pM, respectively,)
46 inding activity were significantly higher in RVLM of CHF compared with Sham rabbits (240.4+/-30.2%, P
48 by activation of glutamatergic receptors in RVLM that also cause proarrhythmogenic changes mediated
49 actor for CVD, increase GABA(A) receptors in RVLM, including its rostral extension (RVLM(RE) ), both
50 and JNK activity increased significantly in RVLM of CHF compared with sham (262.9+/-48.1%, 213.8+/-2
51 GABA(Aalpha1) and GABA(Aalpha2) subunits in RVLM but only GABA(Aalpha2) was lower in the RVLM(RE) of
52 findings suggest the existence of individual RVLM neurons for which the axons branch to drive sympath
55 notropic glutamate receptor antagonist) into RVLM or the retrotrapezoid nucleus (RTN) eliminated or r
56 ine 10 mg/ml) microinjected bilaterally into RVLM had no effect on seizure-induced sympathoexcitation
57 cordingly, microinjections of glutamate into RVLM evoked larger increases in SNA after CIH (P<0.05).
59 agonist, kynurenic acid (50 nl; 100 mM) into RVLM, blocked the seizure-induced 43.2 +/- 12.6% sympath
61 that the pressor response elicited by intra-RVLM ethanol (10 mug) was (i) abolished following local
63 LM with GABA persisted following ipsilateral RVLM GABA(A) receptor blockade (bicuculline, BIC, 400 pm
64 on in eNOS expression within the ipsilateral RVLM and an overexpression of eNOS within the ipsilatera
65 on in nNOS expression within the ipsilateral RVLM and an overexpression of nNOS abundance within the
66 duced nNOS expression within the ipsilateral RVLM quadrant compared to the contralateral RVLM or RVLM
67 itive nerve terminals within the ipsilateral RVLM that were immunoreactive (ir) for the VGLUT2 protei
68 ns retrogradely labeled from the ipsilateral RVLM with cholera toxin subunit B (CTB; 85% on average,
69 ns retrogradely labeled from the ipsilateral RVLM with CTB were c-Fos-ir (16-40%, depending on PVH re
74 ostral ventrolateral portion of the medulla (RVLM) is composed of heterogeneous populations of neuron
76 group of the rostral ventrolateral medulla (RVLM) and the nucleus of the solitary tract (NTS), where
77 eurons in the rostral ventrolateral medulla (RVLM) are more responsive to excitation in sedentary ver
79 eurons of the rostral ventrolateral medulla (RVLM) determine sympathetic outflow to different territo
80 anol into the rostral ventrolateral medulla (RVLM) elicits modest increases in local extracellular si
81 input to the rostral ventrolateral medulla (RVLM) from neurons in the paraventricular nucleus (PVN)
82 eptors in the rostral ventrolateral medulla (RVLM) has been suggested to contribute to hypertension.
84 sst2 ) in the rostral ventrolateral medulla (RVLM) lower sympathetic nerve activity, arterial pressur
85 eurons in the rostral ventrolateral medulla (RVLM) maintain sympathetic vasomotor tone and blood pres
86 AT(1)R in the rostral ventrolateral medulla (RVLM) of rabbits with CHF, its downstream pathway, and i
87 reased in the rostral ventrolateral medulla (RVLM) of rabbits with chronic heart failure (CHF) and in
88 apelin in the rostral ventrolateral medulla (RVLM) on blood pressure, cardiac function, and sympathet
89 nervating the rostral ventrolateral medulla (RVLM) play important roles in the control of sympathetic
90 leased in the rostral ventrolateral medulla (RVLM) plays a critical role in maintaining arterial baro
91 ctions in the rostral ventrolateral medulla (RVLM) region that contains bulbospinal C1 adrenergic neu
92 eurons in the rostral ventrolateral medulla (RVLM) regulate blood pressure through direct projections
93 zation of rat rostral ventrolateral medulla (RVLM) sympathetic premotor neurons and its functional co
94 urones in the rostral ventrolateral medulla (RVLM) that drive this sympathetic nerve activity (SNA) a
96 eus (PVN) and rostral ventrolateral medulla (RVLM) were microdissected for gene expression and protei
97 eurons of the rostral ventrolateral medulla (RVLM) were recorded in anaesthetized sino-aortic denerva
98 n-13 into the rostral ventrolateral medulla (RVLM), a major source of sympathoexcitatory neurones, in
99 vation of the rostral ventrolateral medulla (RVLM), and accordingly, microinjections of glutamate int
100 ostrema (AP), rostral ventrolateral medulla (RVLM), and lateral parabrachial nucleus (lPBN); however,
101 ocated in the rostral ventrolateral medulla (RVLM), are activated by pain, hypoxia, hypoglycemia, inf
102 eurons in the rostral ventrolateral medulla (RVLM), but the underlining electrophysiological mechanis
103 cing from the rostral ventrolateral medulla (RVLM), express NPY Y1 receptor immunoreactivity, and pat
106 in identified rostral ventrolateral medulla (RVLM)-projecting PVN neurones is altered in hypertensive
116 ius (NTS) and rostral ventrolateral medulla (RVLM)] cytokine surges were blunted, whereas oxidative s
117 etic nerve activity (control = 12 +/- 1 min; RVLM-strychnine = 5.1 +/- 1 min), suggesting that RVLM g
118 minergic C1 and non-C1 respiratory-modulated RVLM presympathetic neurons constitute a heterogeneous n
119 ude that the different respiratory-modulated RVLM presympathetic neurons contribute to the central ge
120 ubpopulation of non-C1 respiratory-modulated RVLM presympathetic neurons presented enhanced excitator
121 olateral medulla catecholaminergic neurones (RVLM-C1) modulate sympathetic outflow and breathing unde
122 olateral medulla catecholaminergic neurones (RVLM-C1) to both haemodynamic and respiratory alteration
123 ulating neurotransmitter in the normotensive RVLM to affect vascular tone through interaction with th
124 Histological analysis revealed that ~21% of RVLM bulbospinal neurons were retrogradely labelled by b
130 In sum, selective optogenetic activation of RVLM-CA neurons in conscious mice revealed two important
133 and assessed their impact on the activity of RVLM-projecting PVN neurons (PVN-RVLM neurons), and on P
134 s have addressed a potential contribution of RVLM-C1 neurones to irregular breathing in this context.
135 s study was to determine the contribution of RVLM-C1 neurones to irregular breathing patterns in HF.
136 Previous studies suggest the existence of RVLM neurons with distinct functional classes, such as n
138 that estrogens can modulate the function of RVLM C1 bulbospinal neurons either directly, through ext
141 ady-state conditions GABAergic inhibition of RVLM neurons predominated and glycine contributed less t
143 raphe nuclei was most dense at the level of RVLM, but rostral levels of pallidus were devoid of inne
144 cing, we show that a significant minority of RVLM neurons send axon collaterals to disparate spinal s
147 the CVLM can be activated in the presence of RVLM GABA receptor blockade, but sympathoinhibitory infl
149 hat the axons of a significant proportion of RVLM neurons collateralise widely within the spinal cord
150 Although glycine-dependent regulation of RVLM neurons has been proposed, its role in determining
151 These experiments evaluated the role of RVLM gamma-amino butyric acid (GABA) receptor subtypes a
152 anges may enhance the overall sensitivity of RVLM neurons to excitatory stimuli and contribute to an
155 d that (1) ACTH exerts excitatory effects on RVLM neurons resulting in pressor and tachycardic respon
156 roles of glutamate, PACAP, and microglia on RVLM catecholaminergic neurons during the cardiovascular
158 oduct of ethanol, caused no changes in BP or RVLM phosphatase activity but it produced significant in
162 urones that tonically inhibit presympathetic RVLM neurones and are essential for the production of nu
165 s that axon collaterals of lumbar-projecting RVLM neurons project to, and excite, both functionally s
168 Patch-clamp recordings obtained from PVN-RVLM neurons showed a reduction in I(A) current magnitud
169 d potassium current I(A) is expressed in PVN-RVLM neurones, characterized its biophysical and pharmac
170 ls play little role in generating SFA in PVN-RVLM neurones, their activation nevertheless does dampen
171 ults demonstrate the presence of I(A) in PVN-RVLM neurones, which actively modulates their action pot
173 I(A) availability, action potentials in PVN-RVLM neurons in hypertensive rats were broader, decayed
174 stochemical studies suggest that I(A) in PVN-RVLM neurons is mediated by Kv1.4 and/or Kv4.3 channel s
176 onstructions of intracellularly labelled PVN-RVLM neurons showed a diminished dendritic surface area
177 ngs obtained from retrogradely labelled, PVN-RVLM neurones indicate that a 4-AP sensitive, TEA insens
178 activity of RVLM-projecting PVN neurons (PVN-RVLM neurons), and on PVN influence of renal sympathetic
179 he hypothalamic paraventricular nucleus (PVN-RVLM) contributes to an imbalanced excitatory/inhibitory
182 ased or decreased the firing activity of PVN-RVLM neurones, supporting the presence of subsets of PVN
193 e roles of nNOS and eNOS within the rostral (RVLM) and caudal ventrolateral medulla (CVLM) in modulat
196 Collectively, these data demonstrate that RVLM C1 neurons modulate the activity of other central c
197 In this study, we tested the hypothesis that RVLM ser/thr phosphatases dampen the ERK-dependent press
199 optogenetics in tissue slices, we show that RVLM catecholaminergic neurons activate the locus coerul
202 strychnine = 5.1 +/- 1 min), suggesting that RVLM glycine plays a critical role in regulating the tim
207 l to Fluoro-Gold injection sites in both the RVLM and CVLM, and the remainder were contralateral.
208 ra-toxin-B retrogradely transported from the RVLM were detected in: paratrigeminal nucleus, lateral p
209 (CTB-ir), retrogradely transported from the RVLM, were assessed for expression of glutamic acid deca
210 cell count was significantly greater in the RVLM (P < 0.01) and in the neighbouring rostral ventral
211 Finally, blockade of orexin receptors in the RVLM abolished the increase in ASNA to neuroglucoprivati
212 (V(1A)) receptor expression increases in the RVLM after CIH conditioning (8 h per day for 10 days).
214 l angiotensin binding site is altered in the RVLM and other caudal brainstem regions of SHR, a quanti
215 espiratory output via V(1A) receptors in the RVLM and rVRC, and increased SNA in CIH-conditioned anim
216 activating polypeptide, and microglia in the RVLM and their contribution to cardiovascular autonomic
217 trast, stimulation of synaptic inputs in the RVLM decreased GABAergic inhibition to 53%; and increase
218 her neuroglucoprivation in the PeH or in the RVLM elicits adrenaline release in vivo and 2) whether d
219 ive comparison of AT receptor binding in the RVLM has been made in SHR versus normotensive rats.
221 ed that enhanced functional responses in the RVLM may be due, in part, to changes in the structure of
225 creased the AP-1-DNA binding activity in the RVLM of CHF rabbits compared to the vehicle group (9.14
226 with chronic heart failure (CHF) and in the RVLM of normal rabbits infused with intracerebroventricu
227 pressor action of [Pyr(1) ]apelin-13 in the RVLM of normotensive rats is not mediated via angiotensi
228 he characteristics of AT(1) receptors in the RVLM of rat, the species in which the most experimental
229 -AT, non-AT, angiotensin binding site in the RVLM of SHR may indicate a role for this binding site to
230 ow that apelin expression is enhanced in the RVLM of SHR versus WKY rats and that overexpression of t
231 of apelin was significantly enhanced in the RVLM of spontaneously hypertensive rat (SHR) compared wi
232 lease from the active synaptic inputs in the RVLM produced saturation of GABAergic inhibition and eme
233 and that overexpression of this gene in the RVLM results in chronic blood pressure elevation and car
235 and to a lesser extent MC3 receptors in the RVLM, and (3) the pressor effects of ACTH were mediated
236 itions of increased synaptic activity in the RVLM, glycinergic inhibition is recruited to strengthen
244 units GABA(Aalpha1) and GABA(Aalpha2) in the RVLM/RVLM(RE) of sedentary or physically active (10-12 w
246 ed that blood-borne Ang II can influence the RVLM via a neural connection between the circumventricul
247 summary, most PVH neurons that innervate the RVLM are glutamatergic, and this population includes the
250 idine (AGN; 1.0 microM), for 60 min into the RVLM attenuated increases in mean arterial pressure (MAP
251 enous apelin-13 (200 pmol in 50 nL) into the RVLM caused a 20 mm Hg elevation in blood pressure and a
252 ntagonist strychnine (4 mm, 100 nL) into the RVLM decreased the duration of baroreflex-mediated inhib
253 0 nl) of ACTH (0.5, 1 and 2 mmol/l) into the RVLM elicited increases in MAP and HR; tachycardic respo
255 ually absent when AAV2 was injected into the RVLM of DbetaH(Cre/0);VGLUT2(flox/flox) mice, into the c
256 nnelrhodopsin2(ChR2)-mCherry (AAV2) into the RVLM of dopamine-beta-hydroxylase Cre transgenic mice (D
259 ade tracer Fluoro-Gold was injected into the RVLM or CVLM of these animals, and immunofluorescence st
260 that microinjection of AAV2-apelin into the RVLM resulted in a significant increase in apelin expres
262 zole (TRIM, 1.0 microM) for 120 min into the RVLM, potentiated cardiovascular responses during a stat
263 GABA(A) and GABA(B) receptor blockade of the RVLM (400 pmol BIC+400 pmol CGP35348, 100 nl), inhibitio
264 ardiovascular regulation at the level of the RVLM and highlight that this system is a possible potent
266 GABA(A) receptor-mediated inhibition of the RVLM increases sympathetic outflow and blood pressure su
267 , and electrophysiological recordings of the RVLM presympathetic neurons in in situ preparations from
269 ffects were abolished by pretreatment of the RVLM with the vasopressin V1a receptor antagonist, SR 49
274 of brainstem nuclei with known inputs to the RVLM (nucleus tractus solitarius and caudal VLM) unmaske
275 d if AVP neurons project from the PVN to the RVLM and if arginine vasopressin (V(1A)) receptor expres
276 tion of strychnine (300 pmol, 100 nl) to the RVLM eliminated responses to CVLM inhibition, suggesting
283 antially, providing a mechanism by which the RVLM could contribute chronically to cardiovascular dise
284 examined whether nNOS antagonism within the RVLM and CVLM affected cardiovascular responses during t
285 he endothelial NOS (eNOS) isoform within the RVLM and CVLM might also play a role in integrating card
286 we investigated the role of iNOS within the RVLM and CVLM on cardiovascular responses and glutamater
289 ogically altered by nNOS blockade within the RVLM or CVLM, which in turn might have contributed to th
290 blot analysis of nNOS expression within the RVLM showed significant attenuation of the protein when
296 tors are probably located within or close to RVLM and not in the NTS or in the rVRG-pre-Botzinger/CVL
297 ABA(B) receptors nor a contralateral CVLM to RVLM GABAergic pathway explains residual responses to CV
300 opic evidence that the axons of rostral VLM (RVLM) catecholaminergic neurons contact locus coeruleus,