ライフサイエンスコーパス: pial

1 cs, was probed with a monoclonal antibody in pial and cortical microvessels in rat brain.

2 Blood flow velocity in pial and cortical penetrating vessels measuring <20 micr

3 emarkably, these antibodies also labeled rat pial and ependymal cells as well as reactive astrocytes

4 vascular smooth muscle cells (VSMC) in small pial and intracerebral arteries, which are critical for

5 that neuronal excitation modulates both the pial and meningeal circulation through a critical intera

6 In control brains, pial and parenchymal blood vessels of all sizes were dis

7 structure of the junctional complex between pial and parenchymal vessels and involvement of MMP acti

8 Moreover, the timing of MMP activity in pial and parenchymal vessels correlated with the timing

9 Both pial and parenchymal vessels from mock infected animals

10 a pial artery would (1) attenuate changes in pial arterial diameter during acute hypertension and (2)

11 easurement of blood pressure, heart rate and pial arterial diameter through a cranial window.

12 ral microvascular endothelial cells (HCMEC), pial arterial endothelial cells, and middle meningeal ar

13 Pial arterial filling was scored on a six-point ordinal

14 ignaling and transport between brain and the pial arteries and cerebrospinal fluid in the subarachnoi

15 of nitric oxide synthase (NOS), in cerebral pial arteries and the sphenopalatine ganglia (SPG) of th

16 ssion brain injury (FPI) in the newborn pig, pial arteries constrict and responses to dilator stimuli

17 Previous studies have shown that pial arteries constricted and responses to dilator opioi

18 myogenic responses were similarly altered in pial arteries from TgNotch3(R169C) mice, but not in mese

19 MYOCD in vivo gene transfer to mouse pial arteries increased contractile protein content and

20 Brain parenchymal arterioles (PAs), but not pial arteries, undergo hypotrophic outward remodeling du

21 ngiography generates time-resolved images of pial arteries.

22 followed by delayed, active constriction of pial arteries.

23 One important mechanism to dilate cerebral (pial) arteries is by activation of large-conductance, ca

24 IL, revealed functional defects in cerebral (pial) arteries on the surface of the brain at an early s

25 ociated with marked decreases (mean: 60%) of pial arteriolar blood flow attributable to vasoconstrict

26 nsitive (KATP) potassium channel blockers on pial arteriolar CO2 reactivity, in vivo, were evaluated

27 Pial arteriolar diameter changes in hypercapnia were mea

28 Sco2 and pial arteriolar diameter decreased to hypocapnia (Paco2,

29 d similar decreases in Sco2 and increases in pial arteriolar diameter in response to moderate and sev

30 ges in cerebral oxygen saturation (Sco2) and pial arteriolar diameter measured by near- infrared spec

31 Pial arteriolar diameter to hypercapnia increased in the

32 rin (SnPP), on brain electrical activity and pial arteriolar diameter were examined using quantitativ

33 In anesthetized piglets, pial arteriolar diameters were determined using intravit

34 nitric oxide and adenosine may contribute to pial arteriolar vasodilatation during hypercapnia, and (

35 NOC/oFQ (10(-8), 10(-6) M) induced pial arteriole dilation was decreased by the protein kin

36 We have applied P2 receptor drugs to rat pial arterioles and measured changes in arteriole diamet

37 urface is consistent with diffusion of NO to pial arterioles as the mechanism of dilation to NMDA.

38 Topical ET-1 dilated pial arterioles at 10(-12) M and produced dose-dependent

39 and progressively worsening to involve most pial arterioles by 18 months; soluble Abeta levels are e

40 th compound 48/80 (25 microg/ml) constricted pial arterioles by 26+/-9% at 80 min.

41 In the control piglets, pial arterioles dose-dependently dilated to topical appl

42 to 100 nmol/L) dose-dependently constricted pial arterioles from SHR and WKY rats (n = 6 to 8).

43 Dilation of pial arterioles in response to hypoxia and hypercapnia w

44 hibits Ca2+ sparks, abolished CO dilation of pial arterioles in vivo.

45 nitroprusside (SNP, 10(-4) M) still dilated pial arterioles normally.

46 ffects of ministrokes targeted to individual pial arterioles on motor function in Thy-1 line 18 chann

47 In addition, diameter of pial arterioles remained constant (32+/-5 microm) while

48 K and NaFl from pial vessels and diameter of pial arterioles remained constant.

49 om pial vessels was minimal, and diameter of pial arterioles remained constant.

50 rom pial vessels was minimal and diameter of pial arterioles remained constant.

51 extran-10K from pial vessels and diameter of pial arterioles remained relatively constant during the

52 th or without alcohol, responses of parietal pial arterioles to systemic hypoxia and hypercapnia were

53 y of the blood-brain barrier and diameter of pial arterioles via the activation of inducible nitric o

54 y of the blood-brain barrier and diameter of pial arterioles via the synthesis/release of nitric oxid

55 10,000 Da; FITC-dextran-10K) and diameter of pial arterioles were measured in the absence and presenc

56 0 daltons; FITC-dextran-10K) and diameter of pial arterioles were measured in the absence and presenc

57 The mean diameters of pial arterioles were reduced 30% 4 days following blood

58 led sustained MA-induced vasoconstriction of pial arterioles, consistent with laser Doppler flowmetry

59 plication of L-NMMA produced constriction of pial arterioles, L-NMMA did not alter the permeability c

60 l expression was assessed in SHR and WKY rat pial arterioles, which were monitored by intravital micr

61 nd produced a rapid, sustained dilatation of pial arterioles.

62 noic acid (20-HETE), a potent constrictor of pial arterioles.

63 in clearance of FITC-dextran-10K and dilated pial arterioles.

64 learance of FITC-dextran-10K and diameter of pial arterioles.

65 n presenting at least one cerebral or spinal pial arteriovenous fistula (AVF), and to describe their

66 a closed cranial window was used to measure pial artery diameter and to collect cortical periarachno

67 Topical NOC/oFQ (10(-10) M) had no effect on pial artery diameter by itself but attenuated NMDA (10(-

68 Reductions in pial artery diameter, cerebral blood flow, cerebral perf

69 Reductions in pial artery diameter, cortical CBF, and cerebral perfusi

70 Cerebral blood flow, pial artery diameter, intracranial pressure, and autoreg

71 tive analogue mastoparan-17 had no effect on pial artery diameter.

72 During hypotension, pial artery dilation (PAD) was impaired more in the male

73 nists, partially restored attenuated NOC/oFQ pial artery dilation 1 h after I+R (9+/-1 and 18+/-1 vs.

74 lephrine decreased impairment of hypotensive pial artery dilation after fluid percussion brain injury

75 ed the effect of H/I on Katp and Kca induced pial artery dilation and the roles of tPA and ERK during

76 These data show that pial artery dilation by Kca channel activation is not me

77 f SB 203580 did not prevent impairment of PG pial artery dilation by NOC/oFQ.

78 Since recent studies show that pial artery dilation during a 20 or 40 min hypoxic expos

79 These data suggest that diminished pial artery dilation during longer hypoxic exposure resu

80 el activation and cAMP contribute to hypoxic pial artery dilation in a stimulus duration-dependent ma

81 K(ca) channel activation in NOC/oFQ-induced pial artery dilation in newborn pigs equipped with a clo

82 a) channel activation in hypotension induced pial artery dilation in newborn pigs equipped with a clo

83 of Kca+2 channels and cAMP in opioid-induced pial artery dilation in newborn pigs equipped with close

84 ion and cAMP-dependent mechanisms to hypoxic pial artery dilation in piglets equipped with a closed c

85 However, tPA potentiates impairment of pial artery dilation in response to hypotension after hy

86 annel (Kca) activation contribute to hypoxic pial artery dilation in the piglet, responses to the NO

87 Hypotension induced pial artery dilation is prostaglandin-dependent in the n

88 ve (K(ca)) K channels and cAMP contribute to pial artery dilation observed during a 10-min exposure t

89 generating system blunted mastoparan induced pial artery dilation similar to FPI (10+/-1 and 17+/-1 v

90 Mastoparan (10(-8), 10(-6) M) elicited pial artery dilation that was blunted by FPI and partial

91 acterize the role of vasopressin in impaired pial artery dilation to activators of the ATP sensitive

92 se of prostaglandins contributes to impaired pial artery dilation to the newly described opioid, noci

93 (+) channel-dependent mechanisms in impaired pial artery dilation to the newly described opioid, noci

94 NOC/oFQ), which contributes to impairment of pial artery dilation to the prostaglandins (PG) PGE2 and

95 Vasopressin so administered attenuated pial artery dilation to these K(+) channel activators un

96 ersal of N-methyl-D-aspartate (NMDA)-induced pial artery dilation to vasoconstriction.

97 kephalin (10(-10), 10(-8), 10(-6) M)-induced pial artery dilation was also inhibited within 1 h of FP

98 NMDA induced pial artery dilation was attenuated by I+R or H+I+R; but

99 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI and ME

100 Cromakalim and NS1619 induced pial artery dilation was attenuated following FPI, while

101 studies in piglets show that opioid-induced pial artery dilation was impaired following fluid percus

102 potension and fluid percussion brain injury, pial artery dilation was impaired more in males.

103 Leucine enkephalin and dynorphin-induced pial artery dilation were similarly altered by FPI and p

104 These data show that NOC/oFQ elicits pial artery dilation, at least in part, via cAMP, K(ATP)

105 FPI blunted PGE2 pial artery dilation, but U 0126 and SP 600125 (10(-6) M

106 tenuated N-methyl-D-aspartate (NMDA)-induced pial artery dilation.

107 oxic/ischemic impairment of NOC/oFQ-mediated pial artery dilation.

108 nteraction between opioids and NO in hypoxic pial artery dilation.

109 hese opioids, in turn, contribute to hypoxic pial artery dilation.

110 rent sites in their contributions to hypoxic pial artery dilation.

111 Kca+2 channels contribute to opioid-induced pial artery dilation.

112 s designed to determine if hyperoxia elicits pial artery vasoconstriction and to characterize the con

113 Hyperoxia also elicited pial artery vasoconstriction that was attenuated by BQ12

114 indicate that ET-1 contributes to hyperoxic pial artery vasoconstriction.

115 Papaverine-induced pial artery vasodilation was unchanged by fluid percussi

116 delivered directly to the outer surface of a pial artery would (1) attenuate changes in pial arterial

117 Pial artrioles of rats were monitored in vivo and found

118 atients with at least one cerebral or spinal pial AVF were screened for genetic disease.

119 on between the olfactory axons and the glial-pial barrier.

120 The disruption of the pial basal lamina caused the neuroepithelial cells to re

121 The present experiments demonstrate that the pial basal lamina has an important function during brain

122 ablished at later stages of development, the pial basal lamina of the newly developing neuroepitheliu

123 By correlating the disruptions in the pial basal lamina with changes in the morphology of radi

124 revealed that the collagenase disrupted the pial basal lamina, which was evident by the fragmented d

125 The disruption of pial basal membranes underlying the heterotopias and poo

126 of radial glia/progenitor fibers toward the pial/basal surface.

127 ment of cobblestone cortex, namely defective pial basement membrane (BM), abnormal anchorage of radia

128 ral cortex in the knockout mice, breaches in pial basement membrane allowed emigration of overmigrate

129 exhibit overmigration of neurons beyond the pial basement membrane and a cobblestone-like cortical m

130 This along with the pial basement membrane defects, contributed to the abnor

131 We hypothesize that breaches in pial basement membrane disrupt the neural-meningeal boun

132 olecules and major protein components of the pial basement membrane during normal brain development.

133 amma1 were used to study the function of the pial basement membrane in cortical histogenesis.

134 The pial basement membrane in the mutant embryos assembled b

135 t detect penetration of OSN axons across the pial basement membrane surrounding the olfactory bulb, s

136 Disruptions in the pial basement membrane underlie neural ectopia seen in t

137 The pial basement membrane was normal in the knockout mouse

138 LAMB1 is localized to the pial basement membrane, suggesting that defective connec

139 eye-brain disease, caused by breaches in the pial basement membrane.

140 histogenesis with the presence of an intact pial basement membrane.

141 rized by overmigration of neurons beyond the pial basement membrane.

142 e closely associated with disruptions in the pial basement membrane.

143 f neurons and glia, and fragmentation of the pial basement membrane.

144 ion to extracellular matrix molecules of the pial basement membrane.

145 imodipine induced vasodilation and increased pial blood flow.

146 evidence that GPR56 functions in regulating pial BM integrity during cortical development.

147 causal events are likely the breaches in the pial BM.

148 er microstructure, The gray/white matter and pial boundaries were identified on the high-resolution s

149 oint, half way between gray/white matter and pial boundaries.

150 ce imaging of transport gradients across the pial brain surface following controlled intracisternal i

151 artery-infusion of HENA (45 muM) dilated the pial cerebral arterioles via selective BK-channel target

152 congenic mice as follows: 83% rescue of low pial collateral extent and 4.5-fold increase in blood fl

153 Pial collaterals begin forming between embryonic day 13.

154 Formation of pial collaterals occurs during a narrow developmental wi

155 e differences were confirmed in the cerebral pial cortical circulation where, compared to VEGF(hi/+)

156 evelopment, SC1 localizes to radial glia and pial-derived structures, including the vasculature, chor

157 t attenuated NMDA (10(-8), 10(-6) M) induced pial dilation (control, 9+/-1 and 16+/-1; coadministered

158 with iberiotoxin further decremented hypoxic pial dilation and blocked the hypoxia-associated rise in

159 l antagonist iberiotoxin had no influence on pial dilation during 5 min of hypoxia (pO(2) approximate

160 agonist Rp 8-Bromo cAMPs had no influence on pial dilation during 5 min of hypoxia, decremented the d

161 Recent studies show that pial dilation during a 20- or 40-min hypoxic exposure wa

162 NS1619, a K(ca) channel agonist, induced pial dilation during hypoxia that was attenuated by 20-

163 Met-induced pial dilation during hypoxia was also stimulus duration

164 Decremented hypoxic pial dilation during longer exposure periods results, at

165 indicate that the diminished role of Met in pial dilation during longer hypoxic exposure periods res

166 halin (10(-10), 10(-8), 10(-6) M) attenuated pial dilation induced by this opioid (7+/-1, 13+/-2, and

167 nteraction between opioids and NO in hypoxic pial dilation using newborn pigs equipped with a closed

168 t studies have observed that NOC/oFQ elicits pial dilation via release of cAMP, which, in turn, activ

169 Topical 8-Bromo cAMP (10(-8), 10(-6) M) pial dilation was unchanged by I+R but blunted by H+I+R

170 d the neuroepithelial cells to retract their pial end feet and caused tectal axons to exit the brain

171 tained throughout its depth, even though the pial half appeared darker during epi-illumination and li

172 es are tectal foliation and the formation of pial holes.

173 ligand, collagen, which is localized to the pial layer of the developing cerebellum, thereby leading

174 ity at the surface of the cortex (meningeal, pial layer, vasculature) and around the ventricular wall

175 The vertical migration of neuroblasts to the pial layers of the tectum was inhibited, leading to a di

176 Arteriolar segments were isolated from pial membrane and studied within 10 h.

177 yelinated axon tracts but even ependymal and pial membranes.

178 cluding the vasculature, choroid plexus, and pial membranes.

179 urogenic zone intimately associated with the pial meningeal surface lining the outer edge of the form

180 ) /Iba1(+) macrophages were prominent in the pial meninges and ventricle lining, mainly at P1-P5.

181 We examined the pial microcirculation in rats using intravital fluoresce

182 We examined the pial microcirculation in rats using intravital fluoresce

183 f EBA is unknown, the variable expression in pial microvascular EC may be related to their incomplete

184 Using intravital microscopy to assess the pial microvasculature through a closed cranial window in

185 uniform labelling of EC in cortical vessels, pial microvessels showed a heterogeneity in EBA expressi

186 r endothelial cells, as well as occluded rat pial microvessels, showed that luminal but not abluminal

187 We examined the pial network of the middle cerebral artery, which distri

188 the present and prior studies imply that the pial network reallocates blood in response to changing m

189 ecular identities distinct from those of the pial network.

190 The soma translocated within the pial process toward the pial surface and could also tran

191 hrough its neurites, which sprouted from the pial process.

192 uron maintains its primitive ventricular and pial processes, through which the cell body moves.

193 region of the optic nerve was present in the pial septa that divide the nerve fiber bundles, in the p

194 embrane, lamina cribrosa, optic nerve septa, pial sheath, and vasculature were delineated as unique o

195 7 and P2Y1,2,6 RNA can be amplified from the pial sheet.

196 se cloned with differentiated neurons in the pial side did so.

197 postmitotic-differentiated neurons from the pial side of the cortex were used for cloning.

198 Its filamentous pial, subventricular, and perivascular immunostaining pa

199 gradient, netrin1 protein accumulates on the pial surface adjacent to the path of commissural axon ex

200 nslocated within the pial process toward the pial surface and could also translocate through its neur

201 kinje cell (PC) dendrites extend towards the pial surface and progressively contact immature granule

202 ly postnatal ages, which migrates toward the pial surface and proliferates in situ.

203 ed past microknife cuts which started at the pial surface and sectioned layers I-IV.

204 Pial surface arteries in cats, as well as surface arteri

205 in laminin, and shows discontinuities in the pial surface basal lamina (glia limitans) that probably

206 nd into the telencephalon and grow along the pial surface but not more deeply into this tissue.

207 an extracellular protein expressed near the pial surface during embryonic development that is absent

208 We also found that the BL located at the pial surface formed labyrinthine tube-like structures en

209 rtical CR cells were distributed beneath the pial surface in control mice, but were virtually absent

210 tion seem to include the molecular layer and pial surface in neonates and blood vessels from P7 until

211 t the growth of apical dendrites towards the pial surface is regulated by a diffusible chemoattractan

212 onnection between radial glial cells and the pial surface mediated by LAMB1 leads to this malformatio

213 idase, Diamidino yellow, or fast blue to the pial surface of SI labeled a characteristic pattern of n

214 ray matter was confined to astrocytes at the pial surface of the brain.

215 urons beyond the first cortical layer at the pial surface of the brain.

216 oriented from the ventricular surface to the pial surface of the brain.

217 d population of neurons situated beneath the pial surface of the human embryonic forebrain even befor

218 distribution of basal lamina proteins at the pial surface of the midbrain and the brainstem.

219 ons underwent normal radial migration to the pial surface of the neural tube.

220 y anchoring the neuroepithelial cells to the pial surface of the retina, has an important function in

221 thalamic axons abnormally migrate toward the pial surface of the ventral telencephalon (VT).

222 amidino yellow (DY), applied directly to the pial surface on rostral or caudal areas of rat M2 (RM2 a

223 e cortical sections, cut tangentially to the pial surface or in the coronal plane, were stained for C

224 minals in cortex sectioned tangential to the pial surface revealed several consistent findings.

225 First, during radial migration toward the pial surface the A13 cells differentiate into dopaminerg

226 loss that in most animals extended from the pial surface through layer V.

227 vascular; Type III lesions extended from the pial surface to cortical layer 3 or 4.

228 ctivation was present in a gradient from the pial surface to deeper cortical layers.

229 Lateral MN dendrites proliferated under the pial surface to form a dense, thin (1-2 microm) plexus i

230 ve, migrate through the claustrum toward the pial surface to form layers (2-6a) of the insular cortex

231 hey migrate radially in the direction of the pial surface to take up positions in the cortical plate.

232 laminae and microknife cuts parallel to the pial surface were used to interrupt propagation or to is

233 ertical cells which were oriented toward the pial surface when compared with 9-day dehydrated animals

234 fuse pattern of laminin deposition below the pial surface which correlated with an abrupt termination

235 loping brain and extend radial fibres to the pial surface, along which embryonic neurons migrate to r

236 nchoring of the neuroepithelial cells to the pial surface, and allowing the formation of a defined cy

237 e, radial glia cells were retracted from the pial surface, and radially migrating neurons, including

238 s as a sharp wave front perpendicular to the pial surface, at speeds ranging between 50 and 300 m/sec

239 -treated tecta outpaces the expansion of the pial surface, creating abnormal mechanical stresses.

240 ere usually made 1.2 to 1.5 mm down from the pial surface, in or around layer III.

241 domly rotated sections cut orthogonal to the pial surface, within the region of interest.

242 rbB2 antibody also immunostained glia at the pial surface.

243 atterning as they weave a course towards the pial surface.

244 cones, especially those oriented toward the pial surface.

245 ortical pathological process driven from the pial surface.

246 .5%), located approximately 1.4 mm below the pial surface.

247 xtend an apical dendrite directed toward the pial surface.

248 also varied with the cortical depth from the pial surface.

249 pling T2* at 25%, 50% and 75% depth from the pial surface.

250 ive astroglia were aberrantly present on the pial surface.

251 rectangular network oriented parallel to the pial surface.

252 sometimes extending barely 100 mum below the pial surface.

253 tex at depths of up to -900 microm below the pial surface.

254 o vertical microcolumns perpendicular to the pial surface.

255 n, which spanned from the ventricular to the pial surface.

256 rocesses terminating on blood vessels or the pial surface.

257 ler fibers were most numerous just below the pial surface.

258 the brainstem to form a motor nucleus at the pial surface.

259 aps were sampled at 25%, 50%, 75% depth from pial surface.

260 rodes implanted in Heschl's gyrus (HG), from pial-surface electrodes placed on the lateral superior t

261 maintain contact both at the ventricular and pial surfaces throughout mitotic division, and (2) short

262 tion MRI scans, models of the gray-white and pial surfaces were generated for each individual's corte

263 and no link was found with distance from the pial surfaces.

264 ctivity increase previously seen in the glio-pial tissue of diabetic rats may be due to the selective

265 Conversely, in glio-pial tissue, PKC-alpha and RACK1 were upregulated, where

266 ffer when comparing cerebral cortex and glio-pial tissue.

267 out passively into the brain parenchyma from pial vascular plexuses to meet metabolic needs of growin

268 SE BOLD iso-orientation maps excluding large pial vascular regions were significantly correlated to m

269 Pial vasodilation to a cAMP analogue during hypoxia was

270 SQ 29,548 similarly partially restored such pial vasodilation.

271 d is found in endothelial cells (ECs) of the pial venous plexus.

272 ity-increasing effect of arachidonic acid on pial venular capillaries in vivo using the single microv

273 The permeability response of slightly leaky pial venular capillaries to histamine was investigated u

274 Permeability of pial venular capillaries to Lucifer Yellow (PLY) was mea

275 iocyanate-BSA infusion was used to determine pial-venular permeability.

276 Finally, in a pial vessel disruption cortical stroke model, a unilater

277 nges differed between both types of vessels (pial vessel disruption within days versus weeks for pare

278 f smooth muscle cells (SMCs) in the walls of pial vessels affected by amyloid deposition in the Tg257

279 es in permeability and leukocyte adhesion in pial vessels after a localized, single dose of 20 Gy.

280 While adaptive arteriogenesis of the pial vessels and angiogenesis at the capillary level may

281 FITC-albumin, FITC-dextran-10K and NaFl from pial vessels and diameter of pial arterioles remained co

282 vehicle, clearance of FITC-dextran-10K from pial vessels and diameter of pial arterioles remained re

283 tly attenuated leukocyte adhesion in surface pial vessels and in deep ascending cortical postcapillar

284 sults showed that fast flows up to 3 cm/s in pial vessels and minute flows down to 0.3 mm/s in arteri

285 nicotine blunted NO-induced vasodilation of pial vessels and the increase in cortical blood flow mea

286 ere identified in immune cells extravasating pial vessels as early as 1 day post infection.

287 Most pial vessels consisted of a mixture of EBA positive and

288 Thermocoagulation (TCL) of pial vessels has been shown to result in the same degree

289 ure the diameter changes of single dural and pial vessels in the awake mouse during voluntary locomot

290 vasoconstriction and improved blood flow in pial vessels of PbA-infected mice.

291 radiation did not affect the permeability of pial vessels to the 150-kDa molecule.

292 (saline), clearance of FITC-dextran-10K from pial vessels was minimal and diameter of pial arterioles

293 vehicle, clearance of FITC-dextran-10K from pial vessels was minimal, and diameter of pial arteriole

294 saline), clearance of FITC-dextran-10 K from pial vessels was modest and remained relatively constant

295 d in blood vessels located in leptomeninges (pial vessels) and brain parenchyma (parenchymal vessels)

296 imarily of the superficial glia limitans and pial vessels, but trended toward a decrease in cerebral

297 ml) was required to increase permeability in pial vessels, suggesting that different tissues exhibit

298 I ganglionic cells in the SPG send fibers to pial vessels.

299 CGRP dilated dural, but not pial, vessels and significantly reduced spontaneous loco

300 In pial window preparations, chronic nicotine blunted NO-in