ライフサイエンスコーパス: i.c.v.

1 i.c.v. benoxathian also inhibited the activity of oxytoc

2 i.c.v. GLP-1R blockade with the antagonist exendin(9-39)

3 i.c.v. infusion of the alpha1-adrenoreceptor antagonist

4 i.c.v. pretreatment with MK-801, an NMDA receptor antago

5 vity of beta-endorphinergic neurons of HRP-1 i.c.v. injected animals showed a daily rhythm, with high

6 hinergic neurons was also observed in Rcho-1 i.c.v. injected animals, which showed very low and uncha

7 terectomized rats and very low in the Rcho-1 i.c.v. injected hysterectomized and sham-hysterectomized

8 The results show that (1) i.c.v. injection of a high dose of OFQ/N (9-18 micro g)

9 f ischemic stroke, administration of PAN-811 i.c.v. 1 h after middle cerebral artery occlusion result

10 In acute i.c.v. studies, the bivalent ligands functioned as agoni

11 In addition, i.c.v. or i.v. pretreatment with the I1-imidazoline rece

12 evious results showing that C75 administered i.c.v. rapidly activates hypothalamic neurons of the arc

13 L-NAME administered i.c.v. decreased 24 h energy intake to a greater extent

14 Co-administration (i.c.v.) of CGRP (1.5 microg) with the mu and kappa opioi

15 After i.c.v. infusion of saline, subjects strongly preferred t

16 After i.c.v. injection to rats, (+/-)-trans H2-PAT (4-40 nmole

17 After i.c.v. injection, I-gp120 appeared in the serum and was

18 ine-regulated transcript CART (55-102) after i.c.v. administration in mouse models of acute and persi

19 markedly reduced c-fos in these areas after i.c.v. ANG II, while the high-dose losartan together wit

20 During the first day after i.c.v. administration, 1.25 micromol RTI-76 had no effec

21 by the cervical nodes was much greater after i.c.v. than after i.v. injection of I-gp120.

22 that the anxiolytic effect of NPS seen after i.c.v. or intra-PVN infusion requires responsive OXT neu

23 animals on significantly fewer trials after i.c.v. infusion of the 2 highest doses of M40, whereas t

24 less prolactin exposure was reinstated by an i.c.v. injection of prolactin.

25 inociception elicited by i.c.v. improgan and i.c.v. morphine.

26 ienced males, VNX does not impair mating and i.c.v.-GnRH suppresses Me activation.

27 Moreover, i.p. and i.c.v. administrations of SR11935, a brain-penetrant and

28 animals' responses to PGE2, i.c.v. I.p. and i.c.v. rmIL-1beta induced similar fevers in WT and COX-1

29 Only combined MOB stimulation and i.c.v.-GnRH produced a significant increase in Fos in th

30 alone had no effect on sucrose intake at any i.c.v. dose tested.

31 selective CRF(2) antagonist astressin(2)-B (i.c.v.), at a 20 : 1 antagonist: agonist ratio, blocked

32 a 20 : 1 antagonist: agonist ratio, blocked i.c.v. r/hCRF and rUcn 1 induced inhibition of gastric t

33 Both i.c.v. and systemic anti-Abeta antibodies reversed the b

34 Both i.c.v. infusion and repeated bolus injections into the c

35 (i.p., 10 mg/kg) or directly into the brain (i.c.v., 1.5 nmol/mouse), it decreased both food intake d

36 effects of oral diazoxide were abolished by i.c.v. administration of the K(ATP) channel blocker glib

37 Both pressor responses were abolished by i.c.v. pretreatment with indomethacin (200 micro g/5 mic

38 ng to the region of the SON are activated by i.c.v. carbachol and that these receptors are likely to

39 animals fell by 30-50%, which was blocked by i.c.v. injections of P57AS3.

40 e rapid suppression of food intake caused by i.c.v.-administered C75, a fatty acid synthase inhibitor

41 tely blocked the antinociception elicited by i.c.v. improgan and i.c.v. morphine.

42 hibit SIA, although analgesia was induced by i.c.v. administration of Hcrt-1.

43 n also increases c-Fos expression induced by i.c.v. amphetamine in several subcortical dopamine (DA)

44 nd pattern of cellular activation induced by i.c.v. amphetamine is altered by a regimen of food restr

45 activity in these areas than that induced by i.c.v. ANG II alone.

46 ificantly reduces the hypothermia induced by i.c.v. injection of 9 micro g OFQ/N (P<0.01).

47 ults suggest that the hypothermia induced by i.c.v. injection of a high dose of OFQ/N (9 or 18 micro

48 re OFQ/N) reduces the hypothermia induced by i.c.v. injection of OFQ/N at dose of 18 micro g (P>0.05)

49 , Fos-like immunoreactivity (FLI) induced by i.c.v. MK-801 was evaluated in an effort to identify res

50 st, the colonic motor stimulation induced by i.c.v. r/hCRF and rUcn 1 and 1h restraint stress were an

51 sent from the PVN and SON of rats treated by i.c.v. infusion of vehicle or either dose of lactate.

52 Central (i.c.v.) administration of 2 microl PRL-AB diluted up to

53 ism of antinociception induced by centrally (i.c.v.) administered U50,488 following peripheral admini

54 hen given into the lateral cerebroventricle (i.c.v.).

55 he first experiment, 3rd cerebroventricular (i.c.v.) administration of either 1 or 5 microl of NT-AS,

56 Rats were administered MPEP or CHPG i.c.v. beginning 15 or 135 min after induction of ischem

57 Chronic i.c.v. studies revealed that MDAN ligands whose spacer w

58 In Experiment 3, chronic i.c.v. leptin infusion in ad libitum fed rats decreased

59 Rats received chronic i.c.v. infusion of the orexigenic melanocortin receptor

60 Continuous i.c.v. microinfusion of rrTNF alpha exacerbates the hype

61 urotransmission is decreased upon continuous i.c.v. microinfusion of TNF.

62 In contrast, i.c.v. leptin increased basal and baroreflex control of

63 /- 5 g (ghrelin+CD) vs. 152 +/- 5 g (control i.c.v. saline+CD), P<0.001], but the combination of ghre

64 content of ATP in the hypothalami of control i.c.v. injected animals fell by 30-50%, which was blocke

65 Conversely, i.c.v. administration of exogenous adiponectin produces

66 ismatch oligodeoxynucleotides (2 microg/day, i.c.v.) for 3 consecutive days.

67 ore restricted neuronal population than does i.c.v. colchicine.

68 ion in the brain and that a single, low-dose i.c.v. injection of FGF19 dramatically improved glucose

69 Following i.c.v. administration, mod2B was widely distributed and

70 Twenty-one days following i.c.v. injection of 6-OHDA (200 microg) hypothalamus, ne

71 Immediately following i.c.v. alpha-MSH(1-13) administration, rats were exposed

72 lude that increases in NOS-II mRNA following i.c.v. administration of IL-1beta lead to increases in N

73 Fourth-i.c.v. urocortin administration (3 microg) produced subs

74 substantially greater than that after fourth-i.c.v. injection.

75 cular administration, suggesting that fourth-i.c.v. effects are mediated in part by stimulation of CR

76 ermia in adult rats; (2) OFQ/N (1.8 micro g, i.c.v., t=+30 s after morphine) can decrease morphine-in

77 es for feeding, both Hcrt-1 and Hcrt-2 given i.c.v. into conscious, unrestrained rats stimulated sign

78 e excitatory effects on startle of CRF given i.c.v. on Day 2.

79 by morphine given s.c. L-NAME, itself, given i.c.v. at a dose of 1 mg did not evoke any change in T(b

80 tassium (K-ATP) channels with glibenclamide (i.c.v.) abolished salvage only in the SHR rat.

81 nfused with the MC3/4R agonist MTII (10 ng/h i.c.v.) for 12 days, followed by 7 days at 50 ng/h.

82 ducing CAA and associated micro-hemorrhages, i.c.v.-targeted passive immunotherapy offers a promising

83 However, i.c.v. administration of alpha-MSH prevents only the ore

84 However, i.c.v. pretreatment with yohimbine (30 microg) had no ef

85 r in males and pro-oestrus females; however, i.c.v. leptin increased mean arterial pressure (MAP) onl

86 lsulfonylphenyl)-5-(4-pyridyl)-1H-imidazole (i.c.v.)] and found that it selectively blocked the condi

87 and 8.7+/-0.7 respectively vs. 0.3+/-0.3 in i.c.v. vehicle/no stress).

88 the CRF(2) agonist mouse (m) Ucn 2, injected i.c.v. inhibited gastric emptying and stimulated distal

89 F and stress similarly as NBI-27914 injected i.c.v. at 100 microg/rat.

90 None of the CRF antagonists injected i.c.v. alone influenced gut transit.

91 nist, NBI-27914 (50-100 microg/rat) injected i.c.v., abolished the colonic response to i.c.v. CRF and

92 n with galanin, 5 microg of MCH was injected i.c.v. with or without 10 microg of galanin.

93 ) in rats pre-labeled with [3H]myo-inositol (i.c.v. 24 h pre-treatment).

94 crog/rat) injected intracerebroventicularly (i.c.v.) or 1 h water avoidance stress stimulated defecat

95 Intracerebroventricular (i.c.v.) administration of AICAR rapidly lowers hypothala

96 Intracerebroventricular (i.c.v.) administration of both PrRP-20 and PrRP-31 (0.4

97 Intracerebroventricular (i.c.v.) administration of C75 to fasted mice rapidly (<

98 Intracerebroventricular (i.c.v.) administration of CDP-choline was made and blood

99 Intracerebroventricular (i.c.v.) administration of CGS-21680 (0.25 and 1.0 nmol)

100 Intracerebroventricular (i.c.v.) administration of prolactin also increased the p

101 Intracerebroventricular (i.c.v.) administration of the three active mGluR5 antago

102 Intracerebroventricular (i.c.v.) angiotensin (ANG) II causes a reliable pressor r

103 Intracerebroventricular (i.c.v.) IL-1ra (500 microgram in 5 microliter) significa

104 Intracerebroventricular (i.c.v.) injection of an adiponectin neutralizing antibod

105 Intracerebroventricular (i.c.v.) injection of NPB in mice induces hyperphagia dur

106 Intracerebroventricular (i.c.v.) injection of Rcho-1 into hysterectomized rats wa

107 Intracerebroventricular (i.c.v.) injections of the purified P57AS3 demonstrated t

108 Intracerebroventricular (i.c.v.)-GnRH restores mating in sexually naive VNX males

109 In Experiment 1, intracerebroventricular (i.c.v.) infusion of leptin (0.5 microg/0.5 microl/hr for

110 intake after acute intracerebroventricular (i.c.v.) of L-NAME was also measured.

111 In addition, intracerebroventricular (i.c.v.) NPS evoked a significant somatodendritic release

112 P-1) peptides after intracerebroventricular (i.c.v.) administration in the rat.

113 tinociception after intracerebroventricular (i.c.v.) administration, but the mechanism of action of t

114 and/or 7 days after intracerebroventricular (i.c.v.) AF64A administration.

115 were recorded after intracerebroventricular (i.c.v.) challenge with recombinant murine (rm) IL-6 (10

116 in rat brain after intracerebroventricular (i.c.v.) injection of a newly developed selective sst(2)

117 4, 6 and 24 h after intracerebroventricular (i.c.v.) injection of interleukin-1beta (IL-1beta) or veh

118 120 (I-gp120) after intracerebroventricular (i.c.v.) injection.

119 ei of rats given an intracerebroventricular (i.c.v.) infusion of morphine over 5 days, which is known

120 cular catheters and intracerebroventricular (i.c.v.) cannula.

121 pertonic saline and intracerebroventricular (i.c.v.) injection of Ang-II increased Fos-IR in both spo

122 rathecal (i.t.) and intracerebroventricular (i.c.v.) injection of HE in a rat model of neuropathic sp

123 nt mice to i.p. and intracerebroventricular (i.c.v.) injections of recombinant murine (rm) interleuki

124 Both intracerebroventricular (i.c.v.) IL-1beta and exposure to inescapable tail shock

125 ed and evaluated by intracerebroventricular (i.c.v.) administration in the tail-flick test in mice.

126 effects elicited by intracerebroventricular (i.c.v.) administration of clonidine result from stimulat

127 crodialysis, and by intracerebroventricular (i.c.v.) administration of GRP to audiogenic seizure-pron

128 or cells induced by intracerebroventricular (i.c.v.) administration of IL-1beta (20 ng).

129 e synthase (NOS) by intracerebroventricular (i.c.v.) administration of NG-nitro-l-arginine methyl est

130 old greater than by intracerebroventricular (i.c.v.) administration.

131 effects induced by intracerebroventricular (i.c.v.) carbachol injections.

132 pression induced by intracerebroventricular (i.c.v.) infusion of angiotensin II (Ang II).

133 saline, followed by intracerebroventricular (i.c.v.) infusion of IFN-alpha (1000 IU in 5 microl) or v

134 rphine dependent by intracerebroventricular (i.c.v.) infusion of the opioid at increasing doses over

135 Central intracerebroventricular (i.c.v.) administration of an insulin mimetic resulted in

136 (-1)) by continuous intracerebroventricular (i.c.v.) infusion through pre-implanted cannula connected

137 Continuous intracerebroventricular (i.c.v.) microinfusion of TNF-antibodies (Abs) starting a

138 stress by examining intracerebroventricular (i.c.v.) administration of mUcn 3 in animal models of act

139 Following intracerebroventricular (i.c.v.) administration of GALC we noted a significant, 1

140 risoria) following intracerebroventricular (i.c.v.) injection of various melanocortin receptor agoni

141 (i.v.) but not for intracerebroventricular (i.c.v.) activity.

142 contrast to leptin, intracerebroventricular (i.c.v.) administration of ADP decreased body weight main

143 antagonist (10 mug, intracerebroventricular (i.c.v.), 24 and 48 h after the stressor) prevented the d

144 se of the effect of intracerebroventricular (i.c.v.) administration of 5 microg MCH on food intake wa

145 gated the effect of intracerebroventricular (i.c.v.) administration of L-NAME on the hyperthermia ind

146 ying the effects of intracerebroventricular (i.c.v.) administration of WAY100635 (1-100 microg), a se

147 sted the effects of intracerebroventricular (i.c.v.) injection of alpha-MSH on lipopolysaccharide (LP

148 ined the effects of intracerebroventricular (i.c.v.) injections of endomorphin-1 (EM-1) and endomorph

149 and tolerability of intracerebroventricular (i.c.v.) rhPDGF-BB administration in individuals with PD.

150 eritoneal (i.p.) or intracerebroventricular (i.c.v.) administration of SR-3306, a brain-penetrant and

151 factors, we perform intracerebroventricular (i.c.v.) injections of recombinant FGF1 or FGF19 in an aw

152 ffects of prolonged intracerebroventricular (i.c.v.) versus systemic delivery of anti-Abeta antibodie

153 Adult rats received intracerebroventricular (i.c.v.) administration of either phosphate buffer (PBS)

154 tela furo) received intracerebroventricular (i.c.v.) infusions of 4 doses of the galanin receptor ant

155 parenteral routes [intracerebroventricular (i.c.v.), intrathecal, and subcutaneous].

156 y demonstrated that intracerebroventricular (i.c.v.) administration of protein kinase C (PKC) or prot

157 ously reported that intracerebroventricular (i.c.v.) injection of either a PKC or PKA inhibitor compl

158 es demonstrate that intracerebroventricular (i.c.v.) injections of the non-N-methyl-d-aspartate (NMDA

159 Here, we show that intracerebroventricular (i.c.v.) leptin increases lumbar (LSNA) and renal (RSNA)

160 Their response to intracerebroventricular (i.c.v.) administration of NPY and related peptides is ei

161 nvestigated whether intracerebroventricular (i.c.v.) infusion of this monocarboxylate fuel attenuates

162 were implanted with intracerebroventricular (i.c.v.) and i.v. cannulae.

163 atum, together with intracerebroventricular (i.c.v.) injection of hrIL-1beta, produced a similar rise

164 eptor blockade with intracerebroventricular (i.c.v.) kynurenate eliminated PND and the response of RT

165 nistered centrally (intracerebroventricular, i.c.v.) or systemically (subcutaneously and orally).

166 central (0.3-3 nmol intracerebroventricular, i.c.v.) administration of this peptide dose-dependently

167 are administered intracerebroventricularly (i.c.v.) as well as systemically, it would seem to reflec

168 when administered intracerebroventricularly (i.c.v.) or when overexpressed in transgenic mice.

169 ase, administered intracerebroventricularly (i.c.v.) to awake and freely moving rats increased mean a

170 when administered intracerebroventricularly (i.c.v.).

171 was administered intracerebroventricularly (i.c.v.).

172 was administered intracerebroventricularly (i.c.v.; 100 microg) to determine whether results obtaine

173 (aCSF)) injected intracerebroventricularly (i.c.v.) increased already enhanced levels of oxytocin, b

174 peptides injected intracerebroventricularly (i.c.v.) on gastric and colonic motility, and the CRF rec

175 ats were injected intracerebroventricularly (i.c.v.) with 0.2 or 0.4 microg of kainic acid following

176 r cellular dehydration and intraventricular (i.c.v.) colchicine injections.

177 g and locomotor effects of intraventricular (i.c.v.) MK-801 are potentiated by chronic food restricti

178 nt tested whether repeated intraventricular (i.c.v.) infusion of AVP would lead to an increase in the

179 ed drug infusion pump and an investigational i.c.v. catheter.

180 Losartan at 0.5 mg/kg (i.c.v.) abolished central ANG II-induced pressor respons

181 High-dose losartan (5 mg/kg, i.c.v.) showed a potentiation of the pressor response to

182 ormal C57black6 mice (n = 3 each, 40 mug/kg, i.c.v.); we found retention of Ran-SPION-rIgP/cIgY-MAP2

183 nt with indomethacin (200 micro g/5 micro l, i.c.v.), an inhibitor of cyclo-oxygenase, showing that t

184 antagonist, PD 145065 (48 micro g/2 micro l, i.c.v.).

185 body weight loss measured 24 h after lateral-i.c.v. injection was substantially greater than that aft

186 itude and duration from responses to lateral-i.c.v. delivery.

187 Unlike leptin, i.c.v. insulin infusion increased basal and baroreflex c

188 ition in which GnRH does not enhance mating, i.c.v.-GnRH combined with MOB stimulation suppressed Fos

189 nce paradigm we found that galanin (1 microg i.c.v.) alone does not possess reinforcing or aversive p

190 Specifically, oxytocin (1 microg i.c.v.) given before ethanol (1.5 g/kg i.p.) attenuated

191 NNC 26-9100 treatment (0.2 microg i.c.v. in 2 microL) improved learning, which was blocked

192 nally, the effects of galanin (10, 20 microg i.c.v.) on delayed match-to-position (DMTP) performance

193 amined the effects of galanin (10, 20 microg i.c.v.) on the performance of a simple operant response

194 oked at the effects of galanin (5, 20 microg i.c.v.) on the performance of non-delayed match-to-posit

195 ppression of LH pulses induced by 1.5 microg i.c.v. CGRP and significantly attenuated the suppression

196 imals treated 90 min earlier with 1.5 microg i.c.v. CGRP.

197 f pulsatile LH secretion induced by 5 microg i.c.v. CGRP.

198 , nor-binaltorphimine (Nor-BNI; 20.0 microg, i.c.v.) reproduced the effect of naltrexone in BSTLD and

199 RF receptor agonist urocortin (0-5.0 microg, i.c.v.), and the CRF receptor antagonist [D-Phe(12), Nle

200 e selective mu antagonist, CTAP (2.0 microg, i.c.v.), reproduced the effect of naltrexone in NACshell

201 e CRF receptor agonist h/rCRF (0-5.0 microg, i.c.v.), the CRF receptor agonist urocortin (0-5.0 micro

202 ptor antagonist d-PheCRF(12-41) (3.0 microg, i.c.v.).

203 pha) MeLeu(37)] h/rCRF(12-41) (0-5.0 microg, i.c.v.).

204 ndently blocked the effect of CRF (1 microg, i.c.v.) on startle at doses that had no effect on baseli

205 Treatment with alpha-MSH (1 microg, i.c.v.) suppressed LPS-induced increases in core body te

206 antagonist, alpha-helical CRF9-41 (1 microg, i.c.v.), on the test day, prior to exposure to cocaine-a

207 ected with mUcn 3 (0, 0.1, 1.0 or 10 microg, i.c.v.) 10 min prior to testing and activity was monitor

208 ected with mUcn 3 (0, 0.1, 1.0 or 10 microg, i.c.v.) 10 min prior to testing and examined in the elev

209 peptide, beta-endorphin (betaEND, 10 microg, i.c.v.) was significantly and dose-dependently reduced b

210 itory effect of WAY100635 (10 or 100 microg, i.c.v.) in only two of six rats.

211 The AS ODN probes (25 microg, i.c.v.) were administered once 24 h prior to morphine (5

212 BQ123 (3 microg, i.c.v.) and BMS182874 (50 microg, i.c.v.) significantly

213 ntricular administration of CRF (0.3 microg, i.c.v.) blocked the decrease in extracellular 5-HT in bo

214 tment with a single dose of BQ123 (3 microg, i.c.v.) reversed tolerance to morphine antinociception i

215 HT in the lateral septum by CRF (0.3 microg, i.c.v.) was blocked by pretreatment with the CRF recepto

216 onized clonidine antinociception (40 microg, i.c.v.), supraspinal alpha(2) receptors seem to mediate

217 ral cell adhesion molecule (NCAM) (5 microg, i.c.v.) into the lateral ventricle of rats and tested th

218 tered once 24 h prior to morphine (5 microg, i.c.v.) or M6G (250 ng) and spontaneous free feeding was

219 (3 microg, i.c.v.) and BMS182874 (50 microg, i.c.v.) significantly enhanced antinociceptive effect of

220 ective opioid antagonist nor-BNI (60 microg, i.c.v.), despite the inability of ppOFQ/N(160-187) to co

221 blocked improgan antinociception (80 microg, i.c.v.), suggesting a mediator role for alpha(2) recepto

222 In contrast, nicotine (3-30 microgram i.c.v.) produced increases in hotplate latency in both s

223 SR48692 (2.5 microgram, i.c.v.) inhibited acid secretion, suggesting that SR4869

224 b]pyridine (CP 93,129) (3 and 10 micrograms, i.c.v.) each dose-dependently reduced the self-administr

225 ptor antagonist nor-BNI (1 micro g/5 microl, i.c.v., t=-30 s before OFQ/N) reduces the hypothermia in

226 of [3H]IP at 0.3 to 3 micromol/8 microliter i.c.v. with lower doses resulting in less efficacious or

227 s toxin treatment (1 microgram/5 microliter, i.c.v.; 48 hr before the 8-OH-DPAT challenge) did not in

228 tely 300-fold greater potency than morphine (i.c.v.).

229 ist, beta-funaltrexamine (betaFNA: 2-20 mug, i.c.v.), significantly and dose-dependently reduced feed

230 In the NY1DD mice, naloxone (i.c.v.) possessed approximately 300-fold greater potency

231 We microinjected either FGF2 (200 ng, i.c.v.) or the FG loop (FGL) of neural cell adhesion mol

232 either intracerebroventricularly (30-300 ng, i.c.v.) or directly into the LC (intra-LC; 2-20 ng) were

233 f a pressor dose of angiotensin II (0.1 nmol i.c.v.); however, the magnitude of blood pressure elevat

234 However, 10 nmol (i.c.v.) (S)-3.4-DCPG did reverse amphetamine-induced hyp

235 In vivo, exogenous N/OFQ (0.03-1 nmol, i.c.v.) or a synthetic N/OFQ receptor agonist given syst

236 r agonist, melanotan-II (MTII: 0.01-10 nmol, i.c.v.).

237 by intracerebroventricular (ED(50)>100 nmol, i.c.v.) or intraplantar (ED(50)>500 nmol) routes suggest

238 ethyl ester hydrochloride (RTI-76; 100 nmol, i.c.v.), an irreversible inhibitor of the DA transporter

239 ethyl ester hydrochloride (RTI-76; 100 nmol, i.c.v.), to assess whether the inhibitory mechanism of c

240 analgesic activity supraspinally (3.4 nmol, i.c.v.) and spinally (4.3 nmol, i.t.).

241 3/4 receptor antagonist, SHU-9119 (0.5 nmol, i.c.v.), especially at those intake periods (24-48 h) wh

242 GNTI (0.032-0.32 nmol; i.c.v.), administered 15 min prior to food access, reduc

243 The dose of i.c.v. renin that induced expression of immediate early

244 test showed that the antidiabetic effect of i.c.v. FGF19 was solely due to increased GE and not to c

245 rapid (< or = 2 h) and reciprocal effects of i.c.v. C75 on the expression of hypothalamic orexigenic

246 eported experiments evaluated the effects of i.c.v. gp120 administration and subsequent IL-1beta acti

247 ata suggesting that the divergent effects of i.c.v.-delivered anti-Abeta antibodies result from gradu

248 ive was to assess safety and tolerability of i.c.v.-delivered rhPDGF-BB.

249 (P>0.05); (4) 60 micro g/5 microl AS oligo (i.c.v. treatment on days 1, 3 and 5) against OFQ/N recep

250 In addition, SIB-1663 (s.c. or i.c.v.) attenuated antinociceptive activity NIC given by

251 Intravenous or i.c.v. pretreatment with yohimbine, the alpha2-adrenocep

252 IL-18 i.p. or i.c.v. is not pyrogenic.

253 her administered intraperitoneally (i.p.) or i.c.v. in WT mice; COX gene-ablated mice, therefore, wer

254 Here, we demonstrate that i.v. or i.c.v. injection of aNSCs engineered to secrete IL-10 (I

255 tibodies that aggravated vascular pathology, i.c.v.-infused antibodies globally reduced CAA and assoc

256 , Toxin i.c.v.+physostigmine i.v. (n=6), PBS i.c.v.+saline i.v. (n=6) and PBS i.c.v. +physostigmine i

257 (n=6), PBS i.c.v.+saline i.v. (n=6) and PBS i.c.v. +physostigmine i.v. (n=6).

258 integrity of the animals' responses to PGE2, i.c.v. I.p. and i.c.v. rmIL-1beta induced similar fevers

259 ti-SVG-30, 0-20 microg, 20-min pretreatment, i.c.v.), a potent CRF(2) peptide antagonist, and tested

260 Moreover, prior i.c.v. administration of an acetyl-CoA carboxylase inhib

261 Prolonged i.c.v. infusions of anti-Abeta antibodies dose-dependent

262 hyperthermia caused by DAMGO (1 micro g/rat, i.c.v.), a selective mu agonist, confirming that NMDA re

263 -R1/R2 antagonist, astressin (10 microg/rat, i.c.v.) inhibited the colonic motor response to i.c.v. C

264 attenuated by leptin (2 or 4 microgram/rat, i.c.v.; two infusions, given 21 hr and 20-30 min before

265 In alert rats, i.c.v. injection of nociceptin caused a significant decr

266 These results indicate that even a single i.c.v. administration of the recombinant enzyme can have

267 Most importantly, animals receiving a single i.c.v. dose of the enzyme at postnatal day 20 survived u

268 st, pretreatment with 2.5 microgram SR48692, i.c.v., did not block neurotensin-induced inhibition of

269 A sublethal i.c.v. dose of quisqualate caused episodes of prolonged

270 morphine at spinal (i.th.) and supraspinal (i.c.v.) sites to the same rat produces antinociceptive s

271 At all doses tested, i.c.v. administration of rhPDGF-BB was well tolerated.

272 Considering that i.c.v. leptin may not diffuse into deep brain regions wh

273 We also demonstrated that i.c.v. administration of the phosphatase inhibitor okada

274 These results indicate that i.c.v. losartan at a high and a low dose has strikingly

275 s agent in individuals with PD and show that i.c.v. administration of PDGF-BB is safe and well tolera

276 We show that i.c.v. injection of FGF19 or FGF1 leads to a approximate

277 The current study shows that i.c.v. administration of the PKC inhibitors bisindolylma

278 The i.c.v. administration of CRH significantly increased NGF

279 The i.c.v. administration of GLP-1 completely prevents the o

280 f glucose administered and is blocked by the i.c.v. administration of an inhibitor of glucose metabol

281 slice punches removed at 24 h following the i.c.v. injections.

282 The present study investigated the i.c.v. carbachol-induced activity of the soma of LT proj

283 Results showed that the i.c.v. administration of FIVgp120 (5 ng/10 microliter) p

284 inal tolerance (3-fold) was observed via the i.c.v. route.

285 gnificantly reduced by pretreatment with the i.c.v. muscarinic antagonist, atropine.

286 ed a potentiation of the pressor response to i.c.v. ANG II, accompanied by bradycardia.

287 ed i.c.v., abolished the colonic response to i.c.v. CRF and dose-dependently reduced that induced by

288 .v.) inhibited the colonic motor response to i.c.v. CRF and stress similarly as NBI-27914 injected i.

289 here were no differences in the responses to i.c.v. PGE2 among the WT and COX knockout mice.

290 Lep(ob/ob) mice were especially sensitive to i.c.v. and systemic ADP, which resulted in increased the

291 imals: Toxin i.c.v.+saline i.v. (n=9), Toxin i.c.v.+physostigmine i.v. (n=6), PBS i.c.v.+saline i.v.

292 methodology in four groups of animals: Toxin i.c.v.+saline i.v. (n=9), Toxin i.c.v.+physostigmine i.v

293 o morphine antinociception, mice pre-treated i.c.v. with the PKC inhibitors bisindolylmaleimide I, Go

294 put to the amygdala in naive-VNX males using i.c.v.-GnRH and pharmacological stimulation (bicuculline

295 njected into the lateral cerebral ventricle (i.c.v.).

296 In addition, third ventricle (i.c.v.) administration of P57, which reduces subsequent

297 Fourth ventricular (i.c.v.) administration of ondansetron (10.0 microg/3.0 m

298 he expression of conditioned defeat, whereas i.c.v. injections of D-Phe CRF(12-41) successfully reduc

299 GRP-induced suppression of LH pulses, whilst i.c.v. co-administration of CGRP (1.5 microg) with the d

300 og of IL-1beta, alone or in combination with i.c.v. administration of GABA-A and GABA-B receptor anta