ライフサイエンスコーパス: isoflurane

1 eling using photoactivatable isoflurane (azi-isoflurane).

2 activity and general anesthetic state under isoflurane.

3 e commonly used volatile general anesthetic, isoflurane.

4 intain incubation and allow anesthesia using isoflurane.

5 of equianesthetic doses of pentobarbital or isoflurane.

6 hage-vehicle, and subarachnoid hemorrhage+2% isoflurane.

7 -sleep-active VLPO neurons are unaffected by isoflurane.

8 the magnitude of this cell death response to isoflurane.

9 in age from P14 to P206 were sedated with 1% isoflurane.

10 ted hemi-parkinsonian rats anesthetized with isoflurane.

11 esence and absence of the general anesthetic isoflurane.

12 e are 10 and 25 times, respectively, that of isoflurane.

13 to hyperpolarizing effects of halothane and isoflurane.

14 has been shown previously to be inhibited by isoflurane.

15 seleit solution, with or without propofol or isoflurane.

16 so required for activation by chloroform and isoflurane.

17 : after 1 hr of propofol discontinuation and isoflurane 0.8%; step 3: after 1 hr of propofol at the s

18 orce from low doses (propofol, 27 +/- 6 muM; isoflurane, 1.0 +/- 0.1%) to moderate doses (propofol, 8

19 order efficacy: halothane (207% [202-212]) > isoflurane (169% [161-176]) > sevoflurane (164% [150-177

20 ) to moderate doses (propofol, 87 +/- 4 muM; isoflurane, 3.0 +/- 0.25%), without significant alterati

21 at had training sessions and were exposed to isoflurane 30 min later had freezing behavior similar to

22 Isoflurane (300 mum) significantly inhibited, while fent

23 ng combinations: Isoflurane (5%)+O(2) (95%); Isoflurane (5%)+N(2)O (75%)+O(2) (25%) and N(2)O (75%)+O

24 er protocol with the following combinations: Isoflurane (5%)+O(2) (95%); Isoflurane (5%)+N(2)O (75%)+

25 rats were randomly assigned to receive 1.8% isoflurane/70% nitrous oxide (N(2)O) anesthesia for 4h o

26 Isoflurane, a volatile anesthetic agent, has been recogn

27 dies show that general anesthetics including isoflurane activate VLPO neurons, and may contribute to

28 Whole cell recordings revealed that the isoflurane-activated background potassium current observ

29 ngle-cell multiplex RT-PCR conducted on both isoflurane-activated, putative sleep-promoting VLPO neur

30 -159, and similar results were observed with isoflurane activation of wild-type TASK-3.

31 Moreover, isoflurane affected neuronal plasticity by facilitating

32 d when paraoxon-treated rats were exposed to isoflurane after SE.

33 ated structural and dynamical modulations by isoflurane aid in the understanding of the underlying me

34 Isoflurane also entered the channel after the pore was d

35 Isoflurane also impaired the cognitive functions of 10-w

36 Isoflurane also increased firing rate of RTN chemosensit

37 Isoflurane also induced autophagy in mouse in vivo as sh

38 tter understanding of the mechanism by which isoflurane alters protein function requires the detailed

39 anti-epileptogenic interventions were used; isoflurane anaesthesia and losartan.

40 Early treatments with either isoflurane anaesthesia or losartan prevented early micro

41 emale animals and appeared to be enhanced by isoflurane anaesthesia.

42 in clearance and changes in plasma volume in isoflurane-anaesthetized mice (C57BL/6J) pre-treated wit

43 re also calculated, and shown to be 3 mM for isoflurane and 10 muM for propofol; both anesthetics hav

44 Rats were anesthetized with 1.5% isoflurane and 95% oxygen.

45 e therefore set out to assess the effects of isoflurane and desflurane on mitochondrial function, cyt

46 hways are critical in the TCR, and ketamine, isoflurane and fentanyl differentially alter the synapti

47 amines the mechanisms of action of ketamine, isoflurane and fentanyl on the synaptic TCR responses in

48 r antecedent neuronal activity, we show that isoflurane and halothane increase the number of active n

49 rectly depolarized by the general anesthetic isoflurane and hyperpolarized by norepinephrine, a wake-

50 would be augmented when preconditioning with isoflurane and hypoxic preconditioning are combined.

51 In primary mouse cortical neurons, both isoflurane and hypoxic preconditioning induced autophagy

52 Isoflurane and hypoxic preconditioning protected against

53 plore the role of SPK2-mediated autophagy in isoflurane and hypoxic preconditioning.

54 rysanthemi, can be functionally inhibited by isoflurane and other anesthetics.

55 These results indicate that isoflurane and propofol anesthesia affect postnatal hipp

56 Isoflurane and propofol anesthesia altered postnatal hip

57 Isoflurane and propofol are known to depress cardiac con

58 urthermore, molecular modeling predicts that isoflurane and propofol bind to this pocket by forming H

59 block inhibition by the general anesthetics isoflurane and propofol of the prokaryotic pentameric ch

60 s hypothesis, we investigated the effects of isoflurane and propofol on new cell proliferation and co

61 Affinities of isoflurane and propofol to the allosteric site are also

62 both single and double occupancy binding of isoflurane and propofol to the GLIC pore.

63 Met-956 selectively abolishes activation by isoflurane and propofol without affecting actions of A-9

64 ction and uncovered the molecular targets of isoflurane and propofol.

65 Volatile anaesthetics such as halothane, isoflurane and sevoflurane inhibit membrane currents con

66 59W, V136E, and L122D were resistant to both isoflurane and TCE activation.

67 Isoflurane and TCE likely share commonalities in their m

68 ether we induced anesthesia with urethane or isoflurane and whether awake mice were stationary or run

69 on using an anesthetic conserving device and isoflurane, and 322 received standard IV sedation.

70 eterologous expression systems, sevoflurane, isoflurane, and desflurane at subsurgical concentrations

71 er anesthetic for AD patients as compared to isoflurane, and elucidate the potential mitochondria-ass

72 We also showed that the general anesthetic isoflurane, and to a lesser extent propofol, reverses TX

73 , insulin and glucose (6 mU/g, 1 mg/g) under isoflurane, and under ketamine-xylazine anesthesia to su

74 nder isoflurane, ketamine/xylazine, ketamine/isoflurane, and urethane anesthesia demonstrated that th

75 anesthetic combinations (ketamine/xylazine, isoflurane, and urethane) markedly suppressed calcium tr

76 to determine the effects of laparotomy under isoflurane anesthesia (Anesthesia/Surgery) on these beha

77 rhesus macaques were exposed for 5 hours to isoflurane anesthesia according to current clinical stan

78 measure baseline sleep loss and responses to isoflurane anesthesia at 1% and 2%.

79 the hippocampus after a clinically relevant isoflurane anesthesia exposure conducted at an early pos

80 A brief burst-suppressing isoflurane anesthesia has been shown to rapidly alleviat

81 trained state and demonstrate the effects of isoflurane anesthesia on radiotracer uptake.

82 Isoflurane anesthesia produced learning impairment in ag

83 We show that a single isoflurane anesthesia produces antidepressant-like behav

84 Optical imaging experiments in mice under isoflurane anesthesia showed that both cortical spreadin

85 Sprague-Dawley rats under isoflurane anesthesia were exposed to a series of 3 sub-

86 Awake tissue Po2 is about half that under isoflurane anesthesia, and within the cortex, vascular a

87 Under isoflurane anesthesia, the mice were subjected to intest

88 In resting newborn piglets (n=6) on isoflurane anesthesia, we measured a median total cerebr

89 Five rhesus macaques were tested under isoflurane anesthesia.

90 f age and C57BL/6 age-matched controls under isoflurane anesthesia.

91 VLPO neurons themselves is not required for isoflurane anesthesia.

92 2), after sino-aortic denervation, or during isoflurane anesthesia.

93 raphy (EEG) activation under continuous deep isoflurane anesthesia.

94 o accelerated behavioral emergence from deep isoflurane anesthesia; this was prevented with beta or a

95 fentanyl-fluanisone/midazolam) and volatile (isoflurane) anesthetics in mice.

96 Isoflurane anesthetized and intubated pigs were randomiz

97 hysiologically defined slow calcium waves in isoflurane anesthetized rats.

98 yomicrospectrophotometry) were determined in isoflurane anesthetized rats.

99 rophenol (DNP) were compared using 16.4 T in isoflurane anesthetized wild type (WT) and HD mice at 9

100 re scanned under the awake (n = 6 scans) and isoflurane-anesthetized (n = 4 scans) conditions.

101 Isoflurane-anesthetized adult male wild-type C57B/6 or a

102 Dynamic PET was performed for 60 min on 23 isoflurane-anesthetized male C57BL/6 mice after intraven

103 In isoflurane-anesthetized male rats, trigeminal ganglia we

104 lly microinjected into the DMH/PeF region of isoflurane-anesthetized male Sprague-Dawley rats (n = 19

105 binding potential (BPND) would be higher in isoflurane-anesthetized monkeys.

106 mins of untreated ventricular fibrillation, isoflurane-anesthetized pigs received 5 mins of either s

107 In protocol A, 24 isoflurane-anesthetized pigs underwent 15 mins of untrea

108 the ventro-postero-lateral (VPL) nucleus in isoflurane-anesthetized rats.

109 ses of carrier (R)-rolipram in conscious and isoflurane-anesthetized rats.

110 Preclinical PET studies were performed with isoflurane-anesthetized rats.

111 blood sampling were obtained for 4 groups of isoflurane-anesthetized Wistar rats: controls (n = 7); p

112 ects on leak channels; a similar anesthetic, isoflurane, appears to work a different way.

113 the observation that the synaptic targets of isoflurane are located in local cortical circuits rather

114 esponses and encourage further evaluation of isoflurane as a rapid-acting antidepressant devoid of th

115 opofol, barbiturates, and the volatile agent isoflurane, at low millimolar concentrations, but not by

116 At 24 hrs, isoflurane attenuated neuronal cell death in the cortex,

117 teins with meta-Azi-propofol (AziPm) and Azi-isoflurane (Azi-iso) and molecular docking were also use

118 obed by photolabeling using photoactivatable isoflurane (azi-isoflurane).

119 tudies prove that the neurons depolarized by isoflurane belong to the subpopulation of VLPO neurons r

120 onsistent with their functional responses to isoflurane, beta2 but not alpha7 showed pronounced dynam

121 Isoflurane binding introduced strong anticorrelated moti

122 The isoflurane binding site in the I domain involves an arra

123 Mutagenesis of the alpha'1 helix showed that isoflurane binding sites at the betaI domain were signif

124 studies suggested the existence of multiple isoflurane binding sites in NaV, but experimental bindin

125 An extensive search for isoflurane binding sites in the nicotinic acetylcholine

126 Isoflurane binding sites on the full ectodomain LFA-1 we

127 Two isoflurane binding sites were identified using photolabe

128 Point mutations were introduced around isoflurane binding sites.

129 osteric to the ICAM-1 binding site, and that isoflurane binding stabilizes LFA-1 in the closed confor

130 (19)F probes in NMR experiments to quantify isoflurane binding to the bacterial voltage-gated sodium

131 olecular dynamics simulations suggested that isoflurane binding was more stable in the resting than i

132 the extracellular entrance was observed upon isoflurane binding.

133 Isoflurane-binding sites in beta2 and alpha7 were found

134 modulate etomidate binding to the GABA(A)R: isoflurane binds directly to the site with millimolar af

135 Specifically, isoflurane binds persistently to three classes of sites

136 We discovered that isoflurane binds to an allosteric cavity previously impl

137 This study suggested that isoflurane binds to both the alphaI and betaI domains al

138 (iii) Isoflurane binds to the subunit centers of both nAChR al

139 Isoflurane bound to several locations within GLIC, inclu

140 An orientation preference was observed for isoflurane bound to T189 and S208, but not to S129 and L

141 The inhalation anesthetic isoflurane, but not desflurane, has been shown to induce

142 Here we show that isoflurane, but not desflurane, induces opening of mitoc

143 animals to the general anesthetic effects of isoflurane, but that the sedation produced by VLPO neuro

144 Isoflurane can impair cognitive functions of animals und

145 We, therefore, set out to assess whether isoflurane can induce apoptosis by regulating Bcl-2 fami

146 Furthermore, we find that isoflurane causes a sustained increase in activity in th

147 e have also observed (unpublished data) that isoflurane causes apoptosis of cellular profiles in the

148 Here, we show that isoflurane causes robust activation of CO(2)/pH-sensitiv

149 ues in the S5, S6, and the first pore helix; isoflurane competitively disrupts A-967079 antagonism, a

150 Surprisingly, isoflurane completely inhibited the amplitude of eIPSCs

151 Isoflurane concentrations that anesthetize only Ndufs4(K

152 20-month-old) rats prior to a 3h exposure to isoflurane, control, propofol, or 10% intralipid.

153 store righting or produce EEG changes during isoflurane CSSGA in 5/5 mice.

154 Thus, propofol and isoflurane decrease force development by directly depres

155 ntact and skinned preparations, propofol and isoflurane depressed maximum Ca(2+)-activated force and

156 In contrast, several volatile (isoflurane, desflurane) and i.v. (propofol) general anes

157 opofol, ketamine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic drugs (topiramate

158 n-response of TASK-3 to several anesthetics (isoflurane, desflurane, sevoflurane, halothane, alpha-ch

159 he VLPO of a mouse lightly anesthetized with isoflurane, dexmedetomidine increased behavioral arousal

160 However, isoflurane did not affect the cognitive functions of IL-

161 es in the nAChR transmembrane domain: (i) An isoflurane dimer occludes the pore, contacting residues

162 Brains exposed to isoflurane displayed significant apoptosis in both the w

163 Isoflurane disrupted the quaternary structure of GLIC, a

164 We conclude that isoflurane disrupts the development of hippocampal neuro

165 Both propofol and isoflurane dose dependently depressed force from low dos

166 ence time (r=0.54); an interaction-effect of isoflurane dose was observed (burst-suppression ratio: p

167 This isoflurane effect was attenuated by lidocaine, a local a

168 IL-1beta may play an important role in this isoflurane effect.

169 We measured isoflurane effects on time to loss of righting reflex, o

170 Isoflurane-exposed rats had reduced freezing behavior du

171 Isoflurane exposure after IRI led to significant attenua

172 Finally, isoflurane exposure led to increased TGF-beta1 levels in

173 ial learning and memory that are impaired by isoflurane exposure.

174 with non-injurious hypoxia or the anesthetic isoflurane express different genes but are equally prote

175 xia (95% N(2), 5% CO(2) for 15 min, HPC), 1% isoflurane for 15 min (APC) or their combination (CPC) f

176 ated by exposing the neuronal cultures to 2% isoflurane for 1h at various times after the onset of th

177 10-week old mice were exposed to 1.2 or 1.4% isoflurane for 2 h.

178 hippocampal neuronal cultures exposed to 2% isoflurane for 30min at 24h before a 1h oxygen-glucose d

179 posure of the infant rhesus macaque brain to isoflurane for 5 hours is sufficient to cause widespread

180 xposure of 6-day-old (P6) rhesus macaques to isoflurane for 5 hours triggers a robust neuroapoptosis

181 ow for the first time that treatment with 2% isoflurane for 6 h can increase pro-apoptotic factor Bax

182 smission alone can affect the emergence from isoflurane general anesthesia.

183 We aimed to determine whether isoflurane, given after intestinal ischemia, protects ag

184 The common inhalation anesthetic isoflurane has been shown to induce apoptosis, which the

185 Volatile anesthetics, including isoflurane, have anti-inflammatory effects.

186 We conclude that combined isoflurane-hypoxia preconditioning augments neuroprotect

187 Our studies showed that isoflurane impaired the cognitive functions of the rats

188 Our results suggest that isoflurane impairs the learning but may not affect the r

189 strong decreases in the source entropy under isoflurane in area V1 and the prefrontal cortex (PFC)-as

190 tials in two ferrets after administration of isoflurane in concentrations of 0.0%, 0.5%, and 1.0%.

191 ble to inhibition by the volatile anesthetic isoflurane in electrophysiology measurements.

192 atory neurotransmission is hypersensitive to isoflurane in Ndufs4(KO) mice due to the inhibition of p

193 ation with propofol and during sedation with isoflurane in patients with severe subarachnoid hemorrha

194 reversed the VLPO depolarization induced by isoflurane in slices in vitro.

195 Structures of ELIC co-crystallized with isoflurane in the absence or presence of an agonist reve

196 side are disconnected, we observe binding of isoflurane in the central cavity.

197 We also found that isoflurane increased activity of the parvalbumin interne

198 Both propofol and isoflurane increased autophagy induction (P < 0.05) in a

199 Isoflurane increased the expression of interleukin 1beta

200 Isoflurane increases regional cerebral blood flow in com

201 sitive RTN neurons was strongly increased by isoflurane, independent of prevailing pH conditions.

202 Volatile anesthetics (VAs), such as isoflurane, induce a general anesthetic state by binding

203 Nitrous oxide together with isoflurane induced a statistically significant decrease

204 ("shaker") channels: reduced sensitivity to isoflurane-induced anesthesia.

205 Isoflurane-induced autophagy in mice lacking the SPK1 is

206 ced autophagy, and SPK2 inhibitors abolished isoflurane-induced disruption of the Beclin 1/Bcl-2 asso

207 VLPO neurons produces an acute resistance to isoflurane-induced hypnosis.

208 eased the paired-pulse ratio, and attenuated isoflurane-induced inhibition of eIPSCs.

209 ine A, a blocker of mPTP opening, attenuates isoflurane-induced mPTP opening, caspase 3 activation, a

210 be additive to the potential consequences of isoflurane-induced neuroapoptosis.

211 The isoflurane-induced ROS accumulation can be attenuated by

212 ts suggest that volatile anesthetics such as isoflurane inhibit NaV by stabilizing the inactivated st

213 ed inhaled anesthetics such as halothane and isoflurane inhibit the archetypical voltage-gated Kv3 ch

214 istent with allosteric interactions, whereas isoflurane inhibition was nearly complete, apparently co

215 dence for a direct pore-binding mechanism of isoflurane inhibition, which has a general implication f

216 e notion that binding at these sites renders isoflurane inhibition.

217 We conclude that isoflurane inhibits NaChBac by two distinct mechanisms:

218 However, it remains to be determined how isoflurane interacts with the full ectodomain LFA-1 and

219 Isoflurane introduced into the aqueous phase readily par

220 Isoflurane is a volatile anesthetic that has a vasodilat

221 Given that isoflurane is a widely used volatile anesthetic, and is

222 The volatile anesthetic isoflurane is capable of inducing preconditioning and po

223 Immobility induced by another VA, isoflurane, is not affected by these treatments, thereby

224 MRI recordings under isoflurane, ketamine/xylazine, ketamine/isoflurane, and

225 These results suggest that isoflurane may induce apoptosis through Bcl-2 family pro

226 Finally, isoflurane may induce the opening of mPTP via increasing

227 hippocampus and cortex of rats treated with isoflurane/ N(2)O anesthesia at 18-months-old, leading t

228 igs in each experimental group): thiopental, isoflurane, nitrous oxide and isoflurane plus nitrous ox

229 ce or presence of an agonist revealed double isoflurane occupancies inside the pore near T237(6') and

230 rousal and reduced the depressant effects of isoflurane on barrel cortex somatosensory-evoked potenti

231 anisms may also contribute to the effects of isoflurane on IPSCs.

232 neral anesthesia, we examined the effects of isoflurane on properties of GABAergic inhibitory current

233 assess the effects of chloroform or the VGA isoflurane on TRP channel activation.

234 fects of the most common general anesthetic, isoflurane, on time perception and the circadian clock u

235 dazolam and barbiturates have failed, use of isoflurane or ketamine anesthesia has been tried at a me

236 Here, we demonstrate that isoflurane or propofol anesthesia decreases hippocampal

237 Isoflurane or propofol did not affect new cell prolifera

238 Furthermore, isoflurane or propofol may prevent or reverse TXA-induce

239 99% expression of InsP3R-1 were treated with isoflurane or propofol.

240 Isoflurane or sevoflurane administered after the ischemi

241 ng IV propofol (n = 74) or inhaled volatile (isoflurane or sevoflurane) anesthetic agent (n = 67).

242 We found that exposure to either isoflurane (p=0.017) or propofol (p=0.006) decreased hip

243 ): thiopental, isoflurane, nitrous oxide and isoflurane plus nitrous oxide.

244 Our findings demonstrate that isoflurane post-conditioning protects against small inte

245 not better than NMDA receptor inhibition or isoflurane postconditioning alone for neuroprotection.

246 r activation, isoflurane preconditioning, or isoflurane postconditioning alone.

247 I inhibition, isoflurane preconditioning, or isoflurane postconditioning alone.

248 on with either isoflurane preconditioning or isoflurane postconditioning induced a better neuroprotec

249 Isoflurane preconditioning and isoflurane postconditioning may involve CaMKII inhibitio

250 combination of NMDA receptor inhibition and isoflurane postconditioning was not better than NMDA rec

251 fter the onset of the simulated reperfusion (isoflurane postconditioning).

252 of NMDA receptors may mediate the effects of isoflurane postconditioning, but not isoflurane precondi

253 Isoflurane posttreatment delays the development of posts

254 We examined whether isoflurane posttreatment is protective against early bra

255 tive effect than NMDA receptor inhibition or isoflurane preconditioning alone.

256 Isoflurane preconditioning and isoflurane postconditioni

257 The combination of isoflurane preconditioning and postconditioning induced

258 ongly indicate that autophagy is involved in isoflurane preconditioning both in vivo and in vitro and

259 combination of NMDA receptor inhibition and isoflurane preconditioning caused a better neuroprotecti

260 denosine A2A receptor activation with either isoflurane preconditioning or isoflurane postconditionin

261 The combination of CaMKII inhibition and isoflurane preconditioning or postconditioning did not p

262 fect than adenosine A2A receptor activation, isoflurane preconditioning, or isoflurane postconditioni

263 de better protection than CaMKII inhibition, isoflurane preconditioning, or isoflurane postconditioni

264 These results suggest that isoflurane preconditioning- and postconditioning-induced

265 ects of isoflurane postconditioning, but not isoflurane preconditioning.

266 e Sprague-Dawley rats were anesthetized with isoflurane, prepared for parasagittal fluid percussion i

267 Moreover, in the latter model, isoflurane prevented BBB dysfunction and neurodegenerati

268 steady-state general anesthesia (CSSGA) with isoflurane produced behavioral and EEG evidence of arous

269 B dysfunction and neurodegeneration, whereas isoflurane reduced neuroinflammation in the kainate mode

270 The addition of N(2)O to isoflurane reduced the time to loss of the righting refl

271 The significance of isoflurane's effect was assessed in both intracellular a

272 ld affect the onset, depth, or recovery from isoflurane's general anesthetic effects.

273 e 1 phosphate receptor inhibitor VPC23019 on isoflurane's protective action against postsubarachnoid

274 Isoflurane sedation was changed to midazolam in two nons

275 Isoflurane sedation with the AnaConDa during 24 hours th

276 Thus, changes in information transfer under isoflurane seem to be a consequence of changes in local

277 on the uptake of the inhalation anesthetics isoflurane, sevoflurane, and desflurane when used in rou

278 Isoflurane significantly decreased the number of maturin

279 Isoflurane significantly improved neurobehavioral functi

280 PnO of male mice (n = 18) anesthetized with isoflurane significantly increased ACh release in the Pn

281 In the absence of isoflurane, spontaneous recurrent seizures were common i

282 tivation-sensitive antibodies suggested that isoflurane stabilized LFA-1 in the closed conformation.

283 n mouse brain in the awake and anesthetized (isoflurane) states.

284 We previously demonstrated that isoflurane targets lymphocyte function-associated antige

285 In these animals, isoflurane transiently enhanced activity of the respirat

286 nerated in the forebrain white matter of the isoflurane-treated group was 6.3% of the total populatio

287 Similarly, the inhaled anesthetic isoflurane triggered a persistent increase in tonic curr

288 When isoflurane was administered during kainate injection, du

289 Isoflurane was either administered during (kainate) or a

290 eneral anesthetics (etomidate, propofol, and isoflurane) was greater at negative membrane potentials.

291 The beneficial effects of isoflurane were abolished by N, N-dimethylsphingosine an

292 Furthermore, the protective effects of isoflurane were abolished by treatment with a TGF-beta1

293 Rats anesthetized with isoflurane were given intravenous infusions (9 mL/kg ove

294 The effects of isoflurane were investigated in two rat models of SE-ind

295 higher concentrations of both halothane and isoflurane were required to render TASK knock-out animal

296 The effects of isoflurane were similar on evoked field excitatory posts

297 gnificantly shorter in patients sedated with isoflurane when compared with IV sedation although no di

298 re, it has been shown in animal studies that isoflurane, when used as a preconditioning agent, has ne

299 We report novel preclinical findings with isoflurane, which exerts various nonanesthetic effects t

300 spectroscopy showed a strong interaction of isoflurane with S129, T189, and S208; relatively weakly