ライフサイエンスコーパス: pilocarpine

1 tra-amygdala kainic acid and intraperitoneal pilocarpine).

2 tatus epilepticus-induced epilepsy (systemic pilocarpine).

3 ight eye and -0.52 mm in the left eye, under pilocarpine).

4 or acetylcholine and for the partial agonist pilocarpine.

5 uced by the non-selective muscarinic agonist pilocarpine.

6 given at the first behavioral seizure after pilocarpine.

7 nse to the chemoconvulsants, kainic acid and pilocarpine.

8 before pilocarpine and 0.68 +/- 0.29 D after pilocarpine.

9 esponse when given 2, but not 8, days before pilocarpine.

10 n the fresh anterior epithelium responded to pilocarpine.

11 anterior epithelial specimens in response to pilocarpine.

12 hr after induction of status epilepticus by pilocarpine.

13 ced with injections of either kainic acid or pilocarpine.

14 ntitis on the salivary secretory response to pilocarpine.

15 the maximal response to the partial agonist, pilocarpine.

16 lepticus (SE) was induced in rats by lithium pilocarpine.

17 e and 1 hour after topical administration of pilocarpine, 1%, in 1 eye of healthy volunteers and pilo

18 cessfully before and after administration of pilocarpine, 1%, in 9 healthy eyes (9 individuals) and p

19 Prophylactic therapy with pilocarpine, 2%, eyedrops may be useful for individuals

20 pine, 1%, in 1 eye of healthy volunteers and pilocarpine, 2%, in 1 eye of patients with glaucoma.

21 e, 1%, in 9 healthy eyes (9 individuals) and pilocarpine, 2%, in 10 eyes with glaucoma (10 patients)

22 us epilepticus after systemic treatment with pilocarpine 31-61 days earlier were video-monitored for

23 atus epilepticus following administration of pilocarpine (380 mg/kg).

24 tudy of 60 patients, we investigated whether pilocarpine, 5 mg orally every 8 h for 1 wk after 131I t

25 ml(-1)) induced much lower sweat rates than pilocarpine (56.8+/-1.62 g m(-2) hour(-1) vs 8.2+/-1.2 g

26 -/-) mice following in vivo stimulation with pilocarpine, a cholinergic agonist.

27 induced by intraperitoneal administration of pilocarpine, a muscarinic acetylcholine receptor agonist

28 induced by intraperitoneal administration of pilocarpine, a muscarinic acetylcholine receptor agonist

29 show that oral treatment of caged bees with pilocarpine, a muscarinic agonist, induced an increase i

30 lated tear production following injection of pilocarpine, a muscarinic receptor agonist.

31 Pilocarpine activates extracellular regulated kinase 1/2

32 ncy to limbic motor seizures following acute pilocarpine administration in the absence of differences

33 ge in pupillary diameter at 30 minutes after pilocarpine administration was smaller in the CXL group

34 the 2 sets of serial scans (before and after pilocarpine administration) were selected for analysis b

35 Following pilocarpine administration, mean (SD) intraocular pressu

36 en SNC80 (30 or 60 mg/kg) was given prior to pilocarpine administration, trends toward increased late

37 of rats exhibiting prolonged SE compared to pilocarpine alone, further suggesting that SNC80 has pro

38 rall seizure severity compared to rats given pilocarpine alone, suggesting that SNC80 was anticonvuls

39 Pilocarpine also fails to stimulate insulin secretion an

40 The synthesis of a chiral pilocarpine analogue 3 in which the lactone ring is repl

41 dative amplitude was 10.08 +/- 1.15 D before pilocarpine and 0.68 +/- 0.29 D after pilocarpine.

42 T protocol also included the installation of pilocarpine and apraclonidine eye drops.

43 Pilocarpine and atropine were applied topically to manip

44 ions (e.g., the muscarinic receptor agonists pilocarpine and cevimeline) that induce saliva secretion

45 cations (e.g., muscarinic receptor agonists: pilocarpine and cevimeline) that induce saliva secretion

46 hen activated by other ligands (for example, pilocarpine and choline).

47 Whereas pilocarpine and glycopyrrolate increased and decreased s

48 ECHO decreased the accommodative response to pilocarpine and increased intraocular pressure, as has b

49 both TrkB and PLCgamma1 in hippocampi in the pilocarpine and kindling models in wild-type mice.

50 Pilocarpine and latanoprost, known to enhance aqueous hu

51 of intrinsic efficacy, from the low-efficacy pilocarpine and oxotremorine to high-efficacy acetylchol

52 es evoked by two different chemoconvulsants, pilocarpine and picrotoxin.

53 anisms (4-Aminopyridine, Pentylenetetrazole, Pilocarpine and Strychnine) resulted in distinct spatiot

54 SE was induced by pilocarpine, and animals were studied 10 minutes (refrac

55 t cell contractility (isoproterenol, Y27632, pilocarpine, and nifedipine).

56 unit alpha2delta4, which was augmented after pilocarpine- and kainic acid-induced status epilepticus.

57 HCN1 mRNA expression was evident also in the pilocarpine animal model of TLE.

58 Moreover, pilocarpine blocked CCh-stimulated PIP2 hydrolysis in M3

59 The M(1) muscarinic agonist pilocarpine blocked phosphorylation of both catenins, wh

60 ted rats, or animals that were injected with pilocarpine but did not develop status epilepticus.

61 significant amounts of fluid in response to pilocarpine, but protein concentrations were decreased.

62 mmodative response amplitude is reduced with pilocarpine by shifting the eye to a more myopic state a

63 Taken together, our findings show that pilocarpine can act as either an agonist or antagonist o

64 Pilocarpine caused a myopic shift in resting refraction

65 Similarly, microneedle delivery of pilocarpine caused rapid and extensive rabbit pupil cons

66 Similar experiments were performed using pilocarpine-coated microneedles, and the rabbit pupil si

67 over a 30-minute period to a dose of topical pilocarpine compared with controls.

68 corneal aberration and retinal injury after pilocarpine delivery using dual-function optimized carri

69 leads to fast polymer degradation and early pilocarpine depletion in vivo, which is disadvantageous

70 Under the conditions of the study, pilocarpine did not reduce the occurrence of radiation s

71 In contrast to CCh or Oxo-M, pilocarpine does not induce Ca(2+) mobilization via endo

72 ost 50% of immature granule cells exposed to pilocarpine-epileptogenesis exhibited aberrant hilar bas

73 efore (immature), or 3 weeks after (newborn) pilocarpine-epileptogenesis.

74 e is in a specific class of drug, along with pilocarpine, epinephrine, and bimatoprost that in humans

75 These data suggest that pilocarpine expands the Schlemm canal in eyes with and w

76 coma medications (P < .001), prescription of pilocarpine hydrochloride (adjusted ratio of persistence

77 The in vivo effect of pilocarpine hydrochloride on the Schlemm canal may help

78 rats with temporal lobe epilepsy induced by pilocarpine hydrochloride treatment.

79 ograms, SE induced by the muscarinic agonist pilocarpine in mice is preceded by a specific increase i

80 eritoneal injections of kainic acid (KA) and pilocarpine in mice with a conditional deletion of Orai1

81 lectin-3 (Gal-3) was strongly upregulated by pilocarpine in microglial cells.

82 Miosis was induced by topical 1% pilocarpine in the right eye of 14 healthy subjects with

83 imal stimulation evoked by acetylcholine and pilocarpine in two different responses.

84 Further, KA and pilocarpine increased the frequency of spontaneous IPSCs

85 s (ACh, nicotine, muscarine, bethanechol and pilocarpine) increased [Ca2+]i.

86 epilepticus by intrahippocampal injection of pilocarpine induced biphasic changes in pO2 in the hippo

87 een done on its role in the lithium chloride-pilocarpine induced epileptic model.

88 However, when applied at higher doses, pilocarpine induced only modestly reduced (5 mg/kg, s.c.

89 ssociation in the hippocampus in response to pilocarpine induced-seizure before transcriptional up-re

90 hanges in pupillary diameter correlated with pilocarpine-induced A-IOL axial shift.

91 t substantially altered during the course of pilocarpine-induced accommodation or atropine-induced cy

92 at the ablation of adult neurogenesis before pilocarpine-induced acute seizures in mice leads to a re

93 terized pupillography, at baseline and after pilocarpine-induced anisocoria.

94 e here the role of this endogenous lectin in pilocarpine-induced cell death in adult mice.

95 different time points in the development of pilocarpine-induced epilepsy in the rat: latency, first

96 anule cells in the temporal dentate gyrus of pilocarpine-induced epileptic rats.

97 channel (TRPC) 7 significantly reduces this pilocarpine-induced increase of gamma wave activity, pre

98 Pregnancy and CI each increased pilocarpine-induced lacrimal fluid production, whereas p

99 mice lacking the corresponding gene Lgals1, pilocarpine-induced neuronal death was essentially aboli

100 ry gland function was monitored by measuring pilocarpine-induced saliva volume.

101 Pilocarpine-induced saliva was simultaneously collected

102 FN-mediated signaling, was characterized for pilocarpine-induced salivation, the presence of serum au

103 ciences were monitored for blood glucose and pilocarpine-induced salivation.

104 We subjected young mice to pilocarpine-induced SE for 2 h and then administered A1-

105 croglia marker IBA1 in the hippocampus after pilocarpine-induced SE from 4 hrs to 35 days.

106 Therefore, using a pilocarpine-induced SE model of mTLE in mice of either s

107 bute to their relative lower activity in the pilocarpine-induced SE model.

108 itiated to evaluate the time course by which pilocarpine-induced SE produced changes in CB(1) recepto

109 Within 1-2 weeks after pilocarpine-induced SE, bromodeoxyuridine (BrdU) labelin

110 During pilocarpine-induced SE, in vivo disruption of STEP activ

111 Cs from adult male rats several months after pilocarpine-induced SE, when they are considered to have

112 h was augmented early and persistently after pilocarpine-induced SE.

113 unds were infused between 2 and 5 days after pilocarpine-induced SE.

114 in local pO2 and LFP-related currents during pilocarpine-induced seizure activity.

115 We report that pilocarpine-induced seizures accelerated the morphologic

116 ecreased the number of rats exhibiting acute pilocarpine-induced seizures and overall seizure severit

117 R7943 significantly reduced the incidence of pilocarpine-induced seizures and status epilepticus in 2

118 ity may contribute to the pathophysiology of pilocarpine-induced seizures and status epilepticus.

119 Significant effects of SNC80 on pilocarpine-induced seizures did not correlate with the

120 to find that doses of VU0255035 that reduce pilocarpine-induced seizures do not induce deficits in c

121 Rats that had pilocarpine-induced seizures had an increased incidence

122 ation in vivo and is efficacious in reducing pilocarpine-induced seizures in mice.

123 esting that SNC80 did not dramatically alter pilocarpine-induced seizures in the absence of behaviora

124 vivo, inhibition or knockdown of PTEN after pilocarpine-induced seizures protected CNS neurons from

125 enriched, or differentially expressed under pilocarpine-induced seizures, and validated TGFBR2 and t

126 dicated by reduced latency and threshold for pilocarpine-induced seizures, but seemed normal in other

127 In vivo, pilocarpine-induced seizures, previously shown to up-reg

128 cell death, but surprisingly have unaltered pilocarpine-induced seizures.

129 NC80, has complex, dose-dependent effects on pilocarpine-induced seizures.

130 hippocampus, particularly in astrocytes, by pilocarpine-induced seizures; and infusion of anti-pro-N

131 cornu ammonis 1 region of hippocampus after pilocarpine-induced severe seizures was significantly am

132 ly assessing granule cell excitability after pilocarpine-induced status epilepticus (SE) and monitori

133 ts levels was noticed as early as 24 h after pilocarpine-induced status epilepticus (SE) and persiste

134 cutaneous metrazol (scMet) seizure tests and pilocarpine-induced status epilepticus (SE) model.

135 Male rats underwent pilocarpine-induced status epilepticus (SE) or sham trea

136 Here, we used a rat model of pilocarpine-induced status epilepticus (SE) to investiga

137 s of CA1 hippocampal pyramidal neurons after pilocarpine-induced status epilepticus (SE), accompanied

138 Under both control conditions and after pilocarpine-induced status epilepticus (SE), ERK/MAPK ac

139 rentially synapse onto adult-born DGCs after pilocarpine-induced status epilepticus (SE), whereas nor

140 temporal lobe epilepsy and in mice following pilocarpine-induced status epilepticus (SE).

141 or in hippocampi of epileptic rats following pilocarpine-induced status epilepticus (SE).

142 model of temporal lobe epilepsy obtained via pilocarpine-induced status epilepticus (SE).

143 of granule cells born either before or after pilocarpine-induced status epilepticus (SE).

144 imes (1-60 d) after an epileptogenic injury, pilocarpine-induced status epilepticus (STEP).

145 campal slices from rats that had experienced pilocarpine-induced status epilepticus and developed a r

146 Kv3.4 (gene Kcnc4) occurred after 1 month of pilocarpine-induced status epilepticus and persisted dur

147 ature EPSCs, was significantly reduced after pilocarpine-induced status epilepticus and remained low

148 mong granule cells born up to 5 weeks before pilocarpine-induced status epilepticus and these cells w

149 ases in alpha4 and Egr3 mRNAs in response to pilocarpine-induced status epilepticus are accompanied b

150 al changes, we subjected rat pups to lithium-pilocarpine-induced status epilepticus during postnatal

151 r delta subunit expression was altered after pilocarpine-induced status epilepticus in C57BL/6 mice i

152 reatment with rapamycin, beginning 1 d after pilocarpine-induced status epilepticus in mice, would su

153 Results following pilocarpine-induced status epilepticus indicate that neu

154 Pilocarpine-induced status epilepticus led to a signific

155 To measure directly the long-term effects of pilocarpine-induced status epilepticus on vesicular rele

156 At 5 d after pilocarpine-induced status epilepticus the spontaneous f

157 which were reduced short-term (5 days after pilocarpine-induced status epilepticus) but later reboun

158 om rats 3-7 d after an epileptogenic injury (pilocarpine-induced status epilepticus).

159 e-treated control mice, in mice 5 days after pilocarpine-induced status epilepticus, and after status

160 ctivity in situ, delayed seizure onset after pilocarpine-induced status epilepticus, and attenuated s

161 After pilocarpine-induced status epilepticus, many granule cel

162 Within 3-7 d after pilocarpine-induced status epilepticus, miniature IPSC f

163 Previously, we showed that, following pilocarpine-induced status epilepticus, there are two in

164 n this study we found that, 1-2 months after pilocarpine-induced status epilepticus, there were signi

165 ated during the first 24 h following lithium-pilocarpine-induced status epilepticus, when neuronal de

166 eous limbic motor seizures 5 weeks following pilocarpine-induced status epilepticus.

167 d in mice beginning 1 h after termination of pilocarpine-induced status epilepticus.

168 is affected during epileptogenesis following pilocarpine-induced status epilepticus.

169 beginning within hours after rats sustained pilocarpine-induced status epilepticus.

170 anced by at least 2-fold in the aftermath of pilocarpine-induced status epilepticus.

171 ting after epileptogenic injuries, including pilocarpine-induced status epilepticus.

172 reduced sweating below baseline and blocked pilocarpine-induced sweating completely.

173 er, preserved autonomic function measured by pilocarpine-induced sweating, and prevented the loss of

174 ath, and spontaneous recurrent seizures in a pilocarpine-induced temporal lobe epilepsy model.

175 e hamster ovary-K1 cells overexpressing M3R, pilocarpine induces Ca(2+) transients like those recorde

176 These results suggest that pilocarpine induces Fos expression in the striatum as a

177 ation of the nonselective muscarinic agonist pilocarpine induces pronounced striatal Fos expression.

178 ed changes in mGlu2 and mGlu3 mRNA following pilocarpine-inducted status epilepticus (SE) and subsequ

179 single SE episode, induced by the convulsant pilocarpine, initiates the development of an epileptic c

180 Pilocarpine injection induces epileptic seizures in rode

181 (SD) rats were treated with lithium chloride-pilocarpine injections and divided into an experimental

182 become very popular in the clinical setting (pilocarpine iontophoresis being a prominent exception).

183 Pilocarpine is a prototypical drug used to treat glaucom

184 d in rat models of acute seizures induced by pilocarpine, kainic acid, or pentylenetetrazole.

185 examine in vivo pharmacological efficacy of pilocarpine-loaded antioxidant-functionalized biodegrada

186 cosity of freshly secreted gland fluid after pilocarpine, measured by fluorescence recovery after pho

187 In vivo, neuronal death induced by pilocarpine-mediated seizures was significantly reduced

188 Application of the muscarinic agonist pilocarpine mimicked the effect of IPSPs on MC maximal f

189 ampal, frontal, and occipital neurons in the pilocarpine model by using [Ca(2+)](i) imaging fluoresce

190 The validity of the pilocarpine model has been challenged based largely on c

191 In the pilocarpine model in mice, BUM5, but not bumetanide, cou

192 e validated by examining hippocampi from the pilocarpine model of chronic TLE.

193 The onset of spontaneous seizures in the pilocarpine model of epilepsy causes a hyperpolarized sh

194 vate granule cells of the dentate gyrus in a pilocarpine model of epilepsy.

195 anges in thalamic T-type channels in a mouse pilocarpine model of epilepsy.

196 velopment of spontaneous seizures in the rat pilocarpine model of epilepsy.

197 f chronically epileptic rats obtained by the pilocarpine model of MTLE.

198 to adult-born and early-born DGCs in the rat pilocarpine model of mTLE.

199 Thus, in a pilocarpine model of recurrent seizures in C57BL/6 mice,

200 We found that in the mouse pilocarpine model of status epilepticus (SE), systemic a

201 Chronically epileptic male adult rats in the pilocarpine model of temporal lobe epilepsy (TLE), exhib

202 In the pilocarpine model of temporal lobe epilepsy, mossy fiber

203 nically epileptic dentate gyrus in the mouse pilocarpine model of temporal lobe epilepsy.

204 rsynchronous-onset (HYP) seizures in the rat pilocarpine model of temporal lobe epilepsy.

205 This study examined their fates in the mouse pilocarpine model of temporal lobe epilepsy.

206 ability leading to recurrent seizures in the pilocarpine model of temporal lobe epilepsy.

207 s involving acid-sensing ion channels in the pilocarpine model of temporal lobe epilepsy.

208 and chronic epileptic rats obtained with the pilocarpine model of temporal lobe epilepsy.

209 izures and hippocampal histopathology in the pilocarpine model of temporal lobe epilepsy.

210 targets with GABA immunocytochemistry in the pilocarpine model of temporal lobe epilepsy.

211 Previous studies in the adult rat pilocarpine model of TLE found reduced expression of GAB

212 s during epileptogenesis in male rats in the pilocarpine model of TLE.

213 sponses to a mild insult, we used a low-dose pilocarpine model to induce a brief seizure in LIF knock

214 d the anticonvulsant activity of 2-DG in the pilocarpine model, but only decreased the efficacy of F1

215 ts robustly reduced seizure frequency in the pilocarpine model.

216 2-DG was only effective in the pilocarpine model.

217 In the systemic pilocarpine mouse model of temporal lobe epilepsy, the e

218 In the pilocarpine mTLE model, hilar-ectopic DGCs arise as a re

219 Muscarinic stimulation with pilocarpine nitrate (50 mug ml(-1) to 1.66 mg ml(-1)) pr

220 inhibitor PP2, indicating that the action of pilocarpine on endogenous M3R is biased toward beta-arre

221 esult and the possibility of side-effects of pilocarpine on the nervous system, led us to develop an

222 +/- 0.59; P = 0.234), but not isoproterenol, pilocarpine, or nifedipine.

223 Experimental TLE was triggered by pilocarpine- or kainic acid-induced status epilepticus (

224 owed stronger seizures to KA (P = 0.001) and pilocarpine (P < 0.00001) and loss of chemoconvulsant-in

225 A1 pyramidal neurons >twofold (KA: P = 0.04; pilocarpine: P = 0.0002) which was abolished in Orai1 KO

226 inistration in the absence of differences in pilocarpine pharmacokinetics, and also had a decreased t

227 orts ranging from 0 to 2.5 diopters [D]) and pilocarpine postoperatively.

228 ethonium (C6) and atropine.ACh, nicotine and pilocarpine potentiated the excitatory effect of Na2S2O4

229 igated and progressively reduced the maximal pilocarpine response.

230 Pilocarpine responses consisted of a large release and m

231 E affects the transcriptome, we employed the pilocarpine SE model in mice and Illumina-based high-thr

232 The induction of hippocampal IL-6 after pilocarpine SE was nearly abolished in EP2 conditional K

233 e (38) also exhibited potent activity in the pilocarpine-SE model 30 min postseizure onset.

234 gues 38 and 43 decreased the activity in the pilocarpine-SE model from ED(50) = 81 mg/kg (34) to 94 m

235 In a Li-pilocarpine seizure model in mice, CYM2503 increased the

236 Similar results were obtained at time of pilocarpine seizure.

237 dose (1 mg/kg, s.c.), the muscarinic agonist pilocarpine showed significantly reduced secretory activ

238 Stimulation of KCs with pilocarpine significantly (p < 0.05) elevated both serin

239 Brief activation of mAChRs with pilocarpine significantly enhances KAR-mediated excitoto

240 Male Wistar rats were subjected to LiCl and pilocarpine status epilepticus (SE).

241 Epileptogenesis was initiated using the pilocarpine status epilepticus model in male and female

242 In the rat Li-pilocarpine status epilepticus model, CYM2503, injected

243 Transgenic mice rendered epileptic using the pilocarpine-status epilepticus model of epilepsy were mo

244 In contrast to CCh, pilocarpine stimulated PIP2 hydrolysis only in cells ove

245 acrimal fluid was collected under basal- and pilocarpine-stimulated conditions for protein determinat

246 of FITC-dextran, was threefold increased in pilocarpine-stimulated gland fluid after CFTR inhibition

247 Unexpectedly, the pilocarpine-stimulated in vivo fluid secretion from subm

248 Pilocarpine-stimulated salivary flow was significantly l

249 Pilocarpine-stimulated salivary flow was used to address

250 of both AQP5+/+ and AQP5-/- male mice after pilocarpine stimulation but no change in strand number i

251 Sweat secretion rates after pilocarpine stimulation did not differ in wild-type mice

252 progenitors and mature DGCs in the adult rat pilocarpine temporal lobe epilepsy model.

253 from 100 hippocampi from mice with epilepsy (pilocarpine-temporal lobe epilepsy model) and 100 health

254 6) and PV-Cre (n = 6) mice were treated with pilocarpine to induce SE.

255 e rats were administered the chemoconvulsant pilocarpine to initiate status epilepticus, which was de

256 Pilocarpine-treated and control rats were sacrificed at

257 iloride suppressed limbic seizures in 33% of pilocarpine-treated animals and significantly reduced th

258 By 1 month post-SE, pilocarpine-treated animals began to display epileptic s

259 evealed different levels between control and pilocarpine-treated animals for 27 miRNAs.

260 ss effective in reducing excitability in the pilocarpine-treated animals than in controls.

261 However, in pilocarpine-treated animals, a rich plexus of ChR2-eYFP-

262 In pilocarpine-treated animals, the normal diffuse labeling

263 In pilocarpine-treated chronically epileptic rats, we descr

264 the inner molecular layer per hippocampus in pilocarpine-treated control mice, in mice 5 days after p

265 y recorded from the CA1 and dentate gyrus in pilocarpine-treated epileptic mice with silicon probes d

266 tions of these subunits were also altered in pilocarpine-treated epileptic mice, and related function

267 ecording from slices of entorhinal cortex in pilocarpine-treated epileptic rats to test the dormant i

268 the hilus of the dentate gyrus of epileptic pilocarpine-treated GIN mice, specifically a subpopulati

269 he dentate gyrus of slices obtained from the pilocarpine-treated mice and demonstrated that physiolog

270 bitory responses in dentate granule cells in pilocarpine-treated mice but not in controls.

271 In the pilocarpine-treated mice, alpha4 subunit labeling remain

272 min-containing interneurons was increased in pilocarpine-treated mice, and miniature IPSCs were reduc

273 basket cells, also labeled fewer boutons in pilocarpine-treated mice.

274 ic phasic inhibition of granule cells in the pilocarpine-treated mice.

275 The pilocarpine-treated rat model is used frequently to inve

276 on failures at BC-->GC synapses in epileptic pilocarpine-treated rats are not attributable to smaller

277 Compared with controls, epileptic pilocarpine-treated rats displayed boutons with over twi

278 nfrapyramidal sites in hippocampal slices of pilocarpine-treated rats showed larger population spikes

279 in patients with temporal lobe epilepsy and pilocarpine-treated rats that support the model's validi

280 This study used hippocampal slices from pilocarpine-treated rats to explore the dependence of sy

281 ilities in hippocampal slices from epileptic pilocarpine-treated rats, laser-scanning glutamate uncag

282 h clamp recording in hippocampal slices from pilocarpine-treated rats.

283 nule cells with basal dendrites in epileptic pilocarpine-treated rats.

284 s among layer II stellate cells in epileptic pilocarpine-treated rats.

285 duction in the number of dying neurons after pilocarpine treatment compared with wild type mice.

286 de of the 5-HT(1A) receptor before and after pilocarpine treatment prevented seizure-induced hippocam

287 ll as from CA3 and CA1 pyramidal cells after pilocarpine treatment, changes that likely contribute to

288 morphology was examined 4 and 8 weeks after pilocarpine treatment.

289 y interneurons progressively increased after pilocarpine treatment.

290 were born in the weeks just before and after pilocarpine treatment.

291 us EEG monitoring was begun 2-3 months after pilocarpine treatment.

292 arinic antagonist (dicyclomine) and agonist (pilocarpine) treatments.

293 e induction by maximal electroshock (MES) or pilocarpine, variably including electroencephalography,

294 OL shift under stimulated accommodation with pilocarpine was -0.02+/-0.20 mm.

295 We found that pilocarpine was 1000 times less potent in stimulating mo

296 Strikingly, the sialagogue activity of pilocarpine was abolished in M(1)/M(3) receptor double-K

297 Accommodation response to topical pilocarpine was monitored periodically.

298 milar effect of amiodarone was observed when pilocarpine was used to stimulate inositol phosphate (IP

299 Effects of pilocarpine were blocked by scopolamine, a muscarinic an

300 erior cells of the in vivo bags responded to pilocarpine, whereas no cells in the cultured bags respo