ライフサイエンスコーパス: pilocarpine

1 tatus epilepticus-induced epilepsy (systemic pilocarpine).

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

3 or acetylcholine and for the partial agonist pilocarpine.

4 uced by the non-selective muscarinic agonist pilocarpine.

5 given at the first behavioral seizure after pilocarpine.

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

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

8 ced with injections of either kainic acid or pilocarpine.

9 n the fresh anterior epithelium responded to pilocarpine.

10 anterior epithelial specimens in response to pilocarpine.

11 hr after induction of status epilepticus by pilocarpine.

12 ntitis on the salivary secretory response to pilocarpine.

13 the maximal response to the partial agonist, pilocarpine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

29 Pilocarpine activates extracellular regulated kinase 1/2

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

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

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

33 Following pilocarpine administration, mean (SD) intraocular pressu

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

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

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

37 Pilocarpine also fails to stimulate insulin secretion an

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

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

40 Pilocarpine and atropine were applied topically to manip

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

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

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

44 Whereas pilocarpine and glycopyrrolate increased and decreased s

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

46 mice, after intraperitoneal stimulation with pilocarpine and isoproterenol.

47 In both pilocarpine and kainic acid models, there was greater mo

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

49 Pilocarpine and latanoprost, known to enhance aqueous hu

50 It has been demonstrated that low doses of pilocarpine and other muscarinics substantially increase

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

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

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

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

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

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

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

63 Pilocarpine caused a myopic shift in resting refraction

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

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

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

67 nt-concentrating hormone, TNRNFLRFamide, and pilocarpine] converge onto the same voltage-dependent in

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

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

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

83 Pilocarpine increased in vivo phosphoinositide (PI) hydr

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

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

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

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

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

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

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

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

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

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

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

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

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

97 ring antagonist pirenzepine potently blocked pilocarpine-induced increases in in vivo PI hydrolysis,

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

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

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

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

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

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

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

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

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

112 We report that pilocarpine-induced seizures accelerated the morphologic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

149 Results following pilocarpine-induced status epilepticus indicate that neu

150 Pilocarpine-induced status epilepticus led to a signific

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

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

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

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

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

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

157 After pilocarpine-induced status epilepticus, many granule cel

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

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

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

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

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

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

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

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

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

167 ollowing an initial brain injury produced by pilocarpine-induced status epilepticus.

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

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

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

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

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

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

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

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

176 Pilocarpine injected either subcutaneously or intracereb

177 Pilocarpine injection induces epileptic seizures in rode

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

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

180 Pilocarpine is a prototypical drug used to treat glaucom

181 Since pilocarpine is a relatively weak partial agonist, these

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

183 mide, timolol) or increase outflow facility (pilocarpine, latanoprost) in primates and humans lowered

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

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

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

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

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

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

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

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

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

193 We used the pilocarpine model of epilepsy to demonstrate that regula

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

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

196 vate granule cells of the dentate gyrus in a 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 The pilocarpine model of temporal lobe epilepsy is an animal

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 +/- 0.59; P = 0.234), but not isoproterenol, pilocarpine, or nifedipine.

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

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

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

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

226 ransient initial increase in IOP produced by pilocarpine reported in other animals was also observed

227 igated and progressively reduced the maximal pilocarpine response.

228 Pilocarpine responses consisted of a large release and m

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

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

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

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

233 Similar results were obtained at time of pilocarpine seizure.

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

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

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

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

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

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

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

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

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

243 Pilocarpine-stimulated fluid secretion was 4.3 +/- 0.4 m

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

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

246 Pilocarpine-stimulated salivary flow was significantly l

247 Pilocarpine-stimulated salivary flow was used to address

248 va secreted by Aqp5(-)/- mice in response to pilocarpine stimulation are not caused by changes in who

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

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

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

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

253 he ability of the partial muscarinic agonist pilocarpine to increase in vivo phosphoinositide (PI) hy

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

255 Pilocarpine-treated and control rats were sacrificed at

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

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

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

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

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

261 In pilocarpine-treated animals, the normal diffuse labeling

262 In pilocarpine-treated chronically epileptic rats, we descr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

279 Hippocampal slices from pilocarpine-treated rats were used to explore the effect

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

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

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

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

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

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

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

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

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

289 y interneurons progressively increased after pilocarpine treatment.

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

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

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

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

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

295 Accommodation response to topical pilocarpine was monitored periodically.

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

297 e increases in vivo PI hydrolysis induced by pilocarpine were 60-75% of the magnitude of the full mus

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

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

300 that treatment with the cholinergic agonist pilocarpine, which is effective in monkeys with specific