ライフサイエンスコーパス: prepulse

1 bited by a preceding sub-threshold stimulus (prepulse).

2 educed baseline startle rates (i.e., without prepulse).

3 ied inhibitory interneurons activated by the prepulse.

4 ling stimulus follows 30-300 ms after a weak prepulse.

5 roduced, with the CS serving as a continuous prepulse.

6 f deactivation in response to a depolarizing prepulse.

7 me extent with and without a hyperpolarizing prepulse.

8 imulus is preceded by a weaker stimulus--the prepulse.

9 ter carboxyl termini were less affected by a prepulse.

10 extrinsic inhibition produced by an auditory prepulse.

11 VSMCs of mesenteric arteries after an NH4(+) prepulse.

12 otentials but only after strong depolarizing prepulses.

13 ition is not relieved by strong depolarizing prepulses.

14 SR field EPSP slopes were unaffected by SLM prepulses.

15 of PPI in rats using motivationally salient prepulses.

16 li both in the presence and absence of 70 dB prepulses.

17 facilitated nearly normally by depolarizing prepulses.

18 e-independent and unaffected by depolarizing prepulses.

19 ent and transiently relieved by depolarizing prepulses.

20 r prolongation by brief depolarizing somatic prepulses.

21 elevating [Ca(2)(+)](c) with a conditioning prepulse (-15 mV, 2 s) inactivated I(Ca) measured during

22 yramidal neurons, which was inhibited by SLM prepulses (150-225 ms).

23 ation of Ca(v)1.3 currents by a conditioning prepulse, a process known as voltage-dependent facilitat

24 n the CS(+) group, particularly with a 10-dB prepulse and a 60-ms SOA.

25 Prepulse and non-prepulse conditions were then compared

26 by using a gradient-echo sequence with an MT prepulse and systematic variation of the off-resonance f

27 s, which were potentiated by hyperpolarizing prepulses and inhibited by Cd2+ (200-500 microm).

28 mes (which reflect mode switching) were also prepulse-, and ion-dependent.

29 er masking the TCR with either continuous or prepulsed anti-Valpha3.2 Ab, 2D2 cells were immediately

30 s voltage-dependent, and strong depolarizing prepulses attenuated Hm-3 activity.

31 Most commonly, NaCl or HCl prepulses attenuated the response to quinine.

32 Hyperpolarizing prepulses augmented nearly all fast and slow eacs but on

33 laced using a whole-cell ammonium or acetate prepulse, before locally applying the low dose of ammoni

34 arned component to the inhibitory effects of prepulses, but this issue has yet to be fully investigat

35 ytoskeletal disruption specifically prevents prepulse, CaMK and IQ-dependent LTCC facilitation.

36 tivated Ca(2+) channels in that depolarizing prepulses can regulate their activity, and their carboxy

37 Strong positive prepulses can reverse the inhibitory effect of ProTx-II,

38 so take into account the perturbation that a prepulse challenge brings to the cytoplasmic acid buffer

39 late pH and volume regulation during a NH4Cl prepulse challenge.

40 d power significantly increased in the 70 dB prepulse condition and significantly decreased in the 11

41 on and significantly decreased in the 110 dB prepulse condition.

42 Prepulse conditions significantly decreased the amplitud

43 Prepulse and non-prepulse conditions were then compared using peak amplit

44 a dose-dependent decline in startle rates in prepulse conditions.

45 itation during the attended than the ignored prepulses, demonstrating early and later attentional mod

46 Finally, hyperpolarizing prepulses did not alter currents evoked by exogenous app

47 Of note, hyperpolarizing prepulses did not significantly reduce autaptic currents

48 Thus, the prepulse-driven shift into mode 2 gating results in a lo

49 t persists independently of the depolarizing prepulse duration and remains in the presence of 4-amino

50 ompartmental model support the idea that the prepulse effectively inactivates currents from the axon

51 nd, more powerful PPI mechanism in Tritonia: prepulse-elicited conduction block of action potentials

52 Using the prepulse facilitation (PPF) test, we further examined ch

53 jects showed greater prepulse inhibition and prepulse facilitation during the attended than the ignor

54 fects on inhibition of Ca(2+) current and on prepulse facilitation in the presence of somatostatin to

55 tantially reduced the low level of intrinsic prepulse facilitation present at the basal level of G pr

56 ) curves, and conferred differing degrees of prepulse facilitation to the channel.

57 ents, such as slowed activation kinetics and prepulse facilitation, were not observed for the mutated

58 Prepulse facilitation, which is a characteristic of volt

59 ersed by strong depolarization, resulting in prepulse facilitation.

60 bunits (Gbetagamma) are required for maximal prepulse facilitation.

61 ASRs were evoked by noise bursts; prepulses for PPI were 70 dB sound pressure level tones

62 studies in dissociated neurons show that the prepulse has no visible effect on the voltage dependence

63 The presence of a mild prepulse immediately before the main pulse inhibits star

64 this preliminary patient study, the dual IR prepulse improved contrast, scar visualization, and expe

65 nse in zebrafish larvae is modulated by weak prepulses in a manner similar to mammalian PPI.

66 ects of weak acoustic stimuli that served as prepulses in published reports of prepulse inhibition de

67 ssed PPI using acoustic, tactile, and visual prepulses in young (4 month) and old (23 month) C57BL/6N

68 effect is dominating and, consequently, the prepulse inactivation curves exhibit depolarizing shifts

69 Ca(2+) channel kinetics, voltage dependence, prepulse inactivation, or G protein inhibition but was a

70 strocytes, and pHi recovery from an ammonium prepulse-induced acid load in neurons.

71 peeds neuronal pHi recovery from an ammonium prepulse-induced acid load.

72 The degree of both prepulse-induced inactivation and facilitation decreased

73 Prepulses inhibit startle on the first pairing with a st

74 23), sensorimotor dexterity (2q24 and 2q32), prepulse inhibition (5p15), the California Verbal Learni

75 DCN induces hearing using a novel electrical prepulse inhibition (ePPI) of startle reflex behavior mo

76 In this study, gap prepulse inhibition (gap-PPI) of the acoustic startle re

77 Gap prepulse inhibition (gap-PPI), a translational experimen

78 impaired neurovascular coupling; attenuated prepulse inhibition (males); and hyperkinetic behavior.

79 digm, while hearing status was assessed with prepulse inhibition (PPI) and auditory brainstem respons

80 hors introduce a real-time model of acoustic prepulse inhibition (PPI) and facilitation (PPF) in anim

81 f IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) def

82 They were also tested for prepulse inhibition (PPI) and locomotor activity in the

83 Previous analyses of prepulse inhibition (PPI) and P50 gating measures in thi

84 CCK-1 receptors play a role in prepulse inhibition (PPI) by modulating mesolimbic dopam

85 sure the acoustic startle response (ASR) and prepulse inhibition (PPI) in mice.

86 autism, these offspring display deficits in prepulse inhibition (PPI) in the acoustic startle respon

87 Clozapine increased prepulse inhibition (PPI) in wild-type mice.

88 Prepulse inhibition (PPI) is an example of sensorimotor

89 Prepulse inhibition (PPI) is an operational measure of s

90 Prepulse inhibition (PPI) is an operational measure of s

91 Prepulse inhibition (PPI) is an operational measure of s

92 Prepulse inhibition (PPI) of acoustic startle is a genet

93 rally active causing a dramatic reduction in prepulse inhibition (PPI) of acoustic startle response.

94 Prepulse inhibition (PPI) of startle is being explored b

95 In humans, prepulse inhibition (PPI) of startle is greater during a

96 Prepulse inhibition (PPI) of startle is impaired in schi

97 t deficient sensorimotor gating (measured by prepulse inhibition (PPI) of startle) and mismatch negat

98 ensory gating of auditory evoked potentials, prepulse inhibition (PPI) of startle, and startle amplit

99 ry spatial acuity was measured in mice using prepulse inhibition (PPI) of the acoustic startle reflex

100 Prepulse inhibition (PPI) of the acoustic startle reflex

101 d schizophrenia patients exhibit deficits in prepulse inhibition (PPI) of the acoustic startle respon

102 Sensorimotor gating was measured by prepulse inhibition (PPI) of the acoustic startle respon

103 Rats were tested for prepulse inhibition (PPI) of the acoustic startle respon

104 ulation of the dopamine (DA) system disrupts prepulse inhibition (PPI) of the acoustic startle respon

105 In animals, LSD disrupts prepulse inhibition (PPI) of the acoustic startle respon

106 Translational biomarkers, such as prepulse inhibition (PPI) of the acoustic startle respon

107 Prepulse inhibition (PPI) of the acoustic startle respon

108 tive probe associated with this circuitry is prepulse inhibition (PPI) of the acoustic startle respon

109 e than Long Evans (LE) rats to disruption of prepulse inhibition (PPI) of the startle reflex by the d

110 Prepulse inhibition (PPI) of the startle reflex has been

111 important measure of sensorimotor gating is prepulse inhibition (PPI) of the startle response, impai

112 nformation, a process which is studied using prepulse inhibition (PPI) of the startle response.

113 Prepulse inhibition (PPI) refers to a reduction in the s

114 ity, impaired working memory, and deficit in prepulse inhibition (PPI) that was ameliorated by diazep

115 nt is preceded by a stimulus; this is called prepulse inhibition (PPI) when the prestimulus is weak a

116 etion (Df1) that models 22q11DS have reduced prepulse inhibition (PPI), a behavioral abnormality and

117 Prepulse inhibition (PPI), a form of sensorimotor gating

118 f3b-null mice also have a profound defect in prepulse inhibition (PPI), a measure of sensorimotor gat

119 whether intra-Acb amylin signaling modulates prepulse inhibition (PPI), a measure of sensorimotor gat

120 n amygdala systems that modulate startle and prepulse inhibition (PPI), an operational measure of sen

121 rlocomotion, increased stereotype, defective prepulse inhibition (PPI), and disability in nest buildi

122 ibition of startle by sensory stimuli, i.e., prepulse inhibition (PPI), and is disrupted in patients

123 function demonstrated consistent deficits in prepulse inhibition (PPI), as well as higher startle res

124 The mGlu5 KO mice showed reduced prepulse inhibition (PPI), long-term memory deficits, an

125 In prepulse inhibition (PPI), startle responses to sudden,

126 In prepulse inhibition (PPI), the startle response to a str

127 the hypothesis that PPD in rats would alter prepulse inhibition (PPI), which is an operational measu

128 ed alternation memory tasks, and deficits in prepulse inhibition (PPI).

129 sensorimotor gating deficits, as measured by prepulse inhibition (PPI).

130 automatic, preattentive sensorimotor gating (prepulse inhibition [PPI]) of the startle reflex.

131 ld-type hosts, SCZ glial mice showed reduced prepulse inhibition and abnormal behavior, including exc

132 ell-characterised neural mechanisms, such as prepulse inhibition and antisaccades, to substantially a

133 icits in translational inhibitory biomarkers-prepulse inhibition and antisaccades-that occur after sl

134 ecreased anxiety-related behavior, increased prepulse inhibition and delayed acquisition of rewarded

135 ormal cerebellar and hippocampal morphology, prepulse inhibition and fear conditioning.

136 he PDE4B(Y358C) mutation was observed in the prepulse inhibition and forced swim tests.

137 eased social interaction, and impairments in prepulse inhibition and latent inhibition.

138 rs of early auditory information processing: prepulse inhibition and mismatch negativity (MMN) in SZ

139 The comparison subjects showed greater prepulse inhibition and prepulse facilitation during the

140 nvestigated the effects of antipsychotics on prepulse inhibition and startle habituation in acutely h

141 gnosed with 90.8% accuracy using measures of prepulse inhibition and temporal sensitivity.

142 hether abnormal P50 suppression and abnormal prepulse inhibition are independent neurophysiological c

143 ) and Disc1-Q31L(+/-) offspring, and reduced prepulse inhibition at 16 but not 8 weeks of age.

144 Prepulse inhibition at the other interstimulus intervals

145 containing the human FMR1 gene had levels of prepulse inhibition comparable to WT mice, indicating no

146 iors, with male Val/Val mice exhibited lower prepulse inhibition compared with Met/Met mice, whereas

147 w rescue of key SCZ-related deficits, namely prepulse inhibition decrease, working memory impairment,

148 Mice expressing AAV-DN1 have prepulse inhibition deficits and impairments in working

149 edicated or unmedicated at admission, showed prepulse inhibition deficits compared with healthy subje

150 served as prepulses in published reports of prepulse inhibition deficits in schizophrenia.

151 hat the neurobiological substrate underlying prepulse inhibition deficits may be dysregulated during

152 d that abnormal P50 suppression and abnormal prepulse inhibition do not necessarily occur together.

153 ging and ameliorated a behavioral deficit in prepulse inhibition in adulthood in a DISC1 knockdown mo

154 lation also reduced swim test immobility and prepulse inhibition in P rats and increased locomotor st

155 Patients showed reduced P50 suppression and prepulse inhibition in relation to healthy comparison su

156 f prepulses should not contribute to reduced prepulse inhibition in schizophrenia patients versus con

157 Prepulse inhibition is a type of sensorimotor gating tha

158 y, the effector mechanisms underlying neural prepulse inhibition itself were unaffected by antagonist

159 ndings suggest that antipsychotic effects on prepulse inhibition may not be evident at a time when sc

160 ehavioral phenotypes in open-field activity, prepulse inhibition of acoustic startle response and con

161 r the effects of amphetamine (2-10 mg/kg) on prepulse inhibition of acoustic startle responses.

162 of behavioral alterations and of deficits in prepulse inhibition of acoustic startle, a measure of se

163 ated acoustic startle responses, deficits in prepulse inhibition of acoustic startle, and motor hyper

164 were also observed in locomotor activity and prepulse inhibition of acoustic startle, behaviors that

165 ia assesses the neurophysiologic measures of prepulse inhibition of acoustic startle, P50 event-relat

166 ntitative MRI, and sensorimotor gating using prepulse inhibition of startle in a subset of 12 individ

167 ed sensorimotor gating as measured using the prepulse inhibition of startle response.

168 The prepulse inhibition of startle responses by a weaker pre

169 tory tasks such as frequency discrimination, prepulse inhibition of startle responses, or fear condit

170 Changes in prepulse inhibition of startle was tested after MK-801 (

171 cits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked gamma-activit

172 weight, spontaneous locomotor activity, and prepulse inhibition of startle.

173 Recently prepulse inhibition of the acoustic startle reflex (ASR)

174 the PV neuron population, robustly impaired prepulse inhibition of the acoustic startle reflex (PPI)

175 uisition of contextual fear conditioning and prepulse inhibition of the acoustic startle reflex.

176 ften studied in humans and rodents using the prepulse inhibition of the acoustic startle response (PP

177 ine system increases locomotion and disrupts prepulse inhibition of the acoustic startle response (PP

178 Prepulse inhibition of the acoustic startle response (PP

179 typical antipsychotic clozapine and enhanced prepulse inhibition of the acoustic startle response in

180 Chemospecific ablation of THINs impairs prepulse inhibition of the acoustic startle response sug

181 ater sensitivity to a D2 agonist and smaller prepulse inhibition of the acoustic startle response tha

182 ylyl)methyl]propanamide dihydrochloride), on prepulse inhibition of the acoustic startle response.

183 ng a temporary-threshold shift model and gap-prepulse inhibition of the acoustic startle to assess ti

184 veloped tinnitus as indicated by gap-induced prepulse inhibition of the acoustic startle.

185 h as those reported in studies that measured prepulse inhibition of the human startle response and ha

186 mice deficient in TIMP-2 (knockout) exhibit prepulse inhibition of the startle reflex, suggesting de

187 We show that fear conditioning and prepulse inhibition of the startle response are also dis

188 ial P50 response to repeated stimuli and the prepulse inhibition of the startle response.

189 ivity in a novel environment and deficits in prepulse inhibition of the startle response.

190 motor gating impairments, as assessed by the prepulse inhibition of the startle.

191 were compared on a silent gap variant of the prepulse inhibition paradigm.

192 15 mg/kg, partially reversed the deficits in prepulse inhibition produced by the mutation.

193 These open-field and prepulse inhibition results suggest that the mGAT1 KO mi

194 ry avoidance, increased startle responses in prepulse inhibition tasks, and increased MK-801-induced

195 eline startle responses in the course of the prepulse inhibition test, and lower hedonic responses in

196 ss sensitive to an amphetamine disruption of prepulse inhibition than WT mice but were more sensitive

197 Prepulse inhibition was impaired in both mice and humans

198 Prepulse inhibition was measured by using a series of pr

199 Prepulse inhibition was most prominent at the 120-msec i

200 At the 500-msec interstimulus interval, prepulse inhibition was significantly but negatively cor

201 Social memory, spatial working memory and prepulse inhibition were also impaired.

202 underlie certain core deficits (startle and prepulse inhibition) that are observed in post-traumatic

203 hyperactivity; sensorimotor gating (startle prepulse inhibition) was unaffected.

204 etamine-induced hyperactivity; disruption of prepulse inhibition).

205 out mice had a sexually dimorphic deficit in prepulse inhibition, a gene dosage-dependent decrease in

206 term plasticity are linked to alterations in prepulse inhibition, a measure of sensorimotor gating.

207 the rotorod, but not to any abnormalities in prepulse inhibition, a measure of sensorimotor gating.

208 o showed overgrooming as well as deficits of prepulse inhibition, a widely used endophenotype of schi

209 iors, less depression-like conduct, impaired prepulse inhibition, amphetamine hypersensitivity, and i

210 alpha deficient mice displayed a decrease in prepulse inhibition, an increase in grooming behaviors,

211 diminished startle response, as measured by prepulse inhibition, and impaired social recognition.

212 evelopment decreased startle habituation and prepulse inhibition, and increased avoidance (particular

213 sures were startle responsivity, reactivity, prepulse inhibition, and startle habituation.

214 phenotypes, such as perseveration, disrupted prepulse inhibition, and strong withdrawal from social i

215 in a novelty-induced open field, deficits in prepulse inhibition, hypersensitivity to amphetamine, an

216 erlocomotion, restored amphetamine-disrupted prepulse inhibition, improved social behavior, and novel

217 cluding hyperlocomotor activity, deficits in prepulse inhibition, increased anxiety, impaired social

218 ld test, it restored d-amphetamine-disrupted prepulse inhibition, it induced cognitive improvements i

219 immobility in the forced swim test, reduced prepulse inhibition, mild motor coordination impairments

220 ate that BACE1(-/-) mice exhibit deficits in prepulse inhibition, novelty-induced hyperactivity, hype

221 udy, we used elevated plus-maze, startle and prepulse inhibition, open field, and novel object recogn

222 differ from each other in startle magnitude, prepulse inhibition, or habituation.

223 rate deficits in inhibition when assessed on prepulse inhibition, P50 suppression, and antisaccade pa

224 deficits in working memory, sociability, and prepulse inhibition, paralleled by locomotor hyperactivi

225 ophrenia-relevant behavioral tasks including prepulse inhibition, response to psychotomimetic drugs,

226 Prepulse inhibition, sensory gating, antisaccade, spatia

227 ion without delays, spontaneous alternation, prepulse inhibition, social interaction, anxiety-, stres

228 s displayed more climbing behavior and lower prepulse inhibition, suggesting an increase in central n

229 Transgenic mice were deficient in prepulse inhibition, which was restored by clozapine but

230 ith impaired sensorimotor gating measured by prepulse inhibition--an established endophenotype of sch

231 el and potent mechanism of sensory gating in prepulse inhibition.

232 exhibited increased sociability and impaired prepulse inhibition.

233 Rab3A or synaptotagmin 1 only show decreased prepulse inhibition.

234 d-amphetamine- and DOI-induced disruption of prepulse inhibition.

235 t mice show increased aggression and reduced prepulse inhibition.

236 tial working memory, social interaction, and prepulse inhibition.

237 revious findings, Fmr1KO mice have increased prepulse inhibition.

238 ects were tested on both P50 suppression and prepulse inhibition.

239 significantly affect startle habituation or prepulse inhibition.

240 startle response but exhibit a deficiency in prepulse inhibition.

241 A/2J mice, a strain with low basal levels of prepulse inhibition.

242 hanced susceptibility to stress and impaired prepulse inhibition.

243 ited any impairment in startle reactivity or prepulse inhibition.

244 pment of temporal processing, assessed using prepulse inhibition.

245 social interaction, locomotor activity, and prepulse inhibition.

246 Prepulse inhibiton (PPI) and P50 suppression were assess

247 e experiments examined PPI across a range of prepulse intensities (4-10 dB) and stimulus onset asynch

248 t include, among others, their dependency on prepulse intensity and duration, duration of the lead in

249 , patients exhibited PPI deficits with 60 ms prepulse intervals; these deficits were 'rescued' by amp

250 n after injection: (1) an inversion-recovery prepulse (IR-TFL) or (2) a combination of inversion-reco

251 ecovery and diffusion-based flow suppression prepulses (IR-DIFF-TFL).

252 If the inhibitory impact of a prepulse is learned, PPI should not be evident when the

253 learned, PPI should not be evident when the prepulse is the first stimulus experienced by the subjec

254 effects on PPI interacted significantly with prepulse modality, with deficient acoustic PPI but incre

255 We tested this using a prepulse of VIP during the day before a shift in either

256 slow inactivation assessed with conditioning prepulses of 100, 1000, or 10,000 milliseconds.

257 r, we examined the effect of hyperpolarizing prepulses on autaptic currents in cultured postnatal rat

258 g paper examined the effects of conditioning prepulses on the kinetics of unitary L-type Ca(2+) chann

259 ls were assessed in an acoustic attention-to-prepulse paradigm.

260 t a unique property described previously as "prepulse potentiation," in which activation by a depolar

261 that OCD patients had PPI deficits at single prepulse (PP) intensities.

262 se preceded 120 ms by an 86 dB(A) 5-ms noise prepulse (pp+P).

263 startling stimulus is preceded by a weaker "prepulse." PPI has been found to be altered in patients

264 These findings suggest that hyperpolarizing prepulses preferentially enhance eacs over iacs, and tha

265 Strongly depolarizing prepulses produced an increased frequency of long-durati

266 inhibition was measured by using a series of prepulse-pulse pairs with interstimulus intervals rangin

267 Moderate-depolarizing prepulses resulted in a decrease in the probability of o

268 In addition, hyperpolarizing prepulses revealed a slow eac even after the slow eac ev

269 sodium channel inactivation, hyperpolarizing prepulses reversibly increased fast excitatory autaptic

270 nsitivity to the motor-activating effects of prepulses should not contribute to reduced prepulse inhi

271 Results without a prepulse showed an evolution of N1 amplitudes, increasin

272 (120 dB) alone or preceded 100 ms earlier by prepulse stimuli (3, 6 or 12 dB above 70 dB ambient nois

273 drug effects on startle magnitude without a prepulse stimulus.

274 e responses in 30 of 49 (61%) units when the prepulse-stimulus interval was 1 sec but were ineffectiv

275 The prepulse-stimulus interval was either 1 or 5 sec, during

276 st inactivation studied with 100-millisecond prepulses, suggesting binding to fast-inactivated states

277 Taste prepulses suppressed (or enhanced) subsequent taste resp

278 e response (PPI) model, in which an acoustic prepulse suppresses behavioral output to a startle-induc

279 processes that can be studied using the NH4+ prepulse technique.

280 A depolarizing prepulse to 0 mV reversed THC inhibition of I(Ca), but r

281 First, we inactivated I(Na) using a ramp prepulse to 45 mV.

282 We found that a brief prepulse to voltages near spike threshold evokes the axo

283 LVA could be fully inactivated by prepulses to -50 mV and was partially amiloride sensitiv

284 age, frequency, and duration of conditioning prepulses to provide access to closed, open, and fast- o

285 ded, ignored, and novel tones that served as prepulse tones.

286 Results from prepulse trials only showed noteworthy changes in peak-t

287 The prepulse was a "speaker swap" (SSwap), shifting a noise

288 eac even after the slow eac evoked without a prepulse was completely blocked by the open channel bloc

289 the rate of acid recovery following NH(4)(+) prepulse was decreased significantly (27%) by SLC4A11 si

290 magnitude increased from Trial 1 to 2 if no prepulse was presented (control order).

291 Kv1.1; however, spike modulation by somatic prepulses was abolished.

292 ith the control order, startle inhibition by prepulses was evident in both Orders 1 and 2, and was mo

293 ependent potentiation by strong depolarizing prepulses was reduced in mdx myocytes but could be resto

294 Conditioning prepulses were applied across a wide range of voltages t

295 In 19 (39%) of the units tested, effects of prepulses were large enough to change the order of effec

296 tical pyramidal neurons in slices, using the prepulse, were found to have voltage dependence nearly i

297 Pulses of taste stimuli, called prepulses, were followed by a 3 sec presentation of the

298 data during and after delivery of an ammonia prepulse, which induces an acid load within the cell.

299 of recovery from short and long depolarizing prepulses, which, under drug-free conditions, recruited

300 ivated CTL-mediated killing in vitro only if prepulsed with cognate peptide, or if beta-gal-expressin