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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 me extent with and without a hyperpolarizing prepulse.
7 imulus is preceded by a weaker stimulus--the prepulse.
8 ter carboxyl termini were less affected by a prepulse.
9 f deactivation in response to a depolarizing prepulse.
10 r acidification induced by ammonium chloride prepulse.
11 extrinsic inhibition produced by an auditory prepulse.
12 VSMCs of mesenteric arteries after an NH4(+) prepulse.
13 otentials but only after strong depolarizing prepulses.
14 ition is not relieved by strong depolarizing prepulses.
15  SR field EPSP slopes were unaffected by SLM prepulses.
16  of PPI in rats using motivationally salient prepulses.
17 r prolongation by brief depolarizing somatic prepulses.
18  facilitated nearly normally by depolarizing prepulses.
19 li both in the presence and absence of 70 dB prepulses.
20 e-independent and unaffected by depolarizing prepulses.
21 ent and transiently relieved by depolarizing prepulses.
22  elevating [Ca(2)(+)](c) with a conditioning prepulse (-15 mV, 2 s) inactivated I(Ca) measured during
23 yramidal neurons, which was inhibited by SLM prepulses (150-225 ms).
24 ation of Ca(v)1.3 currents by a conditioning prepulse, a process known as voltage-dependent facilitat
25 cell model with depolarizing/hyperpolarizing prepulses allowed us to highlight time dependency of the
26 n the CS(+) group, particularly with a 10-dB prepulse and a 60-ms SOA.
27                                              Prepulse and non-prepulse conditions were then compared
28 by using a gradient-echo sequence with an MT prepulse and systematic variation of the off-resonance f
29 s, which were potentiated by hyperpolarizing prepulses and inhibited by Cd2+ (200-500 microm).
30 er masking the TCR with either continuous or prepulsed anti-Valpha3.2 Ab, 2D2 cells were immediately
31 ERG currents at a mild pulse shortly after a prepulse at 37 degrees C, but not so much at 22 degrees
32 s voltage-dependent, and strong depolarizing prepulses attenuated Hm-3 activity.
33                   Most commonly, NaCl or HCl prepulses attenuated the response to quinine.
34                              Hyperpolarizing prepulses augmented nearly all fast and slow eacs but on
35 laced using a whole-cell ammonium or acetate prepulse, before locally applying the low dose of ammoni
36 arned component to the inhibitory effects of prepulses, but this issue has yet to be fully investigat
37 tivated Ca(2+) channels in that depolarizing prepulses can regulate their activity, and their carboxy
38                              Strong positive prepulses can reverse the inhibitory effect of ProTx-II,
39 so take into account the perturbation that a prepulse challenge brings to the cytoplasmic acid buffer
40 late pH and volume regulation during a NH4Cl prepulse challenge.
41 d power significantly increased in the 70 dB prepulse condition and significantly decreased in the 11
42 on and significantly decreased in the 110 dB prepulse condition.
43                                              Prepulse conditions significantly decreased the amplitud
44                             Prepulse and non-prepulse conditions were then compared using peak amplit
45 a dose-dependent decline in startle rates in prepulse conditions.
46 itation during the attended than the ignored prepulses, demonstrating early and later attentional mod
47                     Finally, hyperpolarizing prepulses did not alter currents evoked by exogenous app
48                     Of note, hyperpolarizing prepulses did not significantly reduce autaptic currents
49                                    Thus, the prepulse-driven shift into mode 2 gating results in a lo
50 t persists independently of the depolarizing prepulse duration and remains in the presence of 4-amino
51 ompartmental model support the idea that the prepulse effectively inactivates currents from the axon
52 nd, more powerful PPI mechanism in Tritonia: prepulse-elicited conduction block of action potentials
53                                    Using the prepulse facilitation (PPF) test, we further examined ch
54 jects showed greater prepulse inhibition and prepulse facilitation during the attended than the ignor
55 fects on inhibition of Ca(2+) current and on prepulse facilitation in the presence of somatostatin to
56 tantially reduced the low level of intrinsic prepulse facilitation present at the basal level of G pr
57 ) curves, and conferred differing degrees of prepulse facilitation to the channel.
58 ents, such as slowed activation kinetics and prepulse facilitation, were not observed for the mutated
59                                              Prepulse facilitation, which is a characteristic of volt
60 ersed by strong depolarization, resulting in prepulse facilitation.
61 bunits (Gbetagamma) are required for maximal prepulse facilitation.
62            ASRs were evoked by noise bursts; prepulses for PPI were 70 dB sound pressure level tones
63 studies in dissociated neurons show that the prepulse has no visible effect on the voltage dependence
64                       The presence of a mild prepulse immediately before the main pulse inhibits star
65  this preliminary patient study, the dual IR prepulse improved contrast, scar visualization, and expe
66 nse in zebrafish larvae is modulated by weak prepulses in a manner similar to mammalian PPI.
67 ects of weak acoustic stimuli that served as prepulses in published reports of prepulse inhibition de
68 ssed PPI using acoustic, tactile, and visual prepulses in young (4 month) and old (23 month) C57BL/6N
69  effect is dominating and, consequently, the prepulse inactivation curves exhibit depolarizing shifts
70 Ca(2+) channel kinetics, voltage dependence, prepulse inactivation, or G protein inhibition but was a
71 strocytes, and pHi recovery from an ammonium prepulse-induced acid load in neurons.
72 peeds neuronal pHi recovery from an ammonium prepulse-induced acid load.
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 se in fear conditioning (FC), a reduction in prepulse inhibition (PPI) in the KO animal, along with a
88                          Clozapine increased prepulse inhibition (PPI) in wild-type mice.
89                                              Prepulse inhibition (PPI) is an example of sensorimotor
90                                              Prepulse inhibition (PPI) is an operational measure of s
91                                              Prepulse inhibition (PPI) is an operational measure of s
92                                              Prepulse inhibition (PPI) is an operational measure of s
93 , and deficits in spatial working memory and prepulse inhibition (PPI) of acoustic startle in Grin1 m
94                                              Prepulse inhibition (PPI) of acoustic startle is a genet
95 rally active causing a dramatic reduction in prepulse inhibition (PPI) of acoustic startle response.
96                                              Prepulse inhibition (PPI) of startle is being explored b
97                                   In humans, prepulse inhibition (PPI) of startle is greater during a
98                                              Prepulse inhibition (PPI) of startle is impaired in schi
99 t deficient sensorimotor gating (measured by prepulse inhibition (PPI) of startle) and mismatch negat
100 ensory gating of auditory evoked potentials, prepulse inhibition (PPI) of startle, and startle amplit
101 ry spatial acuity was measured in mice using prepulse inhibition (PPI) of the acoustic startle reflex
102                                              Prepulse inhibition (PPI) of the acoustic startle reflex
103 tive probe associated with this circuitry is prepulse inhibition (PPI) of the acoustic startle respon
104 d schizophrenia patients exhibit deficits in prepulse inhibition (PPI) of the acoustic startle respon
105          Sensorimotor gating was measured by prepulse inhibition (PPI) of the acoustic startle respon
106                         Rats were tested for prepulse inhibition (PPI) of the acoustic startle respon
107 ulation of the dopamine (DA) system disrupts prepulse inhibition (PPI) of the acoustic startle respon
108                     In animals, LSD disrupts prepulse inhibition (PPI) of the acoustic startle respon
109            Translational biomarkers, such as prepulse inhibition (PPI) of the acoustic startle respon
110                                              Prepulse inhibition (PPI) of the acoustic startle respon
111 e than Long Evans (LE) rats to disruption of prepulse inhibition (PPI) of the startle reflex by the d
112                                              Prepulse inhibition (PPI) of the startle reflex has been
113  important measure of sensorimotor gating is prepulse inhibition (PPI) of the startle response, impai
114 nformation, a process which is studied using prepulse inhibition (PPI) of the startle response.
115                                              Prepulse inhibition (PPI) refers to a reduction in the s
116 ity, impaired working memory, and deficit in prepulse inhibition (PPI) that was ameliorated by diazep
117 etion (Df1) that models 22q11DS have reduced prepulse inhibition (PPI), a behavioral abnormality and
118                                              Prepulse inhibition (PPI), a form of sensorimotor gating
119 f3b-null mice also have a profound defect in prepulse inhibition (PPI), a measure of sensorimotor gat
120 whether intra-Acb amylin signaling modulates prepulse inhibition (PPI), a measure of sensorimotor gat
121 n amygdala systems that modulate startle and prepulse inhibition (PPI), an operational measure of sen
122 rlocomotion, increased stereotype, defective prepulse inhibition (PPI), and disability in nest buildi
123 ibition of startle by sensory stimuli, i.e., prepulse inhibition (PPI), and is disrupted in patients
124 function demonstrated consistent deficits in prepulse inhibition (PPI), as well as higher startle res
125             The mGlu5 KO mice showed reduced prepulse inhibition (PPI), long-term memory deficits, an
126                                           In prepulse inhibition (PPI), startle responses to sudden,
127                                           In prepulse inhibition (PPI), the startle response to a str
128  the hypothesis that PPD in rats would alter prepulse inhibition (PPI), which is an operational measu
129 ed alternation memory tasks, and deficits in prepulse inhibition (PPI).
130 sensorimotor gating deficits, as measured by prepulse inhibition (PPI).
131 automatic, preattentive sensorimotor gating (prepulse inhibition [PPI]) of the startle reflex.
132 ld-type hosts, SCZ glial mice showed reduced prepulse inhibition and abnormal behavior, including exc
133 ell-characterised neural mechanisms, such as prepulse inhibition and antisaccades, to substantially a
134 icits in translational inhibitory biomarkers-prepulse inhibition and antisaccades-that occur after sl
135 ecreased anxiety-related behavior, increased prepulse inhibition and delayed acquisition of rewarded
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 gnosed with 90.8% accuracy using measures of prepulse inhibition and temporal sensitivity.
141 hether abnormal P50 suppression and abnormal prepulse inhibition are independent neurophysiological c
142 ) and Disc1-Q31L(+/-) offspring, and reduced prepulse inhibition at 16 but not 8 weeks of age.
143                                              Prepulse inhibition at the other interstimulus intervals
144      AICP did not affect basal locomotion or prepulse inhibition but facilitated MK-801-induced hyper
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  served as prepulses in published reports of prepulse inhibition deficits in schizophrenia.
150 hat the neurobiological substrate underlying prepulse inhibition deficits may be dysregulated during
151 d that abnormal P50 suppression and abnormal prepulse inhibition do not necessarily occur together.
152            First, we observed a reduction of prepulse inhibition in A(2A)R knockout mice, similar to
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 ehavioral phenotypes in open-field activity, prepulse inhibition of acoustic startle response and con
160 r the effects of amphetamine (2-10 mg/kg) on prepulse inhibition of acoustic startle responses.
161 of behavioral alterations and of deficits in prepulse inhibition of acoustic startle, a measure of se
162 ated acoustic startle responses, deficits in prepulse inhibition of acoustic startle, and motor hyper
163 were also observed in locomotor activity and prepulse inhibition of acoustic startle, behaviors that
164 ia assesses the neurophysiologic measures of prepulse inhibition of acoustic startle, P50 event-relat
165 osure had the largest effect on activity and prepulse inhibition of startle 1-week post-irradiation t
166 ed sensorimotor gating as measured using the prepulse inhibition of startle response.
167                                          The prepulse inhibition of startle responses by a weaker pre
168 tory tasks such as frequency discrimination, prepulse inhibition of startle responses, or fear condit
169                                   Changes in prepulse inhibition of startle was tested after MK-801 (
170 cits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked gamma-activit
171  weight, spontaneous locomotor activity, and prepulse inhibition of startle.
172                                     Recently prepulse inhibition of the acoustic startle reflex (ASR)
173  the PV neuron population, robustly impaired prepulse inhibition of the acoustic startle reflex (PPI)
174 uisition of contextual fear conditioning and prepulse inhibition of the acoustic startle reflex.
175 ften studied in humans and rodents using the prepulse inhibition of the acoustic startle response (PP
176 ine system increases locomotion and disrupts prepulse inhibition of the acoustic startle response (PP
177                                              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                                              Prepulse inhibition of the acoustic startling reflex (PP
186  mice deficient in TIMP-2 (knockout) exhibit prepulse inhibition of the startle reflex, suggesting de
187 min (PV)-positive GABAergic, neurons reduced prepulse inhibition of the startle response (PPI) and en
188 ivity in a novel environment and deficits in prepulse inhibition of the startle response.
189 ial P50 response to repeated stimuli and the 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 ceptor channel blocker produced a deficit in prepulse inhibition which was prevented by a GluN2C/2D p
203  underlie certain core deficits (startle and prepulse inhibition) that are observed in post-traumatic
204  hyperactivity; sensorimotor gating (startle prepulse inhibition) was unaffected.
205 etamine-induced hyperactivity; disruption of prepulse inhibition).
206 out mice had a sexually dimorphic deficit in prepulse inhibition, a gene dosage-dependent decrease in
207 term plasticity are linked to alterations in prepulse inhibition, a measure of sensorimotor gating.
208 the rotorod, but not to any abnormalities in prepulse inhibition, a measure of sensorimotor gating.
209 o showed overgrooming as well as deficits of prepulse inhibition, a widely used endophenotype of schi
210 iors, less depression-like conduct, impaired prepulse inhibition, amphetamine hypersensitivity, and i
211 alpha deficient mice displayed a decrease in prepulse inhibition, an increase in grooming behaviors,
212  diminished startle response, as measured by prepulse inhibition, and impaired social recognition.
213 evelopment decreased startle habituation and prepulse inhibition, and increased avoidance (particular
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 rate deficits in inhibition when assessed on prepulse inhibition, P50 suppression, and antisaccade pa
223 deficits in working memory, sociability, and prepulse inhibition, paralleled by locomotor hyperactivi
224 ophrenia-relevant behavioral tasks including prepulse inhibition, response to psychotomimetic drugs,
225                                              Prepulse inhibition, sensory gating, antisaccade, spatia
226 ion without delays, spontaneous alternation, prepulse inhibition, social interaction, anxiety-, stres
227 s displayed more climbing behavior and lower prepulse inhibition, suggesting an increase in central n
228            Transgenic mice were deficient in prepulse inhibition, which was restored by clozapine but
229 ith impaired sensorimotor gating measured by prepulse inhibition--an established endophenotype of sch
230  social interaction, locomotor activity, and prepulse inhibition.
231 el and potent mechanism of sensory gating in prepulse inhibition.
232 exhibited increased sociability and impaired prepulse inhibition.
233  altered forebrain development and decreased prepulse inhibition.
234 Rab3A or synaptotagmin 1 only show decreased prepulse inhibition.
235 d-amphetamine- and DOI-induced disruption of prepulse inhibition.
236 t mice show increased aggression and reduced prepulse inhibition.
237 tial working memory, social interaction, and prepulse inhibition.
238 revious findings, Fmr1KO mice have increased prepulse inhibition.
239 ects were tested on both P50 suppression and prepulse inhibition.
240  significantly affect startle habituation or prepulse inhibition.
241 startle response but exhibit a deficiency in prepulse inhibition.
242 A/2J mice, a strain with low basal levels of prepulse inhibition.
243 hanced susceptibility to stress and impaired prepulse inhibition.
244 ited any impairment in startle reactivity or prepulse inhibition.
245 pment of temporal processing, assessed using 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 ne potential following 40 mV hyperpolarising prepulses of 50 ms duration.
258 r, we examined the effect of hyperpolarizing prepulses on autaptic currents in cultured postnatal rat
259 g paper examined the effects of conditioning prepulses on the kinetics of unitary L-type Ca(2+) chann
260 ls were assessed in an acoustic attention-to-prepulse paradigm.
261 t a unique property described previously as "prepulse potentiation," in which activation by a depolar
262 that OCD patients had PPI deficits at single prepulse (PP) intensities.
263 se preceded 120 ms by an 86 dB(A) 5-ms noise prepulse (pp+P).
264  startling stimulus is preceded by a weaker "prepulse." PPI has been found to be altered in patients
265  These findings suggest that hyperpolarizing prepulses preferentially enhance eacs over iacs, and tha
266 inhibition was measured by using a series of prepulse-pulse pairs with interstimulus intervals rangin
267 response to hyperpolarizing and depolarizing prepulses, respectively, whereas other models showed neg
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

 
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