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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
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
28 by using a gradient-echo sequence with an MT prepulse and systematic variation of the off-resonance f
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
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
39 so take into account the perturbation that a prepulse challenge brings to the cytoplasmic acid buffer
41 d power significantly increased in the 70 dB prepulse condition and significantly decreased in the 11
46 itation during the attended than the ignored prepulses, demonstrating early and later attentional mod
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
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
58 ents, such as slowed activation kinetics and prepulse facilitation, were not observed for the mutated
63 studies in dissociated neurons show that the prepulse has no visible effect on the voltage dependence
65 this preliminary patient study, the dual IR prepulse improved contrast, scar visualization, and expe
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
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
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
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
93 , and deficits in spatial working memory and prepulse inhibition (PPI) of acoustic startle in Grin1 m
95 rally active causing a dramatic reduction in prepulse inhibition (PPI) of acoustic startle response.
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
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
107 ulation of the dopamine (DA) system disrupts 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
113 important measure of sensorimotor gating is prepulse inhibition (PPI) of the startle response, impai
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
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
128 the hypothesis that PPD in rats would alter prepulse inhibition (PPI), which is an operational measu
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
138 rs of early auditory information processing: prepulse inhibition and mismatch negativity (MMN) in SZ
141 hether abnormal P50 suppression and abnormal prepulse inhibition are independent neurophysiological c
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,
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.
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
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
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
168 tory tasks such as frequency discrimination, prepulse inhibition of startle responses, or fear condit
170 cits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked gamma-activit
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
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
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
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
200 At the 500-msec interstimulus interval, prepulse inhibition was significantly but negatively cor
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
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,
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
229 ith impaired sensorimotor gating measured by prepulse inhibition--an established endophenotype of sch
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
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
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
261 t a unique property described previously as "prepulse potentiation," in which activation by a depolar
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
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
272 (120 dB) alone or preceded 100 ms earlier by prepulse stimuli (3, 6 or 12 dB above 70 dB ambient nois
274 e responses in 30 of 49 (61%) units when the prepulse-stimulus interval was 1 sec but were ineffectiv
276 st inactivation studied with 100-millisecond prepulses, suggesting binding to fast-inactivated states
278 e response (PPI) model, in which an acoustic prepulse suppresses behavioral output to a startle-induc
284 age, frequency, and duration of conditioning prepulses to provide access to closed, open, and fast- o
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
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
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
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