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1 etamine-induced hyperactivity; disruption of prepulse inhibition).
2 revious findings, Fmr1KO mice have increased prepulse inhibition.
3 hanced susceptibility to stress and impaired prepulse inhibition.
4 ects were tested on both P50 suppression and prepulse inhibition.
5 significantly affect startle habituation or prepulse inhibition.
6 startle response but exhibit a deficiency in prepulse inhibition.
7 A/2J mice, a strain with low basal levels of prepulse inhibition.
8 ited any impairment in startle reactivity or prepulse inhibition.
9 pment of temporal processing, assessed using prepulse inhibition.
10 s, motor coordination, pain sensitivity, and prepulse inhibition.
11 vant to exploratory locomotion, startle, and prepulse inhibition.
12 erstimulus interval, stimulus intensity, and prepulse inhibition.
13 more evident in measures of right eye-blink prepulse inhibition.
14 ersonality disorder showed less asymmetry of prepulse inhibition.
15 enic patients showing the expected deficient prepulse inhibition.
16 ng was examined operationally via the use of prepulse inhibition.
17 of neurotensin had no significant effect on prepulse inhibition.
18 social interaction, locomotor activity, and prepulse inhibition.
19 el and potent mechanism of sensory gating in prepulse inhibition.
20 exhibited increased sociability and impaired prepulse inhibition.
21 Rab3A or synaptotagmin 1 only show decreased prepulse inhibition.
22 d-amphetamine- and DOI-induced disruption of prepulse inhibition.
23 t mice show increased aggression and reduced prepulse inhibition.
24 tial working memory, social interaction, and prepulse inhibition.
25 23), sensorimotor dexterity (2q24 and 2q32), prepulse inhibition (5p15), the California Verbal Learni
26 out mice had a sexually dimorphic deficit in prepulse inhibition, a gene dosage-dependent decrease in
27 the rotorod, but not to any abnormalities in prepulse inhibition, a measure of sensorimotor gating.
28 term plasticity are linked to alterations in prepulse inhibition, a measure of sensorimotor gating.
29 o showed overgrooming as well as deficits of prepulse inhibition, a widely used endophenotype of schi
30 iors, less depression-like conduct, impaired prepulse inhibition, amphetamine hypersensitivity, and i
31 alpha deficient mice displayed a decrease in prepulse inhibition, an increase in grooming behaviors,
32 ith impaired sensorimotor gating measured by prepulse inhibition--an established endophenotype of sch
33 ld-type hosts, SCZ glial mice showed reduced prepulse inhibition and abnormal behavior, including exc
34 ell-characterised neural mechanisms, such as prepulse inhibition and antisaccades, to substantially a
35 icits in translational inhibitory biomarkers-prepulse inhibition and antisaccades-that occur after sl
36 ecreased anxiety-related behavior, increased prepulse inhibition and delayed acquisition of rewarded
39 se and adaptability of the startle response (prepulse inhibition and habituation) have been observed
41 rs of early auditory information processing: prepulse inhibition and mismatch negativity (MMN) in SZ
43 nvestigated the effects of antipsychotics on prepulse inhibition and startle habituation in acutely h
47 diminished startle response, as measured by prepulse inhibition, and impaired social recognition.
48 evelopment decreased startle habituation and prepulse inhibition, and increased avoidance (particular
50 phenotypes, such as perseveration, disrupted prepulse inhibition, and strong withdrawal from social i
51 of SKF 81297 to disrupt acoustic startle and prepulse inhibition appeared to be attenuated in D5-/- m
52 hether abnormal P50 suppression and abnormal prepulse inhibition are independent neurophysiological c
55 containing the human FMR1 gene had levels of prepulse inhibition comparable to WT mice, indicating no
56 iors, with male Val/Val mice exhibited lower prepulse inhibition compared with Met/Met mice, whereas
59 w rescue of key SCZ-related deficits, namely prepulse inhibition decrease, working memory impairment,
61 edicated or unmedicated at admission, showed prepulse inhibition deficits compared with healthy subje
65 hat the neurobiological substrate underlying prepulse inhibition deficits may be dysregulated during
66 should probably focus on the relationship of prepulse inhibition deficits to measures such as thought
67 s robust as that in previous reports linking prepulse inhibition deficits with other measures, such a
68 patients with schizophrenia would also have prepulse inhibition deficits, thereby reflecting a genet
69 conditions, schizophrenia-linked deficits in prepulse inhibition detected with a relatively strong pr
70 that produce an enhanced sensitivity to the prepulse inhibition-disruptive effects of the DA agonist
71 d that abnormal P50 suppression and abnormal prepulse inhibition do not necessarily occur together.
72 the rotarod test, acoustic startle response, prepulse inhibition, elevated plus-maze, light <--> dark
73 DCN induces hearing using a novel electrical prepulse inhibition (ePPI) of startle reflex behavior mo
76 in a novelty-induced open field, deficits in prepulse inhibition, hypersensitivity to amphetamine, an
77 nce reflects a common endophenotype and that prepulse inhibition identifies a separate endophenotype
78 erlocomotion, restored amphetamine-disrupted prepulse inhibition, improved social behavior, and novel
80 ging and ameliorated a behavioral deficit in prepulse inhibition in adulthood in a DISC1 knockdown mo
81 lation also reduced swim test immobility and prepulse inhibition in P rats and increased locomotor st
82 Patients showed reduced P50 suppression and prepulse inhibition in relation to healthy comparison su
83 f prepulses should not contribute to reduced prepulse inhibition in schizophrenia patients versus con
84 cluding hyperlocomotor activity, deficits in prepulse inhibition, increased anxiety, impaired social
86 ld test, it restored d-amphetamine-disrupted prepulse inhibition, it induced cognitive improvements i
87 y, the effector mechanisms underlying neural prepulse inhibition itself were unaffected by antagonist
88 impaired neurovascular coupling; attenuated prepulse inhibition (males); and hyperkinetic behavior.
89 ndings suggest that antipsychotic effects on prepulse inhibition may not be evident at a time when sc
90 ndently accounted for 60% of the variance in prepulse inhibition measures and contributed 35% of the
91 immobility in the forced swim test, reduced prepulse inhibition, mild motor coordination impairments
92 ate that BACE1(-/-) mice exhibit deficits in prepulse inhibition, novelty-induced hyperactivity, hype
94 ing was abnormal, as measured by deficits in prepulse inhibition of acoustic and tactile startle.
95 ehavioral phenotypes in open-field activity, prepulse inhibition of acoustic startle response and con
97 of behavioral alterations and of deficits in prepulse inhibition of acoustic startle, a measure of se
98 ated acoustic startle responses, deficits in prepulse inhibition of acoustic startle, and motor hyper
99 were also observed in locomotor activity and prepulse inhibition of acoustic startle, behaviors that
100 ia assesses the neurophysiologic measures of prepulse inhibition of acoustic startle, P50 event-relat
102 ntitative MRI, and sensorimotor gating using prepulse inhibition of startle in a subset of 12 individ
105 tory tasks such as frequency discrimination, prepulse inhibition of startle responses, or fear condit
107 cits in auditory-evoked response adaptation, prepulse inhibition of startle, and evoked gamma-activit
108 startle amplitudes and similar magnitudes of prepulse inhibition of startle, suggesting that CREBalph
111 the PV neuron population, robustly impaired prepulse inhibition of the acoustic startle reflex (PPI)
112 uisition of contextual fear conditioning and prepulse inhibition of the acoustic startle reflex.
113 ine system increases locomotion and disrupts prepulse inhibition of the acoustic startle response (PP
115 ften studied in humans and rodents using the prepulse inhibition of the acoustic startle response (PP
116 typical antipsychotic clozapine and enhanced prepulse inhibition of the acoustic startle response in
117 Chemospecific ablation of THINs impairs prepulse inhibition of the acoustic startle response sug
118 ater sensitivity to a D2 agonist and smaller prepulse inhibition of the acoustic startle response tha
119 ylyl)methyl]propanamide dihydrochloride), on prepulse inhibition of the acoustic startle response.
120 ng a temporary-threshold shift model and gap-prepulse inhibition of the acoustic startle to assess ti
122 e normal comparison subjects were tested for prepulse inhibition of the eyeblink component of the sta
123 h as those reported in studies that measured prepulse inhibition of the human startle response and ha
124 potential was significantly correlated with prepulse inhibition of the P13 potential, the N40 potent
125 These results demonstrate the presence of prepulse inhibition of the P13 potential, the N40 potent
126 prepulse intensity and the background level, prepulse inhibition of the SR was reduced or absent whil
127 mice deficient in TIMP-2 (knockout) exhibit prepulse inhibition of the startle reflex, suggesting de
129 -HT)2A receptors are known to be involved in prepulse inhibition of the startle response (PPI), a mea
131 er, heterozygous mice display an increase in prepulse inhibition of the startle response, a manifesta
137 udy, we used elevated plus-maze, startle and prepulse inhibition, open field, and novel object recogn
139 rate deficits in inhibition when assessed on prepulse inhibition, P50 suppression, and antisaccade pa
142 deficits in working memory, sociability, and prepulse inhibition, paralleled by locomotor hyperactivi
143 digm, while hearing status was assessed with prepulse inhibition (PPI) and auditory brainstem respons
144 hors introduce a real-time model of acoustic prepulse inhibition (PPI) and facilitation (PPF) in anim
145 f IL-6 on day 12.5 of mouse pregnancy causes prepulse inhibition (PPI) and latent inhibition (LI) def
149 nd lead times (20-40 ms) and was replaced by prepulse inhibition (PPI) for higher values, especially
150 ring on startle reactivity, habituation, and prepulse inhibition (PPI) in male Lewis, Sprague-Dawley,
152 autism, these offspring display deficits in prepulse inhibition (PPI) in the acoustic startle respon
158 ty to dopamine agonist-induced disruption of prepulse inhibition (PPI) may be a useful model for the
162 rally active causing a dramatic reduction in prepulse inhibition (PPI) of acoustic startle response.
163 tactile startle as well as the magnitude of prepulse inhibition (PPI) of both tactile and acoustic s
167 t deficient sensorimotor gating (measured by prepulse inhibition (PPI) of startle) and mismatch negat
168 ensory gating of auditory evoked potentials, prepulse inhibition (PPI) of startle, and startle amplit
169 vestigated whether individual differences in prepulse inhibition (PPI) of the acoustic startle reflex
170 examine core and shell function, we measured prepulse inhibition (PPI) of the acoustic startle reflex
172 ry spatial acuity was measured in mice using prepulse inhibition (PPI) of the acoustic startle reflex
174 ulation of the dopamine (DA) system disrupts prepulse inhibition (PPI) of the acoustic startle respon
175 locomotor activity in a novel open field and prepulse inhibition (PPI) of the acoustic startle respon
179 tive probe associated with this circuitry is prepulse inhibition (PPI) of the acoustic startle respon
180 d schizophrenia patients exhibit deficits in prepulse inhibition (PPI) of the acoustic startle respon
182 e than Long Evans (LE) rats to disruption of prepulse inhibition (PPI) of the startle reflex by the d
186 deficient sensorimotor gating as measured by prepulse inhibition (PPI) of the startle response, exhib
187 important measure of sensorimotor gating is prepulse inhibition (PPI) of the startle response, impai
189 ed into the nucleus accumbens of rats on the prepulse inhibition (PPI) of their acoustic startle refl
191 ity, impaired working memory, and deficit in prepulse inhibition (PPI) that was ameliorated by diazep
193 nt is preceded by a stimulus; this is called prepulse inhibition (PPI) when the prestimulus is weak a
194 etion (Df1) that models 22q11DS have reduced prepulse inhibition (PPI), a behavioral abnormality and
196 f3b-null mice also have a profound defect in prepulse inhibition (PPI), a measure of sensorimotor gat
197 whether intra-Acb amylin signaling modulates prepulse inhibition (PPI), a measure of sensorimotor gat
200 n amygdala systems that modulate startle and prepulse inhibition (PPI), an operational measure of sen
201 rlocomotion, increased stereotype, defective prepulse inhibition (PPI), and disability in nest buildi
202 ibition of startle by sensory stimuli, i.e., prepulse inhibition (PPI), and is disrupted in patients
203 function demonstrated consistent deficits in prepulse inhibition (PPI), as well as higher startle res
207 the hypothesis that PPD in rats would alter prepulse inhibition (PPI), which is an operational measu
213 oups differed significantly in the amount of prepulse inhibition produced by the 16-dB prepulse, with
215 or the improvement or whether differences in prepulse inhibition reflect other factors, such as acuit
216 zotypal personality disorder all had reduced prepulse inhibition relative to comparison subjects, and
217 ophrenia-relevant behavioral tasks including prepulse inhibition, response to psychotomimetic drugs,
219 suggest a genetically transmitted deficit in prepulse inhibition (sensorimotor gating) in patients wi
221 testing in a carefully designed combined P50/prepulse inhibition session using stimulus characteristi
222 ion without delays, spontaneous alternation, prepulse inhibition, social interaction, anxiety-, stres
223 s displayed more climbing behavior and lower prepulse inhibition, suggesting an increase in central n
224 ry avoidance, increased startle responses in prepulse inhibition tasks, and increased MK-801-induced
225 eline startle responses in the course of the prepulse inhibition test, and lower hedonic responses in
226 ss sensitive to an amphetamine disruption of prepulse inhibition than WT mice but were more sensitive
227 underlie certain core deficits (startle and prepulse inhibition) that are observed in post-traumatic
228 ficits in sensorimotor gating as measured by prepulse inhibition, to the authors' knowledge P50 senso
235 At the 500-msec interstimulus interval, prepulse inhibition was significantly but negatively cor
239 in previous experiments, P50 suppression and prepulse inhibition were not significantly correlated.
240 nstrated greater right versus left eye-blink prepulse inhibition, whereas the probands, their relativ
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