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Journal articles on the topic 'Prepulse inhibition'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Weike, Almut I., Alfons O. Hamm, and Dieter Vaitl. "Sensorimotor Gating and Attitudes Related to Schizotypal Proneness." Psychological Reports 88, no. 3_suppl (June 2001): 1035–45. http://dx.doi.org/10.2466/pr0.2001.88.3c.1035.

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The magnitude of the startle eyeblink response is diminished when the startle-eliciting probe is shortly preceded by another stimulus. This so called prepulse inhibition is interpreted as an automatic sensorimotor gating mechanism. There is substantial support for prepulse inhibition deficits in subjects suffering from schizophrenia spectrum disorders and in psychosis-prone normals as well. Thus, prepulse inhibition deficits may reflect vulnerability on the hypothesized psychopathological continuum from “normal” to “schizophrenia.” The present experiment investigated the amount of prepulse inhibition in a sample selected for “belief in extraordinary phenomena,” an attitude related to measures of psychosis-proneness. Believers and skeptics were tested in an acoustic prepulse-inhibition paradigm. As expected, presentation of prepulses clearly diminished magnitude of startle response, with greatest inhibition effects gained by lead intervals of 60 and 120 msec. Patterns of response were identical for believers and skeptics, i.e., attitude towards extraordinary phenomena did not seem to be related to functional information-processing deficits as has been observed in psychosis-prone normals.

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2

Kawano, Yasuhiro, Eishi Motomura, Koji Inui, and Motohiro Okada. "Effects of Magnitude of Leading Stimulus on Prepulse Inhibition of Auditory Evoked Cerebral Responses: An Exploratory Study." Life 11, no. 10 (September 28, 2021): 1024. http://dx.doi.org/10.3390/life11101024.

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An abrupt change in a sound feature (test stimulus) elicits a specific cerebral response, which is attenuated by a weaker sound feature change (prepulse) preceding the test stimulus. As an exploratory study, we investigated whether and how the magnitude of the change of the prepulse affects the degree of prepulse inhibition (PPI). Sound stimuli were 650 ms trains of clicks at 100 Hz. The test stimulus was an abrupt sound pressure increase (by 10 dB) in the click train. Three consecutive clicks, weaker (−5 dB, −10 dB, −30 dB, or gap) than the baseline, at 30, 40, and 50 ms before the test stimulus, were used as prepulses. Magnetic responses to the ten types of stimuli (test stimulus alone, control, four types of tests with prepulses, and four types of prepulses alone) were recorded in 10 healthy subjects. The change-related N1m component, peaking at approximately 130 ms, and its PPI were investigated. The degree of PPI caused by the −5 dB prepulse was significantly weaker than that caused by other prepulses. The degree of PPI caused by further decreases in prepulse magnitude showed a plateau level between the −10 dB and gap prepulses. The results suggest that there is a physiologically significant range of sensory changes for PPI, which plays a role in the change detection for survival.

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3

Dahmen, Johannes C., and Philip J. Corr. "Prepulse-elicited startle in prepulse inhibition." Biological Psychiatry 55, no. 1 (January 2004): 98–101. http://dx.doi.org/10.1016/s0006-3223(03)00638-3.

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4

Elden, Åke, and Magne Arve Flaten. "The Relationship of Automatic and Controlled Processing to Prepulse Inhibition." Journal of Psychophysiology 16, no. 1 (January 2002): 46–55. http://dx.doi.org/10.1027//0269-8803.16.1.46.

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Abstract When a weak stimulus, or prepulse, is presented immediately prior to a startle reflex-eliciting stimulus, the startle reflex is inhibited. This is called prepulse inhibition (PPI). Directing attention to a prepulse increases PPI. In two experiments (N = 43 and N = 29), attention was directed to the prepulse by having the participants judge the duration of the prepulse. Prepulse inhibition was assessed at stimulus onset asynchronies (SOAs) assumed to index automatic and controlled processing. The prepulse was a 60dB tone, and startle was elicited by 95dB white noise. We predicted that attention directed to the prepulse should increase PPI, and that PPI should increase on trials with correct judgments of prepulse duration compared to trials with incorrect judgments. The results from both experiments showed that attention directed toward the prepulse increased PPI at SOAs assumed to index both automatic and controlled processing. This indicates that controlled attention exerted an influence on automatic processes. There was no evidence that PPI was increased on trials with correct judgment of prepulse duration. It is concluded that attention to the prepulse increased PPI, but PPI did not differentiate between automatic and controlled processing under the present experimental conditions.

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5

Röskam, Stephan, and Michael Koch. "Enhanced prepulse inhibition of startle using salient prepulses in rats." International Journal of Psychophysiology 60, no. 1 (April 2006): 10–14. http://dx.doi.org/10.1016/j.ijpsycho.2005.04.004.

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6

Roussos, P., S. G. Giakoumaki, M. Rogdaki, S. Pavlakis, S. Frangou, and P. Bitsios. "Prepulse inhibition of the startle reflex depends on the catechol O-methyltransferase Val158Met gene polymorphism." Psychological Medicine 38, no. 11 (February 8, 2008): 1651–58. http://dx.doi.org/10.1017/s0033291708002912.

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BackgroundRecent evidence suggests that dopamine (DA) agonist-induced disruption of prepulse inhibition (PPI) depends on basal PPI values, in a manner that suggests an inverted U-shaped relationship between PPI and prefrontal DA levels. This is the first study to examine possible genetic determinants of PPI and the catechol O-methyltransferase (COMT) Val158Met polymorphism, the main catabolic pathway of released DA in the prefrontal cortex (PFC).MethodPPI was measured in 93 healthy males presented with 75-dB and 85-dB prepulses at 60-ms and 120-ms prepulse–pulse intervals. Subjects were grouped according to their COMT status into a Val/Val, a Val/Met and a Met/Met group.ResultsANOVAs showed that at all prepulse and interval conditions, Val/Val individuals had the lowest PPI, Met/Met the highest, and Val/Met were intermediate.ConclusionsThese results suggest that PPI is regulated by DA neurotransmission in the PFC and its levels depend on the COMT Val158Met gene polymorphism. These findings enhance the value of the PPI paradigm in examining individual variability of early information processing in healthy subjects and psychiatric disorders associated with changes in PFC DA activity and attentional deficits such as schizophrenia.

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7

Carlson, Stephanie, and James F. Willott. "Caudal Pontine Reticular Formation of C57BL/6J Mice: Responses to Startle Stimuli, Inhibition by Tones, and Plasticity." Journal of Neurophysiology 79, no. 5 (May 1, 1998): 2603–14. http://dx.doi.org/10.1152/jn.1998.79.5.2603.

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Carlson, Stephanie and James F. Willott. Caudal pontine reticular formation of C57BL/6J mice: responses to startle stimuli, inhibition by tones, and plasticity. J. Neurophysiol. 79: 2603–2614, 1998. C57BL/6J (C57) mice were used to examine relationships between the behavioral acoustic startle response (ASR) and the responses of neurons in the caudal pontine reticular formation (PnC) in three contexts: 1) responses evoked by basic startle stimuli; 2) the prepulse inhibition (PPI) paradigm; and 3) the effects of high-frequency hearing loss and concomitant neural plasticity that occurs in middle-aged C57 mice. 1) Responses (evoked action potentials) of PnC neurons closely paralleled the ASR with respect to latency, threshold, and responses to rapidly presented stimuli. 2) “Neural PPI” (inhibition of responses evoked by a startle stimulus when preceded by a tone prepulse) was observed in all PnC neurons studied. 3) In PnC neurons of 6-mo-old mice with high-frequency (>20 kHz) hearing loss, neural PPI was enhanced with 12- and 4-kHz prepulses, as it is behaviorally. These are frequencies that have become “overrepresented” in the central auditory system of 6-mo-old C57 mice. Thus neural plasticity in the auditory system, induced by high-frequency hearing loss, is correlated with increased salience of the inhibiting tones in both behavioral and neural PPI paradigms.

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8

Lee, Jae-Hun, Jae Yun Jung, and Ilyong Park. "A Gap Prepulse with a Principal Stimulus Yields a Combined Auditory Late Response." Journal of Audiology and Otology 24, no. 3 (July 10, 2020): 149–56. http://dx.doi.org/10.7874/jao.2019.00374.

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Background and Objectives: The gap prepulse inhibition of the acoustic startle response has been used to screen tinnitus in an animal model. Here, we examined changes in the auditory late response under various conditions of gap prepulse inhibition.Subjects and Methods: We recruited 19 healthy adults (5 males, 14 females) and their auditory late responses were recorded after various stimuli with or without gap prepulsing. The N1 and P2 responses were selected for analysis. The gap prepulse inhibition was estimated to determine the optimal auditory late response in the gap prepulse paradigm.Results: We found that the gap per se generated a response that was very similar to the response elicited by sound stimuli. This critically affected the gap associated with the maximal inhibition of the stimulus response. Among the various gap-stimulus intervals (GSIs) between the gap and principal stimulus, the GSI of 150 ms maximally inhibited the response. However, after zero padding was used to minimize artifacts after a P2 response to a gap stimulus, the differences among the GSIs disappeared.Conclusions: Overall, the data suggest that both the prepulse inhibition and the gap per se should be considered when using the gap prepulse paradigm to assess tinnitus in humans.

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9

Schicatano, Edward J., Kavita R. Peshori, Ramesh Gopalaswamy, Eva Sahay, and Craig Evinger. "Reflex Excitability Regulates Prepulse Inhibition." Journal of Neuroscience 20, no. 11 (June 1, 2000): 4240–47. http://dx.doi.org/10.1523/jneurosci.20-11-04240.2000.

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10

Mongeluzi, Donna L., Travis A. Hoppe, and William N. Frost. "Prepulse Inhibition of theTritoniaEscape Swim." Journal of Neuroscience 18, no. 20 (October 15, 1998): 8467–72. http://dx.doi.org/10.1523/jneurosci.18-20-08467.1998.

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11

Lipp, O. V., A. Contarino, and D. A. T. Siddle. "Does startle prepulse inhibition habituate?" Biological Psychology 37, no. 1 (October 1993): 54. http://dx.doi.org/10.1016/0301-0511(93)90044-9.

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12

Poje, Albert B., and Diane L. Filion. "The effects of multiphasic prepulses on automatic and attention-modulated prepulse inhibition." Cognitive Processing 18, no. 3 (April 11, 2017): 261–70. http://dx.doi.org/10.1007/s10339-017-0808-7.

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13

Hong, L. Elliot, Ikwunga Wonodi, Jada Lewis, and Gunvant K. Thaker. "Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients." Neuropsychopharmacology 33, no. 9 (October 24, 2007): 2167–74. http://dx.doi.org/10.1038/sj.npp.1301601.

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14

Li, Liang, Lawrence M. Korngut, Barrie J. Frost, and Richard J. Beninger. "Prepulse inhibition following lesions of the inferior colliculus: prepulse intensity functions." Physiology & Behavior 65, no. 1 (August 1998): 133–39. http://dx.doi.org/10.1016/s0031-9384(98)00143-7.

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15

Matsumoto, Yutaro, Kazuya Shimizu, Kota Arahata, Miku Suzuki, Akira Shimizu, Koki Takei, Junji Yamauchi, Satoko Hakeda-Suzuki, Takashi Suzuki, and Takako Morimoto. "Prepulse inhibition in Drosophila melanogaster larvae." Biology Open 7, no. 9 (September 15, 2018): bio034710. http://dx.doi.org/10.1242/bio.034710.

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16

Hutchison, Kent E., Damaris Rohsenow, Peter Monti, Tibor Palfai, and Robert Swift. "Prepulse Inhibition of the Startle Reflex." Alcoholism: Clinical & Experimental Research 21, no. 7 (October 1997): 1312. http://dx.doi.org/10.1097/00000374-199710000-00023.

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17

Ellenbroek, Bart A., and Alexander R. Cools. "Early maternal deprivation and prepulse inhibition." Pharmacology Biochemistry and Behavior 73, no. 1 (August 2002): 177–84. http://dx.doi.org/10.1016/s0091-3057(02)00794-3.

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18

Frost, William N., Li-Ming Tian, Travis A. Hoppe, Donna L. Mongeluzi, and Jean Wang. "A Cellular Mechanism for Prepulse Inhibition." Neuron 40, no. 5 (December 2003): 991–1001. http://dx.doi.org/10.1016/s0896-6273(03)00731-1.

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19

Perry, William, Mark Geyer, Kristin Cadenhead, Neal Swerdlow, and David Braff. "Schizophrenic patients with normal prepulse inhibition?" Schizophrenia Research 24, no. 1-2 (January 1997): 231. http://dx.doi.org/10.1016/s0920-9964(97)82665-5.

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20

Schmajuk, Nestor A., and José A. Larrauri. "Neural network model of prepulse inhibition." Behavioral Neuroscience 119, no. 6 (2005): 1546–62. http://dx.doi.org/10.1037/0735-7044.119.6.1546.

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21

Erhardt, Sophie, Lilly Schwieler, Carolina Emanuelsson, and Mark Geyer. "Endogenous kynurenic acid disrupts prepulse inhibition." Biological Psychiatry 56, no. 4 (August 2004): 255–60. http://dx.doi.org/10.1016/j.biopsych.2004.06.006.

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22

Kawachi, Y., Y. Matsue, M. Shibata, O. Imaizumi, and J. Gyoba. "P28-18 Self-stimulated prepulse inhibition." Clinical Neurophysiology 121 (October 2010): S272. http://dx.doi.org/10.1016/s1388-2457(10)61113-3.

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23

Vollenweider, Franz X., Martine Barro, Philipp A. Csomor, and Jorame Feldon. "Clozapine Enhances Prepulse Inhibition in Healthy Humans with Low But Not with High Prepulse Inhibition Levels." Biological Psychiatry 60, no. 6 (September 2006): 597–603. http://dx.doi.org/10.1016/j.biopsych.2006.03.058.

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24

Singer, Philipp, Weining Zhang, and Benjamin K. Yee. "SSR504734 enhances basal expression of prepulse inhibition but exacerbates the disruption of prepulse inhibition by apomorphine." Psychopharmacology 230, no. 2 (June 5, 2013): 309–17. http://dx.doi.org/10.1007/s00213-013-3160-3.

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25

Wynn, Jonathan K., Michael E. Dawson, Anne M. Schell, Mark McGee, Dustin Salveson, and Michael F. Green. "Prepulse facilitation and prepulse inhibition in schizophrenia patients and their unaffected siblings." Biological Psychiatry 55, no. 5 (March 2004): 518–23. http://dx.doi.org/10.1016/j.biopsych.2003.10.018.

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26

Tan, Sijie, Changqing Xu, Wanting Zhu, Jesse Willis, Christoph N. Seubert, Nikolaus Gravenstein, Colin Sumners, and Anatoly E. Martynyuk. "Endocrine and Neurobehavioral Abnormalities Induced by Propofol Administered to Neonatal Rats." Anesthesiology 121, no. 5 (November 1, 2014): 1010–17. http://dx.doi.org/10.1097/aln.0000000000000366.

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Abstract Background: The authors studied whether neonatal propofol anesthesia affects development of the endocrine and neural systems. Methods: Sprague–Dawley rats were anesthetized using intraperitoneal propofol for 5 h on postnatal days (P) 4, 5, or 6. Pups that received either saline or intralipid, but not those in the negative control groups, were also maternally separated for 5 h. Serum levels of corticosterone were measured immediately after anesthesia and in adulthood after prepulse inhibition of acoustic startle testing (≥P80), followed by measurement of hippocampal neuronal activity. Results: Propofol acutely increased corticosterone levels to 146.6 ± 23.5 ng/ml (n = 6) versus 16.4 ± 3.5 ng/ml (n = 6) and 18.4 ± 3.2 ng/ml (n = 6) in saline- and intralipd-treated pups, respectively. In adulthood, the propofol group exhibited exacerbated endocrine responses to stress in a form of increased corticosterone levels (1,171.58 ± 149.17 ng/ml [n = 15] vs. 370.02 ± 36.01 ng/ml [n = 10] in the saline group). The propofol group had increased the frequency of miniature inhibitory postsynaptic currents in CA1 neurons of male and female rats, but reduced prepulse inhibition of startle was detected only in males. The Na+–K+–2Cl− cotransporter inhibitor bumetanide, administered to pups before propofol injection, alleviated long-term endocrine and prepulse inhibition abnormalities. Exogenous corticosterone, administered to naive pups, induced synaptic and endocrine but not prepulse inhibition effects, similar to those of propofol. Conclusion: Propofol-caused acute increases in corticosterone levels and γ-aminobutyric acid type A receptor–mediated excitation at the time of anesthesia may play mechanistic roles in development of exacerbated endocrine responses to stress and neurobehavioral abnormalities.

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27

Colecraft, Henry M., Parag G. Patil, and David T. Yue. "Differential Occurrence of Reluctant Openings in G-Protein–Inhibited N- and P/Q-Type Calcium Channels." Journal of General Physiology 115, no. 2 (February 1, 2000): 175–92. http://dx.doi.org/10.1085/jgp.115.2.175.

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Voltage-dependent inhibition of N- and P/Q-type calcium channels by G proteins is crucial for presynaptic inhibition of neurotransmitter release, and may contribute importantly to short-term synaptic plasticity. Such calcium-channel modulation could thereby impact significantly the neuro-computational repertoire of neural networks. The differential modulation of N and P/Q channels could even further enrich their impact upon synaptic tuning. Here, we performed in-depth comparison of the G-protein inhibition of recombinant N and P/Q channels, expressed in HEK 293 cells with the m2 muscarinic receptor. While both channel types display classic features of G-protein modulation (kinetic slowing of activation, prepulse facilitation, and voltage dependence of inhibition), we confirmed previously reported quantitative differences, with N channels displaying stronger inhibition and greater relief of inhibition by prepulses. A more fundamental, qualitative difference in the modulation of these two channels was revealed by a modified tail-activation paradigm, as well as by a novel “slope” analysis method comparing time courses of slow activation and prepulse facilitation. The stark contrast in modulatory behavior can be understood within the context of the “willing–reluctant” model, in which binding of G-protein βγ subunits to channels induces a reluctant mode of gating, where stronger depolarization is required for opening. Our experiments suggest that only N channels could be opened in the reluctant mode, at voltages normally spanned by neuronal action potentials. By contrast, P/Q channels appear to remain closed, especially over these physiological voltages. Further, the differential occurrence of reluctant openings is not explained by differences in the rate of G-protein unbinding from the two channels. These two scenarios predict very different effects of G-protein inhibition on the waveform of Ca2+ entry during action potentials, with potentially important consequences for the timing and efficacy of synaptic transmission.

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28

Neumeister, Heike, Theresa M. Szabo, and Thomas Preuss. "Behavioral and Physiological Characterization of Sensorimotor Gating in the Goldfish Startle Response." Journal of Neurophysiology 99, no. 3 (March 2008): 1493–502. http://dx.doi.org/10.1152/jn.00959.2007.

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Prepulse inhibition (PPI) is typically associated with an attenuation of auditory startle behavior in mammals and is presumably mediated within the brainstem startle circuit. However, the inhibitory mechanisms underlying PPI are not yet clear. We addressed this question with complementary behavioral and in vivo electrophysiological experiments in the startle escape circuit of goldfish, the Mauthner cell (M-cell) system. In the behavioral experiments we observed a 77.5% attenuation (PPI) of startle escape probability following auditory prepulse–pulse stimulation. The PPI effect was observed for prepulse–pulse interstimulus intervals (ISIs) ranging from 20 to 600 ms and its magnitude depended linearly on prepulse intensity over a range of 14 dB. Electrophysiological recordings of synaptic responses to a sound pulse in the M-cell, which is the sensorimotor neuron initiating startle escapes, showed a 21% reduction in amplitude of the dendritic postsynaptic potential (PSP) and a 23% reduction of the somatic PSP following a prepulse. In addition, a prepulse evoked a long-lasting (500 ms) decrease in M-cell excitability indicated by 1) an increased threshold current, 2) an inhibitory shunt of the action potential (AP), and 3) by a linearized M-cell membrane, which effectively impedes M-cell AP generation. Comparing the magnitude and kinetics of inhibitory shunts evoked by a prepulse in the M-cell dendrite and soma revealed a disproportionately larger and longer-lasting inhibition in the dendrite. These results suggest that the observed PPI-type attenuation of startle behavior can be correlated to distinct postsynaptic mechanisms mediated primarily at the M-cell lateral dendrite.

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29

Postma, Peggy, Veena Kumari, Melissa Hines, and Jeffrey A. Gray. "The relationship between prepulse detection and prepulse inhibition of the acoustic startle reflex." Psychophysiology 38, no. 3 (May 2001): 377–82. http://dx.doi.org/10.1111/1469-8986.3830377.

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30

Lipp, Ottmar V., and Steven P. Krinitzky. "The effect of repeated prepulse and reflex stimulus presentations on startle prepulse inhibition." Biological Psychology 47, no. 1 (January 1998): 65–76. http://dx.doi.org/10.1016/s0301-0511(97)00019-7.

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31

Gebhardt, J., S. Schulz-Juergensen, and P. Eggert. "Maturation of prepulse inhibition (PPI) in childhood." Psychophysiology 49, no. 4 (December 16, 2011): 484–88. http://dx.doi.org/10.1111/j.1469-8986.2011.01323.x.

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32

BLUMENTHAL, TERRY D. "Prepulse inhibition decreases as startle reactivity habituates." Psychophysiology 34, no. 4 (July 1997): 446–50. http://dx.doi.org/10.1111/j.1469-8986.1997.tb02388.x.

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33

Pineles, Suzanne L., Terry D. Blumenthal, Andrew J. Curreri, Yael I. Nillni, Katherine M. Putnam, Patricia A. Resick, Ann M. Rasmusson, and Scott P. Orr. "Prepulse inhibition deficits in women with PTSD." Psychophysiology 53, no. 9 (May 30, 2016): 1377–85. http://dx.doi.org/10.1111/psyp.12679.

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34

Swerdlow, N. R., D. P. van Bergeijk, F. Bergsma, E. Weber, and J. Talledo. "The Effects of Memantine on Prepulse Inhibition." Neuropsychopharmacology 34, no. 7 (February 25, 2009): 1854–64. http://dx.doi.org/10.1038/npp.2009.7.

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35

Weiss, I. C., J. Feldon, and A. M. Domeney. "Isolation rearing-induced disruption of prepulse inhibition." Behavioural Pharmacology 10, no. 2 (March 1999): 139–49. http://dx.doi.org/10.1097/00008877-199903000-00003.

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36

Weiss, I. C., J. Feldon, and A. M. Domeney. "Isolation rearing-induced disruption of prepulse inhibition." Behavioural Pharmacology 10, no. 4 (July 1999): 433. http://dx.doi.org/10.1097/00008877-199907000-00011.

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37

Minassian, Arpi, Brook L. Henry, Steven Paul Woods, Florin Vaida, Igor Grant, Mark A. Geyer, and William Perry. "Prepulse Inhibition in HIV-Associated Neurocognitive Disorders." Journal of the International Neuropsychological Society 19, no. 6 (April 3, 2013): 709–17. http://dx.doi.org/10.1017/s1355617713000301.

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AbstractSensorimotor inhibition, or the ability to filter out excessive or irrelevant information, theoretically supports a variety of higher-level cognitive functions. Impaired inhibition may be associated with increased impulsive and risky behavior in everyday life. Individuals infected with HIV frequently show impairment on tests of neurocognitive function, but sensorimotor inhibition in this population has not been studied and may be a contributor to the profile of HIV-associated neurocognitive disorders (HAND). Thirty-seven HIV-infected individuals (15 with HAND) and 48 non-infected comparison subjects were assessed for prepulse inhibition (PPI), an eyeblink startle paradigm measuring sensorimotor gating. Although HIV status alone was not associated with PPI deficits, HIV-positive participants meeting criteria for HAND showed impaired PPI compared to cognitively intact HIV-positive subjects. In HIV-positive subjects, PPI was correlated with working memory but was not associated with antiretroviral therapy or illness factors. In conclusion, sensorimotor disinhibition in HIV accompanies deficits in higher-order cognitive functions, although the causal direction of this relationship requires investigation. Subsequent research on the role of sensorimotor gating on decision-making and risk behaviors in HIV may be indicated. (JINS, 2013, 19, 1–9)

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38

Emoto, Hiroyuki, Masatoshi Tanaka, Masami Yoshida, and Shigeto Yamada. "The effects of corticosterone to prepulse inhibition." Japanese Journal of Pharmacology 82 (2000): 230. http://dx.doi.org/10.1016/s0021-5198(19)48383-2.

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39

Hejl, Anne-Mette, Birte Glenthøj, Torben Mackeprang, Ralf Hemmingsen, and Gunhild Waldemar. "Prepulse inhibition in patients with Alzheimer’s disease." Neurobiology of Aging 25, no. 8 (September 2004): 1045–50. http://dx.doi.org/10.1016/j.neurobiolaging.2003.11.005.

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40

Sato, Kohji. "Why is prepulse inhibition disrupted in schizophrenia?" Medical Hypotheses 143 (October 2020): 109901. http://dx.doi.org/10.1016/j.mehy.2020.109901.

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41

Campbell, L., TW Budd, R. Fulham, M. Hughes, F. Karayanidis, M.-C. Hanlon, W. Stojanov, P. Johnston, and U. Schall. "Functional brain imaging of auditory prepulse inhibition." Acta Neuropsychiatrica 18, no. 6 (December 2006): 280. http://dx.doi.org/10.1017/s092427080003101x.

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42

Kofler, M. "Blink reflex and prepulse inhibition in fibromyalgia." Clinical Neurophysiology 127, no. 3 (March 2016): e47. http://dx.doi.org/10.1016/j.clinph.2015.11.154.

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43

Fang-Jung, W. "Do ? Interactions Regulate Prepulse Inhibition in Rats?" Neuropsychopharmacology 14, no. 4 (April 1996): 265–74. http://dx.doi.org/10.1016/0893-133x(95)00133-x.

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44

Gunduz, Aysegul, Ugur Uygunoglu, Derya Uluduz, Sabahattin Saip, Baki Goksan, Aksel Siva, and Meral E. Kiziltan. "BS18. Reduced prepulse inhibition in trigeminal neuralgia." Clinical Neurophysiology 129 (May 2018): e220. http://dx.doi.org/10.1016/j.clinph.2018.04.566.

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45

Braff, David L., Gregory A. Light, Joel Ellwanger, Joyce Sprock, and Neal R. Swerdlow. "Female schizophrenia patients have prepulse inhibition deficits." Biological Psychiatry 57, no. 7 (April 2005): 817–20. http://dx.doi.org/10.1016/j.biopsych.2004.12.030.

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46

Giakoumaki, Stella G. "Cognitive and Prepulse Inhibition Deficits in Psychometrically High Schizotypal Subjects in the General Population: Relevance to Schizophrenia Research." Journal of the International Neuropsychological Society 18, no. 4 (May 22, 2012): 643–56. http://dx.doi.org/10.1017/s135561771200029x.

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AbstractSchizophrenia and schizotypal personality disorder share common clinical profiles, neurobiological and genetic substrates along with Prepulse Inhibition and cognitive deficits; among those, executive, attention, and memory dysfunctions are more consistent. Schizotypy is considered to be a non-specific “psychosis-proneness,” and understanding the relationship between schizotypal traits and cognitive function in the general population is a promising approach for endophenotypic research in schizophrenia spectrum disorders. In this review, findings for executive function, attention, memory, and Prepulse Inhibition impairments in psychometrically defined schizotypal subjects have been summarized and compared to schizophrenia patients and their unaffected first-degree relatives. Cognitive flexibility, sustained attention, working memory, and Prepulse Inhibition impairments were consistently reported in high schizotypal subjects in accordance to schizophrenia patients. Genetic studies assessing the effects of various candidate gene polymorphisms in schizotypal traits and cognitive function are promising, further supporting a polygenic mode of inheritance. The implications of the findings, methodological issues, and suggestions for future research are discussed. (JINS, 2012, 18, 1–14)

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Bakshi, V. P., M. A. Geyer, N. Taaid, and N. R. Swerdlow. "Similar effects of stimulants on latent inhibition and prepulse inhibition." Biological Psychiatry 35, no. 9 (May 1994): 631. http://dx.doi.org/10.1016/0006-3223(94)90716-1.

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Morton, N., N. S. Gray, J. D. C. Mellers, B. K. Toone, and J. A. Gray. "Relationships between schizotypy, within-subject latent inhibition and prepulse inhibition." Schizophrenia Research 18, no. 2-3 (February 1996): 229. http://dx.doi.org/10.1016/0920-9964(96)85704-5.

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Yang, Xiaoqin, Lei Liu, Pengcheng Yang, Yu Ding, Changming Wang, and Liang Li. "The Effects of Attention on the Syllable-Induced Prepulse Inhibition of the Startle Reflex and Cortical EEG Responses against Energetic or Informational Masking in Humans." Brain Sciences 12, no. 5 (May 18, 2022): 660. http://dx.doi.org/10.3390/brainsci12050660.

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Prepulse inhibition (PPI) is the reduction in the acoustic startle reflex (ASR) when the startling stimulus (pulse) is preceded by a weaker, non-starting stimulus. This can be enhanced by facilitating selective attention to the prepulse against a noise-masking background. On the other hand, the facilitation of selective attention to a target speech can release the target speech from masking, particularly from speech informational masking. It is not clear whether attentional regulation also affects PPI in this kind of auditory masking. This study used a speech syllable as the prepulse to examine whether the masker type and perceptual spatial attention can affect the PPI or the scalp EEG responses to the prepulse in healthy younger-adult humans, and whether the ERPs evoked by the prepulse can predict the PPI intensity of the ASR. The results showed that the speech masker produced a larger masking effect than the noise masker, and the perceptual spatial separation facilitated selective attention to the prepulse, enhancing both the N1 component of the prepulse syllable and the PPI of the ASR, particularly when the masker was speech. In addition, there was no significant correlation between the PPI and ERPs under any of the conditions, but the perceptual separation-induced PPI enhancement and ERP N1P2 peak-to-peak amplitude enhancement were correlated under the speech-masking condition. Thus, the attention-mediated PPI is useful for differentiating noise energetic masking and speech informational masking, and the perceptual separation-induced release of the prepulse from informational masking is more associated with attention-mediated early cortical unmasking processing than with energetic masking. However, the processes for the PPI of the ASR and the cortical responses to the prepulse are mediated by different neural mechanisms.

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Baschnagel, Joseph S., Larry W. Hawk, Craig R. Colder, and Jerry B. Richards. "Motivated attention and prepulse inhibition of startle in rats: Using conditioned reinforcers as prepulses." Behavioral Neuroscience 121, no. 6 (2007): 1372–82. http://dx.doi.org/10.1037/0735-7044.121.6.1372.

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