Sensorimotor Gating (Prepulse Inhibition of Startle) in Children Exposed to a Single Traumatic Event

2009 ◽  
Author(s):  
Robert Pynoos ◽  
Edward Ornitz
Keyword(s):  
Prepulse Inhibition ◽  
Traumatic Event ◽  
Sensorimotor Gating

scholarly journals BDNF haploinsufficiency induces behavioral endophenotypes of schizophrenia in male mice that are rescued by enriched environment

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Mahmoud Harb ◽  
Justina Jagusch ◽  
Archana Durairaja ◽  
Thomas Endres ◽  
Volkmar Leßmann ◽  
...  
Keyword(s):  
Prepulse Inhibition ◽  
Sensorimotor Gating ◽  
Enriched Environment ◽  
Fear Learning ◽  
Set Shifting ◽  
Wild Type ◽  
Mature Adult ◽  
Attentional Set ◽  
Attentional Set Shifting ◽  
The Brain

AbstractBrain-derived neurotrophic factor (BDNF) is implicated in a number of processes that are crucial for healthy functioning of the brain. Schizophrenia is associated with low BDNF levels in the brain and blood, however, not much is known about BDNF’s role in the different symptoms of schizophrenia. Here, we used BDNF-haploinsufficient (BDNF+/−) mice to investigate the role of BDNF in different mouse behavioral endophenotypes of schizophrenia. Furthermore, we assessed if an enriched environment can prevent the observed changes. In this study, male mature adult wild-type and BDNF+/− mice were tested in mouse paradigms for cognitive flexibility (attentional set shifting), sensorimotor gating (prepulse inhibition), and associative emotional learning (safety and fear conditioning). Before these tests, half of the mice had a 2-month exposure to an enriched environment, including running wheels. After the tests, BDNF brain levels were quantified. BDNF+/− mice had general deficits in the attentional set-shifting task, increased startle magnitudes, and prepulse inhibition deficits. Contextual fear learning was not affected but safety learning was absent. Enriched environment housing completely prevented the observed behavioral deficits in BDNF+/− mice. Notably, the behavioral performance of the mice was negatively correlated with BDNF protein levels. These novel findings strongly suggest that decreased BDNF levels are associated with several behavioral endophenotypes of schizophrenia. Furthermore, an enriched environment increases BDNF protein to wild-type levels and is thereby able to rescue these behavioral endophenotypes.

scholarly journals T39. IMPAIRED SENSORIMOTOR GATING USING THE ACOUSTIC PREPULSE INHIBITION PARADIGM IN INDIVIDUALS AT A CLINICAL HIGH RISK FOR PSYCHOSIS

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S246-S246
Author(s):  
Qijing Bo ◽  
Zhen Mao ◽  
Qing Tian ◽  
Weidi Li ◽  
Lei Zhao ◽  
...  
Keyword(s):  
High Risk ◽  
Prepulse Inhibition ◽  
Clinical Characteristics ◽  
Sensorimotor Gating ◽  
Spatial Separation ◽  
Structured Interview ◽  
First Episode ◽  
Clinical High Risk ◽  
Neurocognitive Functions ◽  
First Episode Schizophrenia

Abstract Background Many robust studies on prepulse inhibition (PPI) were conducted in patients with schizophrenia, and, increasingly, evidence has indicated individuals who are at clinical high risk for psychosis (CHR). The specificity of the PPI is insufficient with the classic paradigm. The current study investigated an improved perceived spatial separation PPI (PSSPPI) paradigm in CHR individuals, compared with patients of first-episode schizophrenia (FES) and healthy controls (HC), and the relationship between PPI, demographics, clinical characteristics, and cognitive performance. Methods We included 53 FESs, 55 CHR individuals, and 53 HCs. CHRs were rated on the Structured Interview for Prodromal Syndromes (SIPS). The prepulse inhibition measures of perceived spatial co-location PPI (PSCPPI) and PSSPPI paradigms were applied using 60- and 120-ms lead intervals. The MATRICS Consensus Cognitive Battery (MCCB) was used to assess neurocognitive functions. Results Compared with HC, the CHR group had lower PSSPPI level (ISI=60 ms, P<0.001; ISI=120 ms, P<.001). PSSPPI showed a large effect size (ES) between CHR and HC (ISI=60 ms, ES=0.91; ISI=120 ms, ES=0.98); on PSSPPI using 60-ms lead interval, ES ranged from small to large from CHR to FES. PPI deficits in CHR were unrelated to demographics, clinical characteristics, and cognition. Discussion CHR individuals show a sensorimotor gating deficit similar to FES patients on PSSPPI of the startle response, with greater sensitivity than the classic PPI paradigm. PSSPPI appears a promising objective approach for identifying individuals at clinical high risk for psychosis related to a high risk of transition to schizophrenia.

Sensorimotor Gating and Attitudes Related to Schizotypal Proneness

2001 ◽  
Vol 88 (3_suppl) ◽  
pp. 1035-1045 ◽  
Author(s):  
Almut I. Weike ◽  
Alfons O. Hamm ◽  
Dieter Vaitl
Keyword(s):  
Prepulse Inhibition ◽  
Sensorimotor Gating ◽  
Schizophrenia Spectrum Disorders ◽  
Eyeblink Response ◽  
Startle Eyeblink ◽  
Psychosis Proneness ◽  
Gating Mechanism ◽  
Schizophrenia Spectrum ◽  
Spectrum Disorders ◽  
Information Processing Deficits

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.

scholarly journals Prepulse Inhibition in HIV-Associated Neurocognitive Disorders

2013 ◽  
Vol 19 (6) ◽  
pp. 709-717 ◽  
Author(s):  
Arpi Minassian ◽  
Brook L. Henry ◽  
Steven Paul Woods ◽  
Florin Vaida ◽  
Igor Grant ◽  
...  
Keyword(s):  
Prepulse Inhibition ◽  
Cognitive Functions ◽  
Sensorimotor Gating ◽  
Neurocognitive Disorders ◽  
Hiv Positive ◽  
Causal Direction ◽  
Cognitively Intact ◽  
Eyeblink Startle ◽  
Hiv Associated Neurocognitive Disorders

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)

scholarly journals Meclizine Enhancement of Sensorimotor Gating in Healthy Male Subjects with High Startle Responses and Low Prepulse Inhibition

2013 ◽  
Vol 39 (3) ◽  
pp. 651-659 ◽  
Author(s):  
José A Larrauri ◽  
Lisalynn D Kelley ◽  
Mason R Jenkins ◽  
Eric C Westman ◽  
Nestor A Schmajuk ◽  
...  
Keyword(s):  
Prepulse Inhibition ◽  
Sensorimotor Gating ◽  
Healthy Male ◽  
Male Subjects

scholarly journals Disruption of prepulse inhibition is associated with severity of compulsive behavior and nucleus accumbens dopamine receptor changes in Sapap3 knockout mice

2019 ◽  
Author(s):  
Elizabeth E Manning ◽  
Abigail Y Wang ◽  
Linda M Saikali ◽  
Anna S Winner ◽  
Susanne E Ahmari
Keyword(s):  
Nucleus Accumbens ◽  
Dopamine Receptor ◽  
Prepulse Inhibition ◽  
Knockout Mice ◽  
Sensorimotor Gating ◽  
Striatal Dopamine ◽  
Preclinical Model ◽  
Significant Heterogeneity ◽  
Compulsive Behavior ◽  
Compulsive Disorder

AbstractObsessive compulsive disorder (OCD) is associated with disruption of sensorimotor gating, which may contribute to difficulties inhibiting intrusive thoughts and compulsive rituals. Neural mechanisms underlying these disturbances are unclear; however, striatal dopamine is implicated in regulation of sensorimotor gating and OCD pathophysiology. The goal of this study was to examine the relationships between sensorimotor gating, compulsive behavior, and striatal dopamine receptor levels in Sapap3 knockout mice (KOs), a widely used preclinical model system for OCD research. We found a trend for disruption of sensorimotor gating in Sapap3-KOs using the translational measure prepulse inhibition (PPI); however, there was significant heterogeneity in both PPI and compulsive grooming in KOs. Disruption of PPI was significantly correlated with a more severe compulsive phenotype. In addition, PPI disruption and compulsive grooming severity were associated with reduced dopamine D1 and D2/3 receptor density in the nucleus accumbens core (NAcC). Compulsive grooming progressively worsened in Sapap3-KOs tested longitudinally, but PPI disruption was first detected in high-grooming KOs at 7 months of age. Through detailed characterization of individual differences in OCD-relevant behavioral and neurochemical measures, our findings suggest that NAcC dopamine receptor changes may be involved in disruption of sensorimotor gating and compulsive behavior relevant to OCD.

scholarly journals  Life-Course Contribution of Prenatal Stress in Regulating the Neural Modulation Network Underlying the Prepulse Inhibition of the Acoustic Startle Reflex in Male Alzheimer’s Disease Mice

2019 ◽  
Vol 30 (1) ◽  
pp. 311-325 ◽  
Author(s):  
Zahra Jafari ◽  
Bryan E Kolb ◽  
Majid H Mohajerani
Keyword(s):  
Prepulse Inhibition ◽  
Hpa Axis ◽  
Prenatal Stress ◽  
Acoustic Startle ◽  
Sensorimotor Gating ◽  
Startle Reflex ◽  
Underlying Mechanism ◽  
Acoustic Startle Reflex ◽  
Abnormal Development ◽  
Brain Areas

Abstract The prepulse inhibition (PPI) of the acoustic startle reflex (ASR), as an index of sensorimotor gating, is one of the most extensively used paradigms in the field of neuropsychiatric disorders. Few studies have examined how prenatal stress (PS) regulates the sensorimotor gating during the lifespan and how PS modifies the development of amyloid-beta (Aβ) pathology in brain areas underlying the PPI formation. We followed alternations in corticosterone levels, learning and memory, and the PPI of the ASR measures in APPNL-G-F/NL-G-F offspring of dams exposed to gestational noise stress. In-depth quantifications of the Aβ plaque accumulation were also performed at 6 months. The results indicated an age-dependent deterioration of sensorimotor gating, long-lasting PS-induced abnormalities in PPI magnitudes, as well as deficits in spatial memory. The PS also resulted in a higher Aβ aggregation predominantly in brain areas associated with the PPI modulation network. The findings suggest the contribution of a PS-induced hypothalamic-pituitary-adrenal (HPA) axis hyperactivity in regulating the PPI modulation substrates leading to the abnormal development of the neural protection system in response to disruptive stimuli. The long-lasting HPA axis dysregulation appears to be the major underlying mechanism in precipitating the Aβ deposition, especially in brain areas contributed to the PPI modulation network.

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