The effect of antipsychotic medications on acoustic startle latency in schizophrenia

Fargotstein, Molly; Hasenkamp, Wendy; Gross, Robin E.; Cuthbert, Bruce N.; Green, Amanda; Swails, Lisette W.; Lewison, Barbara; Boshoven, William; Keyes, Megan; Duncan, Erica

doi:10.1016/j.schres.2017.07.030

Cited by 17 publications

(18 citation statements)

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“…Finally, there were no clear effects of psychotropic medication (55) or tobacco use on PPI as has been previously reported (56), but there was a significant effect of cannabis on PPI in the CHR sample with cannabis smokers having greater PPI. Also, of interest is the fact that the normal sex effects on PPI (M>F) were no longer present when cannabis use history was added to the analysis.…”

Section: Figure 4 |supporting

confidence: 69%

Evidence of Slow Neural Processing, Developmental Differences and Sensitivity to Cannabis Effects in a Sample at Clinical High Risk for Psychosis From the NAPLS Consortium Assessed With the Human Startle Paradigm

et al. 2020

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Biomarkers are important in the study of the prodromal period of psychosis because they can help to identify individuals at greatest risk for future psychotic illness and provide insights into disease mechanism underlying neurodevelopmental abnormalities. The biomarker abnormalities can then be targeted with treatment, with an aim toward prevention or mitigation of disease. The human startle paradigm has been used in translational studies of psychopathology including psychotic illness to assess preattentive information processing for over 50 years. In one of the largest studies to date in clinical high risk (CHR) for psychosis participants, we aimed to evaluate startle indices as biomarkers of risk along with the role of age, sex, treatment, and substance use in this population of high risk individuals. Methods: Startle response reactivity, latency, and prepulse inhibition (PPI) were assessed in 543 CHR and 218 Normal Comparison (NC) participants between the ages of 12 and 35.

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Section: Figure 4 |supporting

confidence: 69%

Evidence of Slow Neural Processing, Developmental Differences and Sensitivity to Cannabis Effects in a Sample at Clinical High Risk for Psychosis From the NAPLS Consortium Assessed With the Human Startle Paradigm

et al. 2020

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Section: 1 the Phenotypementioning

confidence: 96%

“…Fargotstein et al (2017) provide the important reminder that PPI is not the only startle reflex parameter that is impaired in schizophrenia patients. They report slowed startle reflex peak latency in their sample of schizophrenia patients -- a common though not ubiquitous finding (see Discussion in Fargotstein et al (2017)). This phenotype was most pronounced in their subgroup of unmedicated schizophrenia patients, suggesting that - as with PPI in many studies - antipsychotics may partially correct this slow-latency phenotype, or that other factors associated with unmedicated status may also contribute to prolonged reflex latency.…”

Section: 1 the Phenotypementioning

confidence: 96%

Sensorimotor gating deficits in schizophrenia: Advancing our understanding of the phenotype, its neural circuitry and genetic substrates

Swerdlow

Light

2018

Schizophrenia Research

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“…Additionally, these mice displayed altered social behavior similar to changes seen in ASD patients [13][14][15] . Df(h22q11)/+ mice displayed a decrease in pre-pulse inhibition and displayed acquired acoustic startle response similar to that seen in SCZ patients 16,22 , which could not be rescued by the antipsychotic drugs haloperidol or clozapine 16 commonly used to treat SCZ 23 . While the three mouse models all present neuropsychiatric disease relevant phenotypes, there is substantial phenotypic variability between them, consistent with the individuals carrying these CNVs who present with different diagnoses [24][25][26] .…”

Section: Introductionmentioning

confidence: 81%

Transcriptomic networks implicate neuronal energetic abnormalities in three mouse models harboring autism and schizophrenia-associated mutations

Gordon

Grønborg-Forsingdal

Klewe

et al. 2019

Preprint

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Genetic risk for psychiatric illness is complex, so identification of shared molecular pathways where distinct forms of genetic risk might coincide is of substantial interest. A growing body of genetic and genomic studies suggest that such shared molecular pathways exist across disorders with different clinical presentations, such as schizophrenia and autism spectrum disorder (ASD).But how this relates to specific genetic risk factors is unknown. Further, whether some of the molecular changes identified in brain relate to potentially confounding antemortem or postmortem factors is difficult to prove. We analyzed the transcriptome from the cortex and hippocampus of three mouse lines modeling human copy number variants (CNVs) associated with schizophrenia and ASD: Df(h15q13)/+, Df(h22q11)/+, and Df(h1q21)/+ which carry the 15q13.3 deletion, 22q11.2 deletion, and 1q21.1 deletion, respectively. Although we found very little overlap of differential expression at the level of individual genes, gene network analysis identified two modules of co-expressed genes that were dysregulated across all three mouse models. One module observed in both cortex and hippocampus was associated with neuronal energetics and firing rate, and overlapped with changes identified in post mortem human brain from SCZ and ASD patients. These data highlight aspects of convergent gene expression in mouse models harboring major risk alleles, and strengthen the connection between neuronal energetic dysfunction and neuropsychiatric disorders in humans. Methods SamplesMice were bred and housed until 8 weeks by Taconic MB (Lille Skensved, Denmark), and then transported to the Lundbeck animal facility. Detailed description of animal housing and handling has been previously described 15 . Adult mice (>10 weeks old) harboring the CNV as well control littermates were sacrificed by cervical dislocation and parietal cortex or hippocampus were dissected by hand and stored at -80°C. With the exception of Df(h15q13)-/-the cortex and hippocampus were dissected from separate animals. All studies were carried out in accordance with Danish legislation, granted by the animal welfare committee, appointed by the Danish Ministry of Food, Agriculture and Fisheries-Danish Veterinary and Food Administration. Samples were lysed and homogenized in RA1 lysis buffer with 1% β-mercaptoethanol (Macherey-Nagel,

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The effect of antipsychotic medications on acoustic startle latency in schizophrenia

Cited by 17 publications

References 50 publications

Evidence of Slow Neural Processing, Developmental Differences and Sensitivity to Cannabis Effects in a Sample at Clinical High Risk for Psychosis From the NAPLS Consortium Assessed With the Human Startle Paradigm

Evidence of Slow Neural Processing, Developmental Differences and Sensitivity to Cannabis Effects in a Sample at Clinical High Risk for Psychosis From the NAPLS Consortium Assessed With the Human Startle Paradigm

Sensorimotor gating deficits in schizophrenia: Advancing our understanding of the phenotype, its neural circuitry and genetic substrates

Transcriptomic networks implicate neuronal energetic abnormalities in three mouse models harboring autism and schizophrenia-associated mutations

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