Prepulse inhibition of startle and the neurobiology of primary nocturnal enuresis

Ornitz, Edward M.; Russell, Andrew; Hanna, Gregory L.; Gabikian, Patrik; Gehricke, Jean Guido; Song, Dale; Guthrie, Donald

doi:10.1016/s0006-3223(98)00205-4

Cited by 118 publications

(99 citation statements)

References 68 publications

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“…In addition, PPI was calculated using two additional estimates of response amplitude: the highest point of a 2 ms running average and log transformation of the peak EMG amplitude. 16 PPI calculations using these measures yielded equivalent results.…”

Section: Startle Testingmentioning

confidence: 89%

“…16 Briefly, acoustic stimuli were presented binaurally through Sony circumaural earphones. Startle stimuli were 105 dB SPL (50 ms duration) white-noise bursts, with 0 ms rise/fall times.…”

Section: Startle Testingmentioning

confidence: 99%

“…Specific details of these test conditions and procedures have been described elsewhere. 16 Data analysis Startle response magnitude was taken to be the peak EMG amplitude occurring within a 105 ms window following the onset of the startle stimulus. Using means of all usable trials, percent PPI was calculated for each subject according to the following formula: %PPI¼[1À(response prepulse þ startle stimulus /response startle stimulus alone )] Â 100).…”

Section: Startle Testingmentioning

confidence: 99%

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Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice

et al. 2004

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Fragile X syndrome (FXS) is the most common single gene (FMR1) disorder affecting cognitive and behavioral function in humans. This syndrome is characterized by a cluster of abnormalities including lower IQ, attention deficits, impairments in adaptive behavior and increased incidence of autism. Here, we show that young males with FXS have profound deficits in prepulse inhibition (PPI), a basic marker of sensorimotor gating that has been extensively studied in rodents. Importantly, the magnitude of the PPI impairments in the fragile X children predicted the severity of their IQ, attention, adaptive behavior and autistic phenotypes. Additionally, these measures were highly correlated with each other, suggesting that a shared mechanism underlies this complex phenotypic cluster. Studies in Fmr1-knockout mice also revealed sensorimotor gating and learning abnormalities. However, PPI and learning were enhanced rather than reduced in the mutants. Therefore, these data show that mutations of the FMR1 gene impact equivalent processes in both humans and mice. However, since these phenotypic changes are opposite in direction, they also suggest that murine compensatory mechanisms following loss of FMR1 function differ from those in humans.

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Section: Startle Testingmentioning

confidence: 89%

“…16 Briefly, acoustic stimuli were presented binaurally through Sony circumaural earphones. Startle stimuli were 105 dB SPL (50 ms duration) white-noise bursts, with 0 ms rise/fall times.…”

Section: Startle Testingmentioning

confidence: 99%

Section: Startle Testingmentioning

confidence: 99%

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Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice

et al. 2004

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“…PPI deficits correlate with clinical severity Light and Braff 1999;Weike et al 2000), cognitive symptoms such as thought disorder (Perry et al 1999), and early age of onset of schizophrenia (Kumari et al 2000), suggesting a strong relationship between disease symptoms and PPI impairment. PPI deficits have also been reported in other 1 disorders that appear to have a common characteristic of loss of gating in sensory, motor or cognitive domains, notably obsessive-compulsive disorder (Swerdlow et al 1993), attention deficit hyperactivity disorder (ADHD) (Hawk et al 2003), Tourette syndrome (Swerdlow et al 2001b), comorbid Tourette syndrome and ADHD (Castellanos et al 1996), Huntington's disease , bipolar disorder with acute psychotic mania (Perry et al 2001), comorbid ADHD and nocturnal enuresis (Ornitz et al 1999), blepharospasm (Gomez-Wong et al 1998), nonepileptic seizures (Pouretemad et al 1998), and post-traumatic stress disorder (Grillon et al 1996).…”

mentioning

confidence: 96%

Two Quantitative Trait Loci for Prepulse Inhibition of Startle Identified on Mouse Chromosome 16 Using Chromosome Substitution Strains

et al. 2005

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Prepulse inhibition (PPI) of acoustic startle is a genetically complex quantitative phenotype of considerable medical interest due to its impairment in psychiatric disorders such as schizophrenia. To identify quantitative trait loci (QTL) involved in mouse PPI, we studied mouse chromosome substitution strains (CSS) that each carry a homologous chromosome pair from the A/J inbred strain on a host C57BL/6J inbred strain background. We determined that the chromosome 16 substitution strain has elevated PPI compared to C57BL/6J (P ¼ 1.6 3 10 ÿ11

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“…However, there is no consensus about relating a preattentional deficit with attention deficit and hyperactivity disorder (ADHD). PPI does not appear to be affected in studies for people with ADHD for children (Castellanos et al, 1996;Ornitz et al, 1992Ornitz et al, , 1999 and adults (Conzelmann et al, 2010;Feifel et al, 2009;Hanlon et al, 2009) diagnosed with ADHD, but there are other publications in which a PPI disruption is observed in ADHD patients. For instance, Schulz-Juergensen et al (2014) showed a preattentional deficit in ADHD patients that was reversed by methylphenidate treatment.…”

Section: Introductionmentioning

confidence: 91%

Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

Ortega-Álvaro

Navarrete

Aracil-Fernández

et al. 2015

Neuropsychopharmacol

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The endocannabinoid system has been widely involved in the pathophysiology of sensorimotor gating deficits. This study aimed to evaluate the pharmacological modulation of the sensorimotor gating impairment induced by cannabinoid CB1 receptor (CB1r) deletion. For this purpose, the prepulse inhibition (PPI) paradigm was used to evaluate the effect of two antipsychotics drugs (risperidone and haloperidol) and a psychostimulant (methylphenidate) on the preattentional deficit presented by CB1KO mice. Furthermore, the effects of the CB1r antagonist AM251 on PPI were evaluated in WT mice. Real-time PCR and immunohistochemical studies were carried out to analyze dopamine transporter (DAT) and α-2C adrenergic receptor (ADRA2C) gene expressions and the distribution of parvalbumin (PV) and cholecystokinin-8 (CCK) immunoreactive (ir) cortical neurons, respectively. Neither risperidone nor haloperidol significantly modified the PPI of WT and CB1KO mice, whereas methylphenidate improved the preattentional deficit of CB1KO mice. In addition, treatment with AM251 (3 mg/kg; i.p.) significantly decreased the PPI of WT animals. The administration of methylphenidate increased DAT and ADRA2C gene expressions in CB1KO mice without producing any effect in WT animals. Immunohistochemical studies revealed that there were no significant changes in CCK immunolabeling between WT and CB1KO mice, whereas the radial distribution of PV-ir neurons was abnormal in CB1KO mice. These data further support the important role of CB1r in sensorimotor gating regulation and the therapeutic usefulness of methylphenidate for the treatment of psychiatric disorders with associated preattentional deficits.

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Prepulse inhibition of startle and the neurobiology of primary nocturnal enuresis

Cited by 118 publications

References 68 publications

Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice

Sensorimotor gating abnormalities in young males with fragile X syndrome and Fmr1-knockout mice

Two Quantitative Trait Loci for Prepulse Inhibition of Startle Identified on Mouse Chromosome 16 Using Chromosome Substitution Strains

Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations

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