Alterations to prepulse inhibition magnitude and latency in adult rats following neonatal treatment with domoic acid and social isolation rearing

Marriott, Amber L.; Tasker, R. Andrew; Ryan, Catherine L.; Doucette, Tracy A.

doi:10.1016/j.bbr.2015.11.009

Cited by 16 publications

(11 citation statements)

References 78 publications

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“…Studies in rats exploring the neural substrates of sensorimotor gating have noted that prepulse effects on startle latency occur separately from PPI (i.e., startle amplitude), so PPI deficits cannot simply reflect reduced prepulse detection because latency modulation may still remain intact (Ison et al, 1973;Swerdlow et al, 1992). Two previous studies support this conclusion because the presence of PPI deficits in animal models of schizophrenia was not associated with differences in startle latency (Lyall et al, 2009;Marriott et al, 2016). This is further exemplified in the present study, in which Cntnap2 Ϫ/Ϫ rats exhibited greater baseline startle responses without effects on latency (Figs.…”

Section: Speed Of Neurotransmission and Startle Response Latencymentioning

confidence: 83%

“…Importantly, sensorimotor gating relies on these central components of the auditory brainstem. For example, lesioning the inferior colliculus causes both a greater startle response and prevents inhibition of startle by a prepulse (Leitner and Cohen, 1985). PPI is impaired in knock-out rats (Figs.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to measuring changes in startle magnitude to assess PPI, the latency of the startle response was also measured in trials with/without the prepulse as an increased latency to the maximum startle amplitude is indicative of sensorimotor gating (Hoffman and Wible, 1970;Ison et al, 1973). The relative changes in latency were calculated as the time to reach the maximum startle magnitude on startle pulse-alone trials subtracted from that during prepulse trials (i.e., positive values represented an increase in latency on prepulse trials; Lyall et al, 2009;Marriott et al, 2016; see Fig. 8A).…”

Section: Methodsmentioning

confidence: 99%

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Altered Auditory Processing, Filtering, and Reactivity in theCntnap2Knock-Out Rat Model for Neurodevelopmental Disorders

et al. 2018

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Sensory processing, and auditory processing in particular, is altered in individuals with neurodevelopmental disorders such as autism spectrum disorders (ASDs). The typical maturation of the auditory system is perturbed in these individuals during early development, which may underlie altered auditory reactivity that persists in later life. Of the many genes that regulate the auditory system development, loss-of-function mutations in the gene are strongly associated with language processing deficits and ASD. Therefore, using a novel knock-out rat model, we tested the impact of loss on auditory processing, filtering, and reactivity throughout development and young adulthood in male and female animals. Although hearing thresholds were not altered in knock-out animals, we found a reduction in response amplitudes and a delay in response latency of the auditory brainstem response (ABR) in juvenile knock-out rats compared with age-matched controls. Amplitudes and latency of the ABR largely normalized by adulthood, indicating a delayed maturation of auditory processing pathways in knock-out rats. Despite the reduced ABR amplitudes, adolescent knock-out animals displayed increased startle reactivity accompanied by disruptions in sensory filtering and sensorimotor gating across various conditions, most of which persisted in adulthood. All of these observations show striking parallels to disruptions reported in ASD. Our results also imply that developmental disruptions of sensory signal processing are associated with persistent changes in neural circuitries responsible for implicit auditory evoked behavior, emphasizing the need for interventions that target sensory processing disruptions early during development in ASD. This is the first study of brainstem auditory processing in a novel knock-out rat model with very high construct and face validity for autism spectrum disorders. Electrophysiological and behavioral measures of implicit auditory-evoked responses were systematically taken across developmental stages. Auditory processing, filtering, and reactivity disruptions show striking similarities to observations in autism. We also show for the first time that, whereas auditory brainstem responses normalize by adulthood, disruptions in brainstem-mediated auditory-evoked behavior persist. This indicates that early developmental perturbations in sensory processing can cause permanent maladaptive changes in circuitries responsible for auditory reactivity, underlining the importance for interventions early during development aiming at normalizing sensory processing.

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Section: Speed Of Neurotransmission and Startle Response Latencymentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Altered Auditory Processing, Filtering, and Reactivity in theCntnap2Knock-Out Rat Model for Neurodevelopmental Disorders

et al. 2018

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“…Administration of low doses of DOM in neonatal rats does not produce overt toxicity or status epilepticus but results in permanent alterations in adult rat behavior that manifest as changes in cognition [17][18][19], attentional processing [20][21][22], anxiety [18,23], seizure threshold [24], and sleep patterns [25] that are consistent with the development of temporal lobe epilepsy (TLE). Moreover, these changes in behavior have been shown to correlate with neuropathological changes in the hippocampal formation such as mossy fiber sprouting (MFS) [17,26] and selective loss of parvalbumin-positive GABAergic interneurons [27] that are also present in both animal models of TLE produced by kainic acid [13,28] as well as human TLE patients [29].…”

Section: Introductionmentioning

confidence: 99%

Progressive changes in hippocampal cytoarchitecture in a neurodevelopmental rat model of epilepsy: implications for understanding presymptomatic epileptogenesis, predictive diagnosis, and targeted treatments

et al. 2017

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Epilepsies affect about 4% of the population and are frequently characterized by a prolonged Bsilent^period before the onset of spontaneous seizures. Most current animal models of epilepsy either involve acute seizure induction or kindling protocols that induce repetitive seizures. We have developed a rat model of epilepsy that is characterized by a slowly progressing series of behavioral abnormalities prior to the onset of behavioral seizures. In the current study, we further describe an accompanying progression of cytoarchitectural changes in the hippocampal formation. Groups of male and female SD rats received serial injections of a low dose of domoic acid (0.020 mg/kg) (or vehicle) throughout the second week of life. Postmortem hippocampal tissue was obtained on postnatal days 29, 64, and 90 and processed for glial fibrillary acidic protein (GFAP), NeuN, and calbindin expression. The data revealed no significant changes on postnatal day (PND) 29 but a significant increase in hilar NeuN-positive cells in some regions on PND 64 and 90 that were identified as ectopic granule cells. Further, an increase in GFAP positive cell counts and evidence of reactive astrogliosis was found on PND 90 but not at earlier time points. We conclude that changes in cellular expression, possibly due to on-going non-convulsive seizures, develop slowly in this model and may contribute to progressive brain dysfunction that culminates in a seizure-prone phenotype.

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“…Different kinds of memory, assessed by the Morris water maze in male mice after 4 weeks of social isolation [14] and by the novel object recognition test in female Lister Hooded rats after 28 days of social isolation, were impaired [15]. Also, attention that is needed for proper cognitive performance was disturbed in socially isolated male Sprague-Dawley rats [16]. …”

Section: Behavioral Changesmentioning

confidence: 99%

Social Isolation Rearing Induces Neuropsychiatric Diseases: Updated Overview

Famitafreshi

Karimian

2018

Complex Psychiatry

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Neuropsychiatric and neurologic diseases cause a great burden for individuals, families, and societies. Social isolation rearing can trigger a variety of psychiatric diseases. New advances suggest that epigenetic factors along with other neurochemical changes can be an important topic in neuropsychiatric diseases. It is thought that the prevention of social isolation rearing that occurs around birth can reduce the occurrence of neuropsychiatric diseases. It has been suggested that the environment can induce epigenetic alternation. So, for the diagnosis of a proportion of neuropsychiatric diseases, assessing epigenetic factors may be helpful. Also, apart from epigenetic factors, new advances have been made about new mechanisms of and treatments for such a disorder.

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Alterations to prepulse inhibition magnitude and latency in adult rats following neonatal treatment with domoic acid and social isolation rearing

Cited by 16 publications

References 78 publications

Altered Auditory Processing, Filtering, and Reactivity in theCntnap2Knock-Out Rat Model for Neurodevelopmental Disorders

Altered Auditory Processing, Filtering, and Reactivity in theCntnap2Knock-Out Rat Model for Neurodevelopmental Disorders

Progressive changes in hippocampal cytoarchitecture in a neurodevelopmental rat model of epilepsy: implications for understanding presymptomatic epileptogenesis, predictive diagnosis, and targeted treatments

Social Isolation Rearing Induces Neuropsychiatric Diseases: Updated Overview

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