ArticleExperimental brain research2009
Neonatal exposure to MK801 promotes prepulse-induced delay in startle response time in adult rats.
Article in Experimental brain research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- Acute and Long-Term Consequences of Neonatal NMDA Blockade in the Cx3cr1 Knock-Out Mouse.Inflammation · 2025Article
- GABAFrontiers in integrative neuroscience · 2021Article
- Effect of Neonatal Treatment With the NMDA Receptor Antagonist, MK-801, During Different Temporal Windows of Postnatal Period in Adult Prefrontal Cortical and Hippocampal Function.Frontiers in behavioral neuroscience · 2021Article
- Neurotoxicity of low-level lead exposure: History, mechanisms of action, and behavioral effects in humans and preclinical models.Neurotoxicology · 2019Review
- Altered Auditory Processing, Filtering, and Reactivity in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Antioxidant Treatment with N-acetyl Cysteine Prevents the Development of Cognitive and Social Behavioral Deficits that Result from Perinatal Ketamine Treatment.Frontiers in behavioral neuroscience · 2017Article
- Strategies to defeat ketamine-induced neonatal brain injury.Neuroscience · 2012Article
- Matrix metalloproteinases 2 and 9 fail to influence drug-induced neuroapoptosis in developing rat brain.Neurotoxicity research · 2011Article
- Is age-dependent, ketamine-induced apoptosis in the rat somatosensory cortex influenced by temperature?Neuroscience · 2010Article
- Postnatal exposure to MK801 induces selective changes in GAD67 or parvalbumin.Experimental brain research · 2010Article
- Article
- Low-level lead exposure triggers neuronal apoptosis in the developing mouse brain.Neurotoxicology and teratologyArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The acoustic startle reflex in rats can be inhibited if a prepulse stimulus is presented just before the startle stimulus (prepulse inhibition; PPI). When postnatal day 7 (P7) rats are exposed to agents that block the NMDA receptor (NMDAR), robust apoptosis is observed within hours and is thought to be followed at later ages by a significant loss of PPI. To understand these observations further, we exposed rat pups to vehicle or the NMDAR antagonist MK801 (1 mg/kg) at P6, P8, and P10. We then examined animals for PPI at P28 and P56. Compared to vehicle controls, we found no evidence for PPI deficits in the MK801-treated group, although we did observe prepulse-induced delay in response time at P56 (but not at P28). In a parallel study, we also performed histological analysis of brain sections for evidence of the pro-apoptotic marker activated caspase-3, 8 h after vehicle or MK801 injection into P6 animals. We found that there was a robust increase in this marker of cell death in the inferior colliculus of MK801 compared to vehicle-treated animals. Thus, transient blockade of the NMDAR during the postnatal period not only promotes early apoptosis in a brain region critical for acoustic processing but also leads to auditory deficits at a later age, suggesting that injury-induced loss of collicular neurons leads to network reorganization in the auditory system that is progressive in nature.
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Registered trials
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