ArticleJournal of molecular neuroscience : MN2007
Blockage of VIP during mouse embryogenesis modifies adult behavior and results in permanent changes in brain chemistry.
Article in Journal of molecular neuroscience : MN, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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
16 citing papers in PubMed, 29 citations in OpenAlex.
- The C9ORF72 repeat expansion alters neurodevelopment.Cell reports · 2023Article
- (Neuro) Peptides, Physical Activity, and Cognition.Journal of clinical medicine · 2020Review
- Vasoactive Intestinal Peptide Decreases β-Amyloid Accumulation and Prevents Brain Atrophy in the 5xFAD Mouse Model of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2019Article
- Retinoprotective Effects of TAT-Bound Vasoactive Intestinal Peptide and Pituitary Adenylate Cyclase Activating Polypeptide.Journal of molecular neuroscience : MN · 2019Article
- Nesting behavior is associated with VIP expression and VIP-Fos colocalization in a network-wide manner.Hormones and behavior · 2015Article
- Pair bond formation is impaired by VPAC receptor antagonism in the socially monogamous zebra finch.Behavioural brain research · 2014Article
- Amygdala nuclei critical for emotional learning exhibit unique gene expression patterns.Neurobiology of learning and memory · 2013Article
- VPAC receptor signaling modulates grouping behavior and social responses to contextual novelty in a gregarious finch: a role for a putative prefrontal cortex homologue.Hormones and behavior · 2013Article
- Multiplex targeted sequencing identifies recurrently mutated genes in autism spectrum disorders.Science (New York, N.Y.) · 2012Article
- Vasoactive intestinal peptide enhances striatal plasticity and prevents dopaminergic cell loss in Parkinsonian rats.Journal of molecular neuroscience : MN · 2012Article
- Neuropeptide GPCRs in neuroendocrinology: the case of activity-dependent neuroprotective protein (ADNP).Frontiers in endocrinology · 2012Article
- Chemical modification of class II G protein-coupled receptor ligands: frontiers in the development of peptide analogs as neuroendocrine pharmacological therapies.Pharmacology & therapeutics · 2010Review
- VIP, from gene to behavior and back: summarizing my 25 years of research.Journal of molecular neuroscience : MN · 2008Article
- Regardless of genotype, offspring of VIP-deficient female mice exhibit developmental delays and deficits in social behavior.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2008Article
- Deficits in social behavior and reversal learning are more prevalent in male offspring of VIP deficient female mice.Experimental neurology · 2008Article
- Vasoactive intestinal peptide (VIP) regulates activity-dependent neuroprotective protein (ADNP) expression in vivo.Journal of molecular neuroscience : MN · 2007Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Vasoactive intestinal peptide (VIP) regulates growth and development during the early postimplantation period of mouse embryogenesis. Blockage of VIP with a VIP antagonist during this period results in growth restriction, microcephaly, and developmental delays. Similar treatment of neonatal rodents also causes developmental delays and impaired diurnal rhythms, and the adult brains of these animals exhibit neuronal dystrophy and increased VIP binding. These data suggest that blockage of VIP during the development of the nervous system can result in permanent changes to the brain. In the current study, pregnant mice were treated with a VIP antagonist during embryonic days 8 through 10. The adult male offspring were examined in tests of novelty, paired activity, and social recognition. Brain tissue was examined for several measures of chemistry and gene expression of VIP and related compounds. Glial cells from the cortex of treated newborn mice were plated with neurons and examined for VIP binding and their ability to enhance neuronal survival. Treated adult male mice exhibited increased anxiety-like behavior and deficits in social behavior. Brain tissue exhibited regionally specific changes in VIP chemistry and a trend toward increased gene expression of VIP and related compounds that reached statistical significance in the VIP receptor, VPAC-1, in the female cortex. When compared to control astrocytes, astrocytes from treated cerebral cortex produced further increases in neuronal survival with excess synaptic connections and reduced VIP binding. In conclusion, impaired VIP activity during mouse embryogenesis resulted in permanent changes to both adult brain chemistry/cell biology and behavior with aspects of autism-like social deficits.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.