ArticleExperimental neurology2012
Antenatal insults modify newborn olfactory function by nitric oxide produced from neuronal nitric oxide synthase.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Olfactory testing in infants with perinatal asphyxia: Enhancing encephalopathy risk stratification for future health outcomes.Neuroscience and biobehavioral reviews · 2025Review
- Development of a New Scoring System in Higher Animals for Testing Cognitive Function in the Newborn Period: Effect of Prenatal Hypoxia-Ischemia.Developmental neuroscience · 2025Article
- Social Odour Perception and Stress Responses in Women's Quality of Partner Relationship and Attachment Style.Behavioral sciences (Basel, Switzerland) · 2023Article
- Smell and Stress Response in the Brain: Review of the Connection between Chemistry and Neuropharmacology.Molecules (Basel, Switzerland) · 2021Review
- Manganese-Enhanced Magnetic Resonance Imaging: Overview and Central Nervous System Applications With a Focus on Neurodegeneration.Frontiers in aging neuroscience · 2018Review
- Role of Prenatal Hypoxia in Brain Development, Cognitive Functions, and Neurodegeneration.Frontiers in neuroscience · 2018Review
- Oxidative Stress in Hypoxic-Ischemic Encephalopathy: Molecular Mechanisms and Therapeutic Strategies.International journal of molecular sciences · 2016Review
- Improved visualization of neuronal injury following glial activation by manganese enhanced MRI.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Newborn feeding, maternal, bonding, growth and wellbeing depend upon intact odor recognition in the early postnatal period. Antenatal stress may affect postnatal odor recognition. We investigated the exact role of a neurotransmitter, nitric oxide (NO), in newborn olfactory function. We hypothesized that olfactory neuron activity depended on NO generated by neuronal NO synthase (NOS). Utilizing in vivo functional manganese enhanced MRI (MEMRI) in a rabbit model of cerebral palsy we had shown previously that in utero hypoxia-ischemia (H-I) at E22 (70% gestation) resulted in impaired postnatal response to odorants and poor feeding. With the same antenatal insult, we manipulated NO levels in the olfactory neuron in postnatal day 1 (P1) kits by administration of intranasal NO donors or a highly selective nNOS inhibitor. Olfactory function was quantitatively measured by the response to amyl acetate stimulation by MEMRI. The relevance of nNOS to normal olfactory development was confirmed by the increase of nNOS gene expression from fetal ages to P1 in olfactory epithelium and bulbs. In control kits, nNOS inhibition decreased NO production in the olfactory system and increased MEMRI slope enhancement. In H-I kits the MEMRI slope did not increase, implicating modification of endogenous NO-mediated olfactory function by the antenatal insult. NO donors as a source of exogenous NO did not significantly change function in either group. In conclusion, olfactory epithelium nNOS in newborn rabbits probably modulates olfactory signal transduction. Antenatal H-I injury remote from delivery may affect early functional development of the olfactory system by decreasing NO-dependent signal transduction.
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