Neonatal exposure to monosodium glutamate results in dysmorphology of orofacial lower motor neurons.

Glutamate is the most abundant excitatory neurotransmitter in the central nervous system, and is stored and released by both neurons and astrocytes. Despite the important role of glutamate as a neurotransmitter, high levels of extracellular glutamate can result in excitotoxicity and apoptosis. Monosodium glutamate (MSG) is a naturally occurring sodium salt of glutamic acid that is used as a flavour enhancer in many processed foods. Neonatal exposure to MSG has been shown to result in neurodegeneration in several forebrain regions, characterised by neuronal loss and neuroendocrine abnormalities. However, the brainstem effects of neonatal MSG exposure have not been investigated. It is therefore hypothesized that MSG exposure during the early postnatal period would impact brainstem lower motor neurons involved in feeding behaviour. The effect of neonatal MSG exposure on brainstem lower motor neurons was investigated by exposing rat pups to either 4 mg/g MSG or saline from postnatal day (P) 4 through 10. On P28, brains were preserved by vascular perfusion with fixative, frozen sectioned and stained for Nïssl substance. The number, size and shape of brainstem motor neurons were compared between MSG and saline-exposed animals. MSG exposure had no impact on the total number of neurons in the nuclei examined. However, MSG exposure was associated with a significant increase in the number of round somata in both the trigeminal and facial nuclei. Furthermore, MSG exposure resulted in significantly smaller neurons in all motor nuclei examined. These results suggest that neonatal exposure to MSG impacts the development of brainstem lower motor neurons which may impact feeding and swallowing behaviours in young animals.

Using cluster analysis to provide new insights into development of very low birthweight (VLBW) premature infants.

BACKGROUND: Very low birthweight (VLBW) premature infant follow-up studies report on single developmental outcome variables but do not assess profiles of development. AIMS: To identify developmental profiles of VLBW premature infants based on cognitive and language development and their association with demographic, perinatal, and behavior variables. STUDY DESIGN: Retrospective chart review. SUBJECTS: 117 children<1250 g BW seen at 18 months post-term on the Bayley Scales-III and Child Behavior Checklist 1 ½-5 (CBCL 1 ½-5), a behavior problem questionnaire. Demographic and perinatal variables were obtained from medical records. OUTCOME MEASURES: Bayley Cognitive, Expressive Language, and Receptive Language scores were used to cluster the subjects into developmental profiles. Demographic, perinatal, and CBCL variables were analyzed as they related to clusters. RESULTS: Children were clustered into 4 groups based on their Bayley Cognitive, Expressive Language, and Receptive Language scores: Consistently High, Consistently Average, Average with Delayed Expressive Language, and Consistently Low. Socioeconomic status, bronchopulmonary dysplasia, Grades III-IV intraventricular hemorrhage, and summary Behavior Problems and Attention Deficit/Hyperactivity (ADHD) Problems scores were significantly related to clusters. CONCLUSION: Cluster analysis defined distinct outcome groups in VLBW premature children and provides an informative means of identifying factors related to developmental outcome. This approach may be useful in predicting later outcome and determining which groups of children will require early intervention.