Auditory hindbrain atrophy and anomalous calcium binding protein expression after neonatal exposure to monosodium glutamate. (6th March 2017)

• Record Type: Journal Article
• Authors: Foran, Lindsey; Blackburn, Kaitlyn; Kulesza, Randy J.
• Is Part Of: Neuroscience. Volume 344(2017)
• Page Start: 406
• Page End: 417
• Publication Date: 2017-03-06
• Subjects: 4V fourth ventricle -- AVCN anterior ventral cochlear nucleus -- CB calbindin -- CI confidence interval -- CR calretinin -- DCN dorsal cochlear nucleus -- LSO lateral superior olive -- MNTB medial nucleus of the trapezoid body -- MSG monosodium glutamate -- MSO medial superior olive -- OC octopus cell -- PB phosphate buffer -- PVCN posterior ventral cochlear nucleus -- RF reticular formation -- SOC superior olivary complex -- SPON superior paraolivary nucleus -- VCN ventral cochlear nucleus; brainstem -- cochlear nucleus -- superior olivary complex -- trapezoid body; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2017.01.004
• Languages: English
• ISSNs: 0306-4522

Abstract

Highlights: MSG is known to be excitotoxic to the brain during the neonatal period. Neonatal exposure results in fewer neurons in the spiral ganglion. Neonatal MSG exposure resulted in significantly fewer neurons in the VCN and SOC. Neonatal MSG exposure resulted in significantly reduced expression of CR and CB. Abstract: 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, elevated 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 flavor enhancer in many processed foods. Previous studies have shown that MSG administration during the early postnatal period results in neurodegenerative changes in several forebrain regions, characterized by neuronal loss and neuroendocrine abnormalities. Systemic delivery of MSG during the neonatal period and induction of glutamate neurotoxicity in the cochlea have both been shown to result in fewer neurons in the spiral ganglion. We hypothesized that an MSG-induced loss of neurons in the spiral ganglion would have a significant impact on the number of neurons in the cochlear nuclei and superior olivary complex (SOC). Indeed, we found that exposure to MSG from postnatal days 4 through 10 resulted in significantly fewer neurons in the cochlear nuclei and SOC and significant dysmorphology in surviving neurons. Moreover, we found that neonatal MSG exposure resulted in a significant decrease in the expression of both calretinin and calbindin. These results suggest that neonatal exposure to MSG interferes with early development of the auditory brainstem and impacts expression of calcium binding proteins, both of which may lead to diminished auditory function.