NMDA Receptors in the Developing Brain and Effects of Noxious Insults

Waters, Karen A.; Machaalani, Rita

doi:10.1159/000077523

Cited by 41 publications

(19 citation statements)

References 121 publications

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“…IHH is a potent pathological noxious insult that induces unique pathophysiological effects on neurons of the brain (Waters and Machaalani, 2004). It is plausible that exposure to hypoxia reduces production/synthesis of orexin at the mRNA level which subsequently manifests at the protein level.…”

Section: Discussionmentioning

confidence: 99%

Cumulative effects of repetitive intermittent hypercapnic hypoxia on orexin in the developing piglet hypothalamus

Hunt

Waters

et al. 2015

Intl J of Devlp Neuroscience

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Orexin neuropeptides (OxA and OxB) and their receptors (OX1R and OX2R) are involved in maintenance of sleep and wakefulness, and are regulated by various environmental stimuli. We studied piglets, in the early neonatal period, exposed to 48-min of intermittent hypercapnic hypoxia (IHH; 7% O2/8% CO2) alternating with air. Three groups of 13-14 day-old piglets with IHH exposure of 1-day (1D-IHH) (n=7), 2-days (2D-IHH) (n=7) and 4-days (4D-IHH) (n=8) were compared to controls (exposed only to air, n=8). Immunoreactivity of OxA and OxB was studied in the piglet hypothalamic regions of the dorsomedial hypothalamus (DMH), perifornical area (PeF) and lateral hypothalamic area (LH). Results showed that after 1D- and 2D-IHH, total OxA and OxB expression decreased by 20% (p ≤ 0.005) and 40% (p<0.001), respectively. After 4D-IHH, the decrease in OxA and OxB was 50% (p<0.001). These findings indicate that a chronic IHH exposure induces greater changes in orexin neuropeptide expression than an acute 1-day exposure in the hypothalamus. This may be causally related to the dysregulation of sleep.

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Section: Discussionmentioning

confidence: 99%

Cumulative effects of repetitive intermittent hypercapnic hypoxia on orexin in the developing piglet hypothalamus

Hunt

Waters

et al. 2015

Intl J of Devlp Neuroscience

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“…In addition to the increase in hypernociceptive behavior, downregulation of expression of the NR1 subunit occurred in the magnesium-deficiency group treated with Cg. This may reflect a necessary adaptive response to avoid excessive neuronal excitability, glutamate-induced NMDA-R overstimulation, and an excitotoxic process that leads to cell death, all of which can be observed in many neurological conditions (36)(37)(38)(39). However, we did not observe a decrease in phospho-NR1; rather, we observed an increase of phospho-NR1 in the magnesium-depleted Cg group in comparison with the Cg group.…”

Section: Discussionmentioning

confidence: 99%

Role ofNMDAreceptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis

Cavalcante

Siqueira

Araújo

et al. 2013

European J Oral Sciences

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Temporomandibular joint (TMJ) arthritis is a common cause of orofacial pain. In the present study, the modulatory effects of N-methyl-d-aspartate receptors (NMDA-Rs) and magnesium were investigated in TMJ arthritis hypernociception. Male Wistar rats received an intra-articular injection of carrageenan (Cg) in the TMJ, and mechanical hypernociception was measured. The NMDA-R antagonist, MK-801, and magnesium chloride (MgCl₂ ) were administered before arthritis induction. Magnesium deficiency was promoted by feeding rats a synthetic magnesium-free diet for 9 d before injection of Cg. The Cg induced mechanical hypernociception that lasted for 120 h. MK-801 inhibited this hypernociceptive state. MgCl₂ pretreatment prevented Cg-induced hypernociception and altered the nociceptive threshold in the absence of Cg. Magnesium deficiency increased hypernociception and induced spontaneous hypernociceptive behavior. TMJ arthritis increased the expression of mRNA for all NMDA-R subunits and immunostaining of phosphorylated NR1 (phospho-NR1). MgCl₂ inhibited expression of NR2B mRNA and phospho-NR1 immunostaining and increased expression of NR3 mRNA. Magnesium deficiency increased expression of both NR1 and NR3 mRNAs and phospho-NR1 immunostaining in the trigeminal subnucleus caudalis. We found that magnesium modulates nociceptive behavior and induces NMDA-R subunit rearrangement in the subnucleus caudalis. The present results may lead to a better understanding of central processing in the nociceptive trigeminal pathway and the development of new approaches to treat orofacial pain with a TMJ origin.

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“…Since NMDARs play an important role on neural cell growth and differentiation in hippocampus, expression of NMDARs in hippocampus has been implicated as important indicators of both learning and neural development [39]. Several studies indicated that there is NMDAR 1A/2B subunits combination in immature brain and NMDAR 1A/2A subunits combination in mature brain [40,41].…”

Section: Discussionmentioning

confidence: 99%

Aluminum alters NMDA receptor 1A and 2A/B expression on neonatal hippocampal neurons in rats

2011

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BackgroundHigh aluminum (Al) content in certain infant formula raises the concern of possible Al toxicity on brain development of neonates during their vulnerable period of growing. Results of in vivo study showed that Al content of brain tissues reached to 74 μM when oral intake up to 1110 μM, 10 times of that in the hi-Al infant formula.MethodsUtilizing a cultured neuron cells in vitro model, we have assessed Al influence on neuronal specific gene expression alteration by immunoblot and immunohistochemistry and neural proliferation rate changes by MTT assay.ResultsMicroscopic images showed that the neurite outgrowth of hippocampal neurons increased along with the Al dosages (37, 74 μM Al (AlCl3)). MTT results also indicated that Al increased neural cell viability. On the other hand, the immunocytochemistry staining suggested that the protein expressions of NMDAR 1A and NMDAR 2A/B decreased with the Al dosages (p < 0.05).ConclusionTreated hippocampal neurons with 37 and 74 μM of Al for 14 days increased neural cell viability, but hampered NMDAR 1A and NMDAR 2A/B expressions. It was suggested that Al exposure might alter the development of hippocampal neurons in neonatal rats.

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NMDA Receptors in the Developing Brain and Effects of Noxious Insults

Cited by 41 publications

References 121 publications

Cumulative effects of repetitive intermittent hypercapnic hypoxia on orexin in the developing piglet hypothalamus

Cumulative effects of repetitive intermittent hypercapnic hypoxia on orexin in the developing piglet hypothalamus

Role ofNMDAreceptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis

Aluminum alters NMDA receptor 1A and 2A/B expression on neonatal hippocampal neurons in rats

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