Dietary therapy restores glutamatergic input to orexin/hypocretin neurons after traumatic brain injury in mice

Sleep
Jonathan E ElliottMiranda M Lim

Abstract

In previous work, dietary branched-chain amino acid (BCAA) supplementation, precursors to de novo glutamate and γ-aminobutyric acid (GABA) synthesis, restored impaired sleep-wake regulation and orexin neuronal activity following traumatic brain injury (TBI) in mice. TBI was speculated to reduce orexin neuronal activity through decreased regional excitatory (glutamate) and/or increased inhibitory (GABA) input. Therefore, we hypothesized that TBI would decrease synaptic glutamate and/or increase synaptic GABA in nerve terminals contacting orexin neurons, and BCAA supplementation would restore TBI-induced changes in synaptic glutamate and/or GABA. Brain tissue was processed for orexin pre-embed diaminobenzidine labeling and glutamate or GABA postembed immunogold labeling. The density of glutamate and GABA immunogold within presynaptic nerve terminals contacting orexin-positive lateral hypothalamic neurons was quantified using electron microscopy in three groups of mice (n = 8 per group): Sham/noninjured controls, TBI without BCAA supplementation, and TBI with BCAA supplementation (given for 5 days, 48 hr post-TBI). Glutamate and GABA were also quantified within the cortical penumbral region (layer VIb) adjacent to the TBI lesion. ...Continue Reading

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Citations

Oct 24, 2018·NeuroRehabilitation·Alphonsa Thomas, Brian D Greenwald
Jun 17, 2020·Obesity Reviews : an Official Journal of the International Association for the Study of Obesity·Jianfei LinFan Jiang
Oct 28, 2020·Journal of Neuroscience Research·Joshua P McGeownRobert Borotkanics

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Brain Injury & Trauma

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