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Selective Alterations of Opiate Receptor Subtypes in Mono sodium Glutamate‐Treated Rats
Author(s) -
Young Elizabeth,
Olney John,
Akil Huda
Publication year - 1983
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1983.tb08126.x
Subject(s) - receptor , medicine , endocrinology , μ opioid receptor , thalamus , δ opioid receptor , chemistry , glutamate receptor , enkephalin , striatum , opioid , biology , neuroscience , dopamine
Neonatal treatment of rats with monosodium glutamate (MSG) has been demonstrated to destroy cell bodies of neurons in the arcuate nucleus including the brain beta‐endorphin (B‐END) system. The effects on opiate receptors of the loss of B‐END is unknown. Neonatal rats were treated with MSG as previously described. After reaching maturity (7‐9 months), MSG‐treated rats and litter‐matched untreated control rats were decapitated and brains dissected into brain regions. Opiate receptor assays were run with [ 3 H]morphine (mu receptor ligand) and [ 3 H]D‐alanine 2 ‐D‐leucine 5 (DADL) enkephalin (delta receptor ligand) for each brain region for both MSG and control rats simultaneously. Scatchard plot analyses showed a selective increase in delta receptors in the thala‐mus only. No corresponding change in mu receptors in the thalamus was found. The cross‐competition IC 50 data supported this conclusion, showing a loss in the potency of morphine in displacing [ 3 H]DADL enkephalin in the thalamus of MSG‐treated rats. This shift in delta receptors produced an IC 50 displacement pattern in thalamus, ordinarily a mu‐rich area, similar to that of striatum or cortex, delta‐rich areas, again indicating an increase in delta receptors. Similar changes in delta receptors in other brain regions were not found. These results represent one of the few examples of a selective and localized shift in delta with no change in mu sites. Furthermore, the delta increase may reflect an up‐regulation of the receptors in thalamus after chronic loss of the endogenous opioid B‐END.