Related Experiment Videos
Differential alterations in opioid analgesia following neonatal monosodium glutamate treatment
Abstract:
Neonatal administration of monosodium glutamate (MSG) produces necrosis of circumventricular structures, including perikarya in the medial-basal hypothalamus that contain beta-endorphin (BEND) and met-enkephalin. Since neonatal MSG treatment alters morphine analgesia, the present study examined neonatal MSG effects upon opioid analgesia observed following either BEND or d-ala d-leu enkephalin (DADL). Rats treated with either MSG or vehicle over the first ten post-natal days, were surgically prepared with a lateral ventricle cannula at 100 days of age. Respective groups received central injections of either BEND (0, 0.1, 0.5 or 1.0 microgram) or DADL (0, 4, 20 or 40 micrograms), and jump thresholds were assessed 15, 30, 45 and 60 min thereafter. Following testing, selected MSG-treated and control animals were prepared for BEND immunocytochemistry. While the magnitude, duration and sensitivity of BEND analgesia on the jump test failed to differ between groups, MSG-treated rats displayed a 10-fold leftward shift in sensitivity and a 200-300% increase in the magnitude of DADL analgesia. Immunocytochemical analysis indicated that MSG treatment depleted perikarya in the medial-basal hypothalamus, periventricular thalamic fibers and periaqueductal gray terminal fields that contained BEND. The differential effects of MSG treatment upon opiate and opioid analgesia are discussed in terms of possible alterations in opiate receptor subpopulations.
Insights
Neonatal monosodium glutamate (MSG) exposure damages brain regions containing beta-endorphin (BEND). MSG altered DADL opioid analgesia but not BEND analgesia, suggesting changes in opioid receptor subtypes.
Area of Science:
- Neuroscience
- Neuropharmacology
- Endocrinology
Background:
- Neonatal monosodium glutamate (MSG) administration causes neuronal damage in specific brain regions.
- These damaged regions include hypothalamic areas containing beta-endorphin (BEND) and met-enkephalin.
- Previous studies indicate MSG alters morphine analgesia.
Purpose of the Study:
- To investigate the effects of neonatal MSG treatment on analgesia induced by central administration of beta-endorphin (BEND) and d-ala d-leu enkephalin (DADL).
- To explore potential alterations in opioid receptor sensitivity following MSG-induced neurotoxicity.
Main Methods:
- Rats received MSG or vehicle during the first ten postnatal days.
- Adult rats (100 days old) were cannulated for intracerebroventricular injections.
- Analgesia was assessed using the jump threshold test after central BEND or DADL administration.
- Immunocytochemistry was used to examine BEND distribution in MSG-treated and control rats.
Main Results:
- Neonatal MSG treatment did not alter the magnitude, duration, or sensitivity of BEND-induced analgesia.
- MSG-treated rats showed a 10-fold increase in sensitivity and 200-300% greater magnitude of DADL analgesia.
- Immunocytochemistry confirmed depletion of BEND-containing perikarya and fibers in MSG-treated rats.
Conclusions:
- Neonatal MSG exposure differentially affects opioid analgesia, specifically enhancing DADL analgesia while sparing BEND analgesia.
- These findings suggest MSG-induced neurotoxicity may lead to alterations in specific opioid receptor subpopulations.