Monosodium glutamate induced lesions of the arcuate nucleus. II. Fluorescence histochemistry of catecholamines

1976 ◽  
Vol 186 (2) ◽  
pp. 197-205 ◽  
Author(s):  
M. A. Holzwarth-Mcbride ◽  
J. R. Sladek ◽  
K. M. Knigge
Keyword(s):  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Fluorescence Histochemistry

Prevention of reflex natriuresis after acute unilateral nephrectomy by neonatal administration of MSG

1987 ◽  
Vol 252 (2) ◽  
pp. F276-F282 ◽  
Author(s):  
S. Y. Lin ◽  
E. Wiedemann ◽  
C. F. Deschepper ◽  
R. H. Alper ◽  
M. H. Humphreys
Keyword(s):  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Brain Regions ◽  
Anterior Lobe ◽  
Unilateral Nephrectomy ◽  
Reflex Pathways ◽  
Before And After ◽  
Hypothalamic Arcuate Nucleus ◽  
The Central Nervous System ◽  
Neonatal Administration

Acute unilateral nephrectomy (AUN) results in natriuresis from the remaining kidney through reflex pathways involving the central nervous system and requiring an intact pituitary gland. The natriuresis is accompanied by an increase in the plasma concentration of a peptide or peptides derived from the N-terminal fragment (NTF) of proopiomelanocortin. We measured plasma immunoreactive NTF-like material (IR-NTF) before and after AUN in control rats and rats treated neonatally with monosodium glutamate (MSG), a procedure that produces neuroendocrine dysfunction by destroying cell bodies in the hypothalamic arcuate nucleus, median eminence, and other brain regions. In control rats, IR-NTF increased from 85.8 +/- 54.9 (SD) to 207 +/- 98.1 fmol/ml after AUN (P less than 0.02) as sodium excretion (UNaV) doubled. In MSG-treated rats, AUN produced no change in plasma IR-NTF concentration (58.8 +/- 21.3 vs. 68.3 +/- 18.5 fmol/ml (P = NS), nor did UNaV increase. Tissue content of IR-NTF was reduced in the arcuate nucleus and anterior lobe of pituitaries from MSG-treated rats compared with controls, but was no different in the neurointermediate lobe. These results indicate that the hypothalamic lesion produced by neonatal administration of MSG prevents both the increase in plasma IR-NTF concentration and the natriuresis after AUN, and therefore lend further support to the concept of a causal relationship between these two consequences of AUN.

MSG lesions decrease body mass of suckling-age rats by attenuating circadian decreases of energy expenditure

2002 ◽  
Vol 283 (3) ◽  
pp. E604-E611 ◽  
Author(s):  
Corinna Schoelch ◽  
Thomas Hübschle ◽  
Ingrid Schmidt ◽  
Barbara Nuesslein-Hildesheim
Keyword(s):  
Energy Expenditure ◽  
Energy Saving ◽  
Lean Body Mass ◽  
Body Mass ◽  
Arcuate Nucleus ◽  
Cell Damage ◽  
Monosodium Glutamate ◽  
Adult Age ◽  
Reduced Body ◽  
Plasma Leptin

Suckling-age rats display endogenous circadian rhythmicity of metabolic rate (MR) with energy-saving, torpor-like decreases, which are sympathetically controlled and suppressed by leptin treatment. We investigated whether neonatal monosodium glutamate (MSG) treatment, known to cause arcuate nucleus damage and adult-age obesity, alters energy balance in the first two postnatal weeks. Continuously recorded MR and core temperatures (Tc) show that MSG treatment disinhibits the periodic, sympathetically controlled, energy-saving drops of Tc and MR. Increased energy expenditure thus explains reduced body fat at normal lean body mass found in MSG-treated pups artificially nourished identically to controls. In MSG-treated mother-reared pups, lean body mass is additionally reduced, suggesting that MSG also reduces suckling. Plasma leptin levels are similar in controls and MSG-treated pups but higher per unit of fat mass in the latter. We conclude that the postweaning development of MSG obesity and depressed thermogenesis are preceded by an early phase of increased energy expenditure with decreased fat deposition during suckling age and hypothesize cell damage in the arcuate nucleus to be involved in both.

Increase in pituitary dopaminergic receptors after monosodium glutamate treatment

1983 ◽  
Vol 245 (3) ◽  
pp. E261-E265
Author(s):  
M. L. Heiman ◽  
N. Ben-Jonathan
Keyword(s):  
Binding Sites ◽  
Anterior Pituitary ◽  
Arcuate Nucleus ◽  
Binding Capacity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Single Class ◽  
Binding Characteristics ◽  
Physiological Conditions ◽  
Da Receptors

We investigated whether a decrease in arcuate nucleus dopamine (DA) levels resulting from neonatal treatment with monosodium glutamate (MSG) affects the anterior pituitary DA receptors in adult male rats. MSG treatment resulted in a significant reduction in medial basal hypothalamic (MBH) DA levels, no change in its norepinephrine (NE) and epinephrine (E) concentrations, and a marked increase in circulating prolactin (PRL). Scatchard analyses of DA binding characteristics to anterior pituitary membranes using [3H]spiperone revealed linear plots, suggesting a single class of high-affinity, low-capacity binding sites. The DA binding capacity was significantly higher in MSG-treated rats than in controls with no change in affinity. The data indicate that anterior pituitary DA receptors change in accordance with altered physiological conditions. The increase in the number of DA receptors following destruction of the arcuate nucleus is probably a direct effect of reduced DA levels reaching the anterior pituitary gland.

Endorphinergic mechanism in the central cardiovascular and analgesic effects of clonidine

1987 ◽  
Vol 65 (8) ◽  
pp. 1624-1632 ◽  
Author(s):  
G. Kunos ◽  
R. Mosqueda-Garcia ◽  
J. A. Mastrianni ◽  
F. V. Abbott
Keyword(s):  
Receptor Antagonist ◽  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Opiate Receptors ◽  
Cardiovascular Effects ◽  
Male Rats ◽  
Sprague Dawley ◽  
Wky Rats ◽  
Sd Rats ◽  
Wistar Kyoto

In urethane-anesthetized male rats, injection of 5 nmol clonidine into the nucleus of the solitary tract (NTS) causes hypotension and bradycardia. These effects are greater in spontaneously hypertensive rats (SHR) and normotensive Sprague–Dawley (SD) rats than in normotensive Wistar–Kyoto (WKY) rats. The effects of clonidine are stereoselectively inhibited by 100 ng intra-NTS naloxone in SHR and SD but not in WKY rats. In SHR, the effects of clonidine are also inhibited by intra-NTS administration of ICI 174864 (a δ-receptor antagonist) but not by β-funaltrexamine (a μ-receptor antagonist), while in SD rats only the μ- and not the δ-antagonist was effective. Neonatal treatment of SHR with monosodium glutamate (MSG) reduced the β-endorphin content of the arcuate nucleus and the NTS, reduced the cardiovascular effects of clonidine, and abolished their naloxone sensitivity. MSG treatment of newborn WKY reduced the β-endorphin content of the arcuate nucleus but not the NTS and did not affect the responses to clonidine. Measurement of pain sensitivity by the formalin test indicated that clonidine was more potent as an analgesic in SHR and SD than in WKY rats, and its effect was inhibited by naloxone (2 mg/kg i.p.) in the former two strains but not in WKY. It is proposed that a naloxone-sensitive component of the cardiovascular effects of clonidine is due to release of a β-endorphin-like opioid from the NTS, and that this mechanism is present in SHR and SD but not in WKY rats. The opiate receptors mediating the effects of the opioid appear to be of the μ-subtype in SD rats and of the δ-subtype in SHR. The results also support a close relationship between central cardiovascular and pain regulatory mechanisms.

Corticoliberin and somatoliberin activity in the pituitary stalk median eminence of rats after neonatal treatment with monosodium glutamate

1982 ◽  
Vol 93 (2) ◽  
pp. 239-245 ◽  
Author(s):  
Zsuzsanna Ács ◽  
F. A. Antoni ◽  
G. B. Makara
Keyword(s):  
Median Eminence ◽  
Arcuate Nucleus ◽  
Monosodium Glutamate ◽  
Plasma Corticosterone ◽  
Pituitary Stalk ◽  
Corticosterone Concentration ◽  
Medial Basal Hypothalamus ◽  
Neonatal Treatment ◽  
Neurotoxic Lesions ◽  
Plasma Gh

Neurotoxic lesions of the arcuate nucleus by neonatal treatment with monosodium glutamate (MSG) resulted in a decrease of plasma GH levels without affecting plasma corticosterone concentration. The corticoliberin activity of the pituitary stalk median eminence (SME) in MSG-treated animals was similar to that of litter-mate controls. Growth hormone releasing (somatoliberin) activity of the SME, tested after placing an anterolateral cut around the medial basal hypothalamus, was significantly lower in MSG-treated than in control animals. It was concluded that a substantial proportion of the somatoliberin neurones are found in the arcuate nucleus.

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