Locomotor and learning deficits in adult rats exposed to monosodium-l-glutamate during early life

Ali, Mohamed M.; Bawari, Meenakshi; Misra, U. K.; Babu, G. Nagesh

doi:10.1016/s0304-3940(00)00958-7

Cited by 50 publications

(29 citation statements)

References 14 publications

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“…However the cognitive affection was much more obvious in the group receiving the higher dose. This finding is also supported by earlier studies (Ali et al, 2000;Olvera-Cortes et al, 2005;Porsolt et al, 1979). Onaolapo et al, 2017, concluded that in their study MSG associated with changes in open field activities, anxiety-related behaviors and brain glutamate/ glutamine levels; its ingestion leads to a stimulation of the brain reward system (Onaolapo et al, 2017).…”

Section: Discussionsupporting

confidence: 79%

Monosodium glutamate affects cognitive functions in male albino rats

Moneim

Yassa

Makboul

et al. 2018

Egypt J Forensic Sci

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Section: Discussionsupporting

confidence: 79%

Monosodium glutamate affects cognitive functions in male albino rats

Moneim

Yassa

Makboul

et al. 2018

Egypt J Forensic Sci

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“…Kunming filial mice which mothers treated with MSG (2.5 mg/g or 4.0 mg/g body weight) per os in 17-21 days of pregnancy had significantly impaired Y-maze discrimination learning in the 60.day, although the neuronal damage of the periventricular organs or the hypothalamus was not observed (Yu et al 1997). Moreover, subneurotoxic doses of MSG (2 mg/g, for 10 days) given perorally to rat neonates led to significant decrease in the active avoidance learning performance at the 90thpost-dosing day, which indicates that early-life MSG exposure could lead to subtle behavioral aberrations in adulthood (Ali et al 2000).…”

Section: Central Nervous Systemmentioning

confidence: 93%

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Husarova¹,

Ostatníková²

2013

JMED

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Monosodium Glutamate (MSG) is one of the world's most widely used food additives. Its toxic effects have been shown in numerous animal studies, however in most of them, the method of administration and the doses were not similar to human MSG intake. In this paper we review animal and human studies in which MSG effects on central nervous system, adipose tissue and liver, reproductive organs and other systems have been shown and we discuss their implications for human MSG intake.

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“…We recorded motor activity in an Opto-Varimex cage (Columbus Instruments, Columbus, Ohio) linked to a computer and placed in a sound-attenuated room illuminated by a 20-W white light. The amount of time spent in ambulatory activity was analyzed using an Auto-Track software 42,43 (Columbus Instruments, Columbus, Ohio). Session duration was 20 min for adult rats and 60 s for 10-day-old pups.…”

Section: Synthesis Of Inhibitorsmentioning

confidence: 99%

Modulation of anxiety through blockade of anandamide hydrolysis

Kathuria

Gaetani

Fegley

et al. 2002

Nat Med

1,261

1,301

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ARTICLESAnandamide, the naturally occurring amide of arachidonic acid with ethanolamine, meets all key criteria of an endogenous cannabinoid substance 1 : it is released on demand by stimulated neurons 2,3 ; it activates cannabinoid receptors with high affinity 1 ; and it is rapidly eliminated through a two-step process consisting of carrier-mediated transport followed by intracellular hydrolysis 2,4 . Anandamide hydrolysis is catalyzed by the enzyme fatty acid amide hydrolase (FAAH), a membrane-bound serine hydrolase 5,6 that also cleaves other bioactive fatty acid ethanolamides such as oleoylethanolamide 7 and palmitoylethanolamide 8 . Mutant mice lacking the gene encoding FAAH (Faah) cannot metabolize anandamide 9 and, although fertile and generally normal, show signs of enhanced anandamide activity at cannabinoid receptors such as reduced pain sensation 9 . This is suggestive that drugs targeting FAAH may heighten the tonic actions of anandamide, while possibly avoiding the multiple and often unwanted effects produced by ∆ 9 -tetrahydrocannabinol (∆ 9 -THC) and other direct-acting cannabinoid agonists 10,11 . To test this hypothesis, potent, selective and systemically active inhibitors of intracellular FAAH activity are needed. However, most current inhibitors of this enzyme lack the target selectivity and biological availability required for in vivo studies [12][13][14] , whereas newer compounds, though promising, have not yet been characterized 15,16 . Thus, the therapeutic potential of FAAH inhibition remains essentially unexplored. Lead identification and optimizationDespite its unusual catalytic mechanism 6 , FAAH is blocked by a variety of serine hydrolase inhibitors, including compounds with activated carbonyls 16 . Therefore we examined whether esters of carbamic acid such as the anti-cholinesterase agent carbaryl (compound 1; Table 1) might inhibit FAAH activity in rat brain membranes. Although compound 1 was ineffective, its positional isomer 2 produced a weak inhibition of FAAH (half-maximal inhibitory concentration (IC 50 ) = 18.6 ± 0.7 µM; mean ± s.e.m., n = 3), which was enhanced by replacing the N-methyl substituent with a cyclohexyl group (compound 3; IC 50 = 324 ± 31 nM). The aryl ester 4, the benzyloxyphenyl group of which can be regarded as an elongated bioisosteric variant of the naphthyl moiety of compound 2, inhibited the activity of FAAH with a potency (IC 50 = 396 ± 63 nM) equivalent to that of compound 3. A conformational analysis of compound 4 revealed families of accessible conformers differing mainly in the torsion angle around the O-CH 2 bond, with substituents in anti or gauche conformations (data not shown). As the latter conformations more closely resembled the shape of the naphthyl derivative 3, we hypothesized that they might be responsible for the interac-

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Locomotor and learning deficits in adult rats exposed to monosodium-l-glutamate during early life

Cited by 50 publications

References 14 publications

Monosodium glutamate affects cognitive functions in male albino rats

Monosodium glutamate affects cognitive functions in male albino rats

Monosodium Glutamate Toxic Effects and Their Implications for Human Intake: A Review

Modulation of anxiety through blockade of anandamide hydrolysis

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