Expression of neuronal nitric oxide synthase mRNA in stress-related brain areas after restraint in rats

Oliveira, Rúbia Maria Weffort de; Bel, Elaine Aparecida Del; Mamede-Rosa, Maria Luiza N.; Padovan, Cláudia Maria; Deakin, Bill; Guimarães, Francisco Silveira

doi:10.1016/s0304-3940(00)01287-8

Cited by 97 publications

(51 citation statements)

References 17 publications

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“…Administration of L-arginine, presumed to increase NO production, abolished the anxiolytic-like response of rats to diazepam in the elevated plus-maze (Volke et al, 1998). There is also increased expression of neuronal NOS mRNA in stress-related brain regions, suggesting an increase in NO during stress (de Oliveira et al, 2000).…”

Section: Discussionmentioning

confidence: 95%

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

Elfline

Branda

Babich

et al. 2004

Neuropsychopharmacol

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Earlier we implicated nitric oxide (NO) in mediation of the behavioral effects of benzodiazepines. Since benzodiazepines work through facilitation of GABAergic inhibitory neurotransmission, this study was designed to determine whether the direct-acting g-aminobutyric acid A (GABA A ) receptor agonist THIP (4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol) evokes behavioral effects similar to those of benzodiazepines and whether behavioral effects of THIP are also NO dependent. When challenged with either chlordiazepoxide or THIP in an elevated plus-maze paradigm, male NIH Swiss mice exhibited a dose-related increase in open-arm activity. The chlordiazepoxide-induced effects were sensitive to antagonism by a benzodiazepine antagonist, and the effects of THIP were blocked by a GABA A receptor antagonist. Pretreatment with the NO synthase (NOS) inhibitor L-N G -nitro arginine antagonized the effects of both chlordiazepoxide and THIP; similar pretreatment with the D-isomer, D-N G -nitro arginine, which is inactive as an NOS inhibitor, was without effect on chlordiazepoxide and THIP. These findings indicate that chlordiazepoxide and THIP evoke similar behavioral effects in mice in the elevated plus-maze through actions on different parts of the GABA A receptor, and that NO appears to play a key role in mediation of the behavioral effects of both chlordiazepoxide and THIP.

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Section: Discussionmentioning

confidence: 95%

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

Elfline

Branda

Babich

et al. 2004

Neuropsychopharmacol

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“…These results indicated that EGb 761 and GKB provide neuroprotection by a mechanism that involves a downregulation of both nNOS and iNOS. Neuroprotective effects of nNOS downregulation may also be conceived upon considering that both traumatic brain injury [Rao et al, 1999] and acute restraint stress [de Oliveira et al, 2000] have been shown to cause increases in nNOS mRNA in various brain areas.…”

Section: Ex Vivo Studiesmentioning

confidence: 99%

Effects of Ginkgo biloba extract (EGb 761) on gene expression: Possible relevance to neurological disorders and age‐associated cognitive impairment

DeFeudis¹

2002

Drug Development Research

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Ginkgo biloba leaf extract (EGb 761), which contains many constituents, including flavonoid glycosides and terpenoids (ginkgolides, bilobalide), is used to treat cerebrovascular and peripheral vascular insufficiency, as well as cognitive impairment and other symptoms of dementia. Recent studies have indicated that these therapeutic effects of EGb 761 probably involve modification of the expression of many genes by actions involving several of its active constituents. As examples: EGb 761 and its ginkgolide B constituent inhibit the expression of the peripheral benzodiazepine receptor in the adrenal cortex and decrease circulating levels of corticosterone in the rat, effects that provide a mechanism for explaining the ''antistress'' action of the extract. Both the flavonoid and terpenoid constituents of EGb 761 decrease the expression of inducible nitric oxide synthase (iNOS), supporting an action of the extract of opposing the deleterious effects of excessive formation of NO. EGb 761 upregulates several genes that encode vital antioxidant enzymes, including heme oxygenase-1 and the regulatory and catalytic subunits of g-glutamyl-cysteinyl synthetase. Dietary treatment of mice with EGb 761 upregulates the expression of genes encoding neuronal tyrosine/threonine phosphatase 1 and microtubule-associated tau in the cerebral cortex, findings that are of interest since these proteins are associated with the intracellular neurofibrillary tangles found in the brain in Alzheimer's disease. Bilobalide upregulates two mitochondrial-DNA-encoded genes, subunit III of cytochrome c oxidase and subunit ND1 of NADH dehydrogenase, indicating a fundamental mechanism that may underlie EGb 761-induced neuroprotection. Collectively, such results indicate that the therapeutic effects of EGb 761 on cognitive impairment (dementia) may involve its action of altering gene expression. Drug Dev.

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“…Asterisks signal significant difference from all other groups. ANOVA followed by Duncan, P<0.05 Moreover, restraint stress increases nNOS mRNA expression (De Oliveira et al 2000b) and NADPHd activity (Krukoff and Khalili 1997) in the dlPAG.…”

Section: Discussionmentioning

confidence: 87%

Ionotropic glutamate-receptor antagonists inhibit the aversive effects of nitric oxide donor injected into the dorsolateral periaqueductal gray of rats

Moreira¹,

Molchanov²,

Guimarães³

2004

Psychopharmacology

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Expression of neuronal nitric oxide synthase mRNA in stress-related brain areas after restraint in rats

Cited by 97 publications

References 17 publications

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

Antagonism by NOS Inhibition of the Behavioral Effects of Benzodiazepine and GABAA Receptor Agonists in the Mouse Elevated Plus-Maze

Effects of Ginkgo biloba extract (EGb 761) on gene expression: Possible relevance to neurological disorders and age‐associated cognitive impairment

Ionotropic glutamate-receptor antagonists inhibit the aversive effects of nitric oxide donor injected into the dorsolateral periaqueductal gray of rats

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