Nitric oxide induces neurotransmitter release from hippocampal slices

Lónárt, György; Wang, Jia; Johnson, Kenneth M.

doi:10.1016/0014-2999(92)90759-w

Cited by 262 publications

(110 citation statements)

References 4 publications

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“…This indicates that the enhanced release is not due to a cytotoxic action on cholinergic neurones, but that the NO donors evoke an exocytotic release of acetylcholine. A similar enhancement of basal acetylcholine release by various NO do- (Prast & Philippu, 1992;Guevara-Guzman et al, 1994;Prast et al, 1995) and in vitro (Lonart et al, 1992;Ohkuma et al, 1995). (Ohkuma et al, 1995).…”

Section: Basal Releasementioning

confidence: 59%

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Hebeiss

Kilbinger

1996

British J Pharmacology

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1 The effects of the nitric oxide (NO) donors, 3-morpholino-sydnonimine (SIN-1), S-nitroso-Nacetylpenicillamine (SNAP) and sodium nitroprusside on basal and electrically evoked release of [3H]-acetylcholine were studied in myenteric plexus longitudinal muscle preparations of the guinea-pig small intestine preincubated with [3H]-choline. 4 It is concluded that NO stimulates basal acetylcholine release from myenteric neurones through activation of guanylyl cyclase. In addition, NO inhibits the depolarization evoked release of acetylcholine by a presynaptic mechanism unrelated to cyclic GMP. The data imply that NO is not only an inhibitory transmitter to intestinal smooth muscles but also a modulator of cholinergic neurotransmission in the myenteric plexus.

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Section: Basal Releasementioning

confidence: 59%

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Hebeiss

Kilbinger

1996

British J Pharmacology

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“…Recently the term "nitrosative stress" has been used to indicate the cellular damage that is elicited by excess of NO and reactive nitrogen species 28 . In addition, NO has been shown to stimulate the release of noradrenaline and glutamate in the hippocampus 29 . This data can support our hypothesis concerning to increased release of this neurotransmitter since we found low levels of glutamate in sclerotic tissues, when compared with autopsy/control tissues.…”

Section: Discussionmentioning

confidence: 99%

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Varella

Santiago

Carrete

et al. 2011

Arq. Neuro-Psiquiatr.

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We investigated a relationship between the FLAIR signal found in mesial temporal sclerosis (MTS) and inflammation. Twenty nine patients were selected through clinical and MRI analysis and submitted to cortico-amygdalo-hippocampectomy to seizure control. Glutamate, TNFα, IL1, nitric oxide (NO) levels and immunostaining against IL1β and CD45 was performed. Control tissues (n=10) were obtained after autopsy of patients without neurological disorders. The glutamate was decreased in the temporal lobe epilepsy (TLE) -MTS group (p<0.001), suggesting increased release of this neurotransmitter. The IL1β and TNFα were increased in the hippocampus (p<0.05) demonstrating an active inflammatory process. A positive linear correlation between FLAIR signal and NO and IL1β levels and a negative linear correlation between FLAIR signal and glutamate concentration was found. Lymphocytes infiltrates were present in hippocampi of TLE patients. These data showed an association between hippocampal signal alteration and increased inflammatory markers in TLE-MTS.

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“…NO is synthesized by the enzyme NO synthase (NOS), which exists in three isoforms that are called neuronal, inducible, and endothelial NOS (nNOS, iNOS, and eNOS). NO can induce neurotransmitter release from hippocampal slices (Lonart et al, 1992) and plays a role in regulating the hippocampal synaptic plasticity (Calabrese et al, 2007). NO converts thiol groups in proteins to form S-nitrosothiols through what is called S-nitrosylation.…”

Section: Inos Nnos and Astrogliosismentioning

confidence: 99%

Genistein inhibits aggregation of exogenous amyloid-beta1–40 and alleviates astrogliosis in the hippocampus of rats

et al. 2012

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We addressed the question of whether injection of Aβ in the rat brain is associated with pathology in the hippocampus, and if genistein has any protective effect against the neuronal damage caused by Aβ 1-40 . Genistein is a plant-derived compound with a structure similar to that of the female sex hormone oestrogen and it was recently shown that pretreatment with a single dose of genistein ameliorated learning and memory deficits in an amyloid beta (Aβ) 1-40 rat model of Alzheimer's disease. Here, we report that injection of the amyloid peptide into the hippocampus of rats led to formation of Aβ 1-40 positive aggregates close to the lateral blade of the dentate gyrus (DGlb). We also observed the following in the hippocampus: extensive cell death in the DGlb (P < 0.0001), CA1 (P = 0.03), and CA3 (P = 0.002); an increased number of iNOS-expressing cells (P = 0.01) and gliosis. Genistein given to rats by gavage one hour before Key words: amyloid-beta, Alzheimer's disease, genistein, neuronal degeneration 1 1 Abbreviations: AD, Alzheimer's disease; iNOS, inducible nitric oxide synthase; nNOS, neuronal nitric oxide synthase; CA1, cornu ammonis 1; CA2, cornu ammonis 2; CA3, cornu ammonis 3; Aβ, amyloid beta; DGlb, lateral blade of dentate gyrus; DGmb, medial blade of dentate gyrus; GFAP, glial fibrillary acidic protein; CC, corpus callosum; MAP, mitogenactivated protein; NFĸB, nuclear factor kappa B; MnSOD, manganese superoxide dismutase; APP, amyloid precursor protein; CrEL, Cremophor EL

show abstract

Nitric oxide induces neurotransmitter release from hippocampal slices

Cited by 262 publications

References 4 publications

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Differential effects of nitric oxide donors on basal and electrically evoked release of acetylcholine from guinea‐pig myenteric neurones

Relationship between fluid-attenuated inversion-recovery (FLAIR) signal intensity and inflammatory mediator's levels in the hippocampus of patients with temporal lobe epilepsy and mesial temporal sclerosis

Genistein inhibits aggregation of exogenous amyloid-beta1–40 and alleviates astrogliosis in the hippocampus of rats

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