Distribution of NADPH-Diaphorase-Positive Neurons in the Mouse Brain: Differences from Previous Findings in the Rat Brain and Comparison with the Distribution of Serotonergic Neurons.

Matsushita, Hiroko; Takeuchi, Yoshihiro; Kawata, Mitsuhiro; Sawada, Tadashi

doi:10.1267/ahc.34.235

Cited by 9 publications

(5 citation statements)

References 70 publications

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“…5A), though without any obvious clustering, as in layer IV. Some cells were found scattered in the white matter, similar to what has been briefly described by Matsushita et al (2001). Usually, the cell body of a NADPH-d neuron located in the Fig.…”

Section: Laminar and Tangential Distribution Of Type I Nadph-d Cells supporting

confidence: 77%

Neuropil reactivity, distribution and morphology of NADPH diaphorase type I neurons in the barrel cortex of the adult mouse

Freire

Franca

Pereira

2005

Journal of Chemical Neuroanatomy

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Section: Laminar and Tangential Distribution Of Type I Nadph-d Cells supporting

confidence: 77%

Neuropil reactivity, distribution and morphology of NADPH diaphorase type I neurons in the barrel cortex of the adult mouse

Freire

Franca

Pereira

2005

Journal of Chemical Neuroanatomy

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“…Stress induced production of NO in hippocampus can negatively alter above functions. NADPH-d positive neurons in hippocampal formation are generally considered to be local circuit neurons [42]. They form a subpopulation of principal pyramidal neurons of this region.…”

Section: Discussionmentioning

confidence: 99%

“…Monopolar and multipolar cells are found in the Oriens layer, pyramidal layer and stratum radiatum. In the dentate gyrus also, number of NADPH-d positive neurons is found in polymorphic layer [22]. Small amount of NO synthesized during neuronal activity mediates diverse physiological functions which include neuronal differentiation, neuronal survival, and synaptic plasticity [23].…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Withania somnifera Dunal.: A Possible Mechanism

2009

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Present study was carried out to understand the possible mechanism of neuroprotective action of the root extract of Withania somnifera Dunal (WS). The study is focused on WS mediated inhibition of nitric oxide production, which is known to mediate neurodegeneration during stress. Adult mice (28 +/- 5 g) were exposed to restraint stress for 30 days. Activity of NADPH diaphorase (NADPH-d) and factors (Acetylcholine, serotonin and corticosterone), which regulates NADPH-d activity were studied. Treatment with WS extract for 30 days during stress, significantly reversed the stress induced NADPH-d activation. Observations suggest that inhibition of NADPH-d by WS is not a direct effect of extract on NADPH-d, instead it inhibits via suppressing corticosterone release and activating cholineacetyltransferase, which in turn increase serotonin level in hippocampus to inhibit NADPH-d. Together, the main mechanism underlying the neuroprotective effects of WS can be attributed to its role in the down regulation of nNOS and neurochemical alterations of specific neurotransmitter systems. These observations thus suggest that WS root extract could be developed as a potential preventive or therapeutic drug for stress induced neurological disorders.

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“…Activation of the nitrergic system has been shown to participate in neural plasticity associated with aversive memories (Hopper and Garthwaite 2006) as well as in unconditioned responses to stress (Beijamini et al 2005). Nitric oxide-producing cells are enriched in regions of the limbic system which organize defensive behavior in mammals (Vincent and Kimura 1992;Wang et al 1995;Matsushita et al 2001;Simpson et al 2003), amphibians (López et al 2005) and fish (Holmqvist et al 2000(Holmqvist et al , 2007Bordieri et al 2005;Giraldez-Perez et al 2008;Mueller et al 2011). In rodents, NO-guanylate cyclase pathway activation peaks immediately after A C C E P T E D M A N U S C R I P T…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Putative involvement of the nitrergic system on the consolidation, but not initiation, of behavioral sensitization after conspecific alarm substance in zebrafish

Lima

Silva

et al. 2015

Pharmacology Biochemistry and Behavior

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Stressful manipulations can sensitize the behavior of an organism, increasing anxiety-like behavior after a delay; this long-term stress sensitization can represent the pathophysiological basis of trauma- and stress-related disorders (TRSDs), of which the most prevalent is post-traumatic stress disorder (PTSD). A role for the glutamate-nitric oxide pathway in this sensitization is implied by behavioral, neurophysiological and genomic data on different species. Here, we report on the long-term sensitization of anxiety-like behavior in zebrafish and the possible participation of nitric oxide in this process. Zebrafish exposed to a conspecific alarm substance (AS) show increased anxiety-like behavior at least 24h after stimulus delivery. Blocking nitric oxide synthesis with l-NAME (5mg/kg) 30min, but not 90min, after AS exposure blocks the sensitization of scototaxis and risk assessment, while treatment 90min after exposure blocks the sensitization of thigmotaxis and erratic swimming; l-NAME was not effective when administered 30min before AS exposure. These data suggest a participation of nitric oxide in the consolidation, but not in the initiation, of behavioral sensitization after predator threat.

show abstract

Distribution of NADPH-Diaphorase-Positive Neurons in the Mouse Brain: Differences from Previous Findings in the Rat Brain and Comparison with the Distribution of Serotonergic Neurons.

Cited by 9 publications

References 70 publications

Neuropil reactivity, distribution and morphology of NADPH diaphorase type I neurons in the barrel cortex of the adult mouse

Neuropil reactivity, distribution and morphology of NADPH diaphorase type I neurons in the barrel cortex of the adult mouse

Neuroprotective Effects of Withania somnifera Dunal.: A Possible Mechanism

Putative involvement of the nitrergic system on the consolidation, but not initiation, of behavioral sensitization after conspecific alarm substance in zebrafish

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