Different Distributions of Nitric Oxide Synthase-Containing Neurons in the Mouse and Rat Hypothalamus

Ng, Yen Kaow; Xue, Yangkui; Wong, Peter T.-H.

doi:10.1006/niox.1999.0247

Cited by 33 publications

(18 citation statements)

References 30 publications

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“…But, NADPH-d containing neurons, especially in the hilus of DG and CA1 subfields, were shown to be vulnerable to systemic KA injection (Miettinen et al, 1995). Though the expression of NADPH-d has been used to detect NOS activity in the hippocampal neurons (Hope et al, 1991;Endoh et al, 1994), recent reports suggest that NADPH-d and NOS may not be the same enzymes though they are found in the same neurons (Wang et al, 1997;Ng et al, 1999;Xu et al, 2000). A few studies have shown that NADPH-d reactivity may reveal the other isoforms of NOS (eNOS and iNOS) in relation to excitotoxic damage and experimental epilepsy (Garthwaite, 1991;Talavera et al, 1997).…”

Section: Involvement Of Nitric Oxide Synthase (Nos) In Da-induced Neumentioning

confidence: 97%

Domoic acid-induced neurotoxicity in the hippocampus of adult rats

2004

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Domoic acid (DA), an agonist of non-N-methyl-D-aspartate (non-NMDA) receptor subtype including kainate receptor, was identified as a potent neurotoxin showing involvement in neuropathological processes like neuronal degeneration and atrophy. In the past decade evidence indicating a role for excitatory amino acids in association with neurological disorders has been accumulating. Although the mechanisms underlying the neuronal damage induced by DA are not yet fully understood, many intracellular processes are thought to contribute towards DA-induced excitotoxic injury, acting in combination leading to cell death. In this review article, we report the leading hypotheses in the understanding of DA-induced neurotoxicity, which focus on the role of DA in neuropathological manifestations, the formation of the retrograde messenger molecule nitric oxide (NO) for the production of free radicals in the development of neuronal damage, the activation of glial cells (microglia and astrocytes) in response to DA-induced neuronal damage and the neuroprotective role of melatonin as a free radical scavenger or antioxidant in DA-induced neurotoxicity. The possible implications of molecular mechanism underlying the neurotoxicity in association with necrosis, apoptosis, nitric oxide synthases (nNos and iNOS) and glutamate receptors (NMDAR1 and GluR2) related genes and their expression in DA-induced neuronal damage in the hippocampus have been discussed.

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Section: Involvement Of Nitric Oxide Synthase (Nos) In Da-induced Neumentioning

confidence: 97%

Domoic acid-induced neurotoxicity in the hippocampus of adult rats

2004

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“…3). While it is well known that pharmacological manipulations of neuronal NOS activity in the mPOA impair male sexual behavior [21,30,39], the role of ACVR2 signaling in these behaviors is unknown. To determine whether the behavioral defects in Acvr2 À/À male mice were due to alterations in NOS, we tested the activity of NOS in the mPOA, cortex, and the rest of the hypothalamus.…”

Section: Absence Of Acvr2 Signaling Does Not Affect Lh and Testosteromentioning

confidence: 99%

Impaired Male Sexual Behavior in Activin Receptor Type II Knockout Mice1

Ma¹,

Reyna²,

Mani³

et al. 2005

Biology of Reproduction

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Integration of multiple hormonal and neuronal signaling pathways in the medial preoptic area (mPOA) is required for elicitation of male sexual behavior in most vertebrates. Perturbation of nitric oxide synthase (NOS) activity in the mPOA causes significant defects in male sexual behavior. Although activins and their signaling components are highly expressed throughout the brain, including the mPOA, their functional significance in the central nervous system (CNS) is unknown. Here, we demonstrate a neurophysiologic role for activin signaling in male reproductive behavior. Adult activin receptor type II null (Acvr2-/-) male mice display multiple reproductive behavioral deficits, including delayed initiation of copulation, reduced mount, and intromission frequencies, and increased mount, intromission, and ejaculation latencies. These behavioral defects in the adult mice are independent of gonadotropin-releasing hormone (GnRH) homeostasis or mating-induced changes in luteinizing hormone (LH) and testosterone levels. The impairment in behavior can be correlated to the nitric oxide content in the CNS because Acvr2-/- males have decreased NOS activity in the mPOA but not the rest of the hypothalamus or cortex. Olfactory acuity tests confirmed that Acvr2-/- mice have no defects in general odor or pheromone recognition. In addition, motor functions are not impaired and the mutants demonstrate normal neuromuscular coordination and balance. Furthermore, the penile histology in mutant mice appears normal, with no significant differences in the expression of penile differentiation marker genes compared with controls, suggesting the observed behavioral phenotypes are not due to structural defects in the penis. Our studies identify a previously unrecognized role of activin signaling in male sexual behavior and suggest that activins and/or related family members are upstream regulators of NOS activity within the mPOA of the forebrain.

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“…Moreover, the system was described in more limited cerebral regions, as the hippocampus, the striatum, or the hypothalamus in the rat (Kharazia et al, 1994;Ng et al, 1999;Valtschanoff et al, 1993); the suprachiasmatic nucleus in the hamster and mouse (Decker and Reuss, 1994;Wang and Morris, 1996); or the vomeronasal organ, the cortex, the claustrum, the laterodorsal tegmental nucleus, and the cerebellum in the mouse (Oermann et al, 1999;Rothe et al, 1999;Schilling et al, 1994;Zancanaro et al, 1999, Guirado et al, 2003. A detailed immunohistochemical distribution of constitutive NOS (cNOS) was performed in rat, using an antibody that recognized both endothelial and neuronal NOS (Rodrigo et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Distribution of nitric oxide synthase immunoreactivity in the mouse brain

Gotti

Sica

Panzica

2005

Microsc. Res. Tech.

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Nitric oxide (NO) is a gaseous intercellular messenger with a wide range of neural functions. NO is synthesized by activation of different isoforms of nitric oxide synthases (NOS). At present NOS immunoreactivity has been described in mouse brain in restricted and definite areas and no detailed mapping studies have yet been reported for NOS immunoreactivity. We have studied the distribution of neuronal NOS-containing neurons in the brain of three months male mice, using a specific commercial polyclonal antibody against the neuronal isoform of nitric oxide synthase (nNOS). Neuronal cell bodies exhibiting nNOS immunoreactivity were found in several distinct nuclei throughout the brain. The neurons that were positively stained exhibited different intensities of reaction. In some brain areas (i.e., cortex, striatum, tegmental nuclei) neurons were intensely stained in a Golgi-like fashion. In other regions, immunoreactive cells are moderately stained (i.e., magnocellular nucleus of the posterior commissure, amygdaloid nucleus, interpeduncular nucleus, lateral periaqueductal gray) or weakly stained (i.e., vascular organ of the lamina terminalis, hippocampus, inferior colliculus, reticular nucleus). In the mouse, the NO-producing system appears well developed and widely diffused. In particular, nNOS immunoreactive neurons seem chiefly present in several sensory pathways like all the nuclei of the olfactory system, as well as in many regions of the lymbic system. These data suggest a widespread role for the NO system in the mouse nervous system.

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Different Distributions of Nitric Oxide Synthase-Containing Neurons in the Mouse and Rat Hypothalamus

Cited by 33 publications

References 30 publications

Domoic acid-induced neurotoxicity in the hippocampus of adult rats

Domoic acid-induced neurotoxicity in the hippocampus of adult rats

Impaired Male Sexual Behavior in Activin Receptor Type II Knockout Mice1

Distribution of nitric oxide synthase immunoreactivity in the mouse brain

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