A critical survey on nitric oxide synthase expression and nitric oxide function in the retinotectal system

Giraldi-Guimarães, Arthur; Batista, Claudia; Carneiro, Kátia; Tenório, Frank; Cavalcante, Leny A.; Mendez-Otero, Rosália

doi:10.1016/j.brainresrev.2007.09.005

Cited by 7 publications

(3 citation statements)

References 267 publications

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“…Following activation of nNOS, NO modulates the release of neurotransmitters by presynaptic terminals through a cGMP-and glutamate-dependent mechanism, enhancing their release in some cases, or decreasing it in others (35). Since in the SC nNOS-immunolabeled cells are predominantly inhibitory GABAergic neurons (10), we could speculate that enhancement occurs in this system.…”

Section: Discussionmentioning

confidence: 99%

NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus

Bittencourt-Navarrete

Nascimento

Santiago

et al. 2009

Braz J Med Biol Res

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Nitric oxide (NO) is a molecular messenger involved in several events of synaptic plasticity in the central nervous system. Ca 2+ influx through the N-methyl-D-aspartate receptor (NMDAR) triggers the synthesis of NO by activating the enzyme neuronal nitric oxide synthase (nNOS) in postsynaptic densities. Therefore, NMDAR and nNOS are part of the intricate scenario of postsynaptic densities. In the present study, we hypothesized that the intracellular distribution of nNOS in the neurons of superior colliculus (SC) superficial layers is an NMDAR activity-dependent process. We used osmotic minipumps to promote chronic blockade of the receptors with the pharmacological agent MK-801 in the SC of 7 adult rats. The effective blockade of NMDAR was assessed by changes in the protein level of the immediate early gene NGFI-A, which is a well-known NMDAR activity-dependent expressing transcription factor. Upon chronic infusion of MK-801, a decrease of 47% in the number of cells expressing NGFI-A was observed in the SC of treated animals. Additionally, the filled dendritic extent by the histochemical product of nicotinamide adenine di-nucleotide phosphate diaphorase was reduced by 45% when compared to the contralateral SC of the same animals and by 64% when compared to the SC of control animals. We conclude that the proper intracellular localization of nNOS in the retinorecipient layers of SC depends on NMDAR activation. These results are consistent with the view that the participation of NO in the physiological and plastic events of the central nervous system might be closely related to an NMDAR activitydependent function.

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Section: Discussionmentioning

confidence: 99%

NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus

Bittencourt-Navarrete

Nascimento

Santiago

et al. 2009

Braz J Med Biol Res

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“…For instance, NO is involved in chemosensory signaling in molluscs (Gelperin 1994;Moroz 2006), such as in mammals (Newland and Yates 2008). It is required for vision of insects (Bicker 2001) and vertebrates (reviewed by Giraldi-Guimarães et al 2007). It regulates motor activity of the enteric nervous system in snails (Rőszer et al 2004) and in vertebrates (Salzman 1995).…”

Section: Introductionmentioning

confidence: 99%

Hypothermia translocates nitric oxide synthase from cytosol to membrane in snail neurons

et al. 2010

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Neuronal nitric oxide (NO) levels are modulated through the control of catalytic activity of NO synthase (NOS). Although signals limiting excess NO synthesis are being extensively studied in the vertebrate nervous system, our knowledge is rather limited on the control of NOS in neurons of invertebrates. We have previously reported a transient inactivation of NOS in hibernating snails. In the present study, we aimed to understand the mechanism leading to blocked NO production during hypothermic periods of Helix pomatia. We have found that hypothermic challenge translocated NOS from the cytosol to the perinuclear endoplasmic reticulum, and that this cytosol to membrane trafficking was essential for inhibition of NO synthesis. Cold stress also downregulated NOS mRNA levels in snail neurons, although the amount of NOS protein remained unaffected in response to hypothermia. Our studies with cultured neurons and glia cells revealed that glia-neuron signaling may inhibit membrane binding and inactivation of NOS. We provide evidence that hypothermia keeps NO synthesis "hibernated" through subcellular redistribution of NOS.

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“…NO has previously been implicated in the maturational refinement of unisensory visual processes in the superficial layers of the SC (Mize et al, 1996;Cork et al, 2000;Scheiner et al, 2001;Mendez-Otero et al, 2007). As a diffusible gas, NO can spread from the release site to exert both synaptic and nonsynaptic effects, and it can have especially potent effects on immature neural processes in the surrounding region (Kiss and Vizi, 2001;Vizi et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Maturation of multisensory integration in the superior colliculus: Expression of nitric oxide synthase and neurofilament SMI-32

Fuentes–Santamaría¹,

McHaffie²,

Stein³

2008

Brain Research

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Nitric oxide (NO) containing (nitrergic) interneurons are well-positioned to convey the cortical influences that are crucial for multisensory integration in superior colliculus (SC) output neurons. However, it is not known whether nitrergic interneurons are in this position early in life, and might, therefore, also play a role in the functional maturation of this circuit. In the present study, we investigated the postnatal developmental relationship between these two populations of neurons using B-nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH) histochemistry and SMI-32 immunocytochemistry to label presumptive interneurons and output neurons, respectively. SMI-32 immunostained neurons were proved to mature and retained immature anatomical features until approximately 8 postnatal weeks. In contrast, nitrergic interneurons developed more rapidly. They had achieved their adult-like anatomy by 4 postnatal weeks and were in a position to influence the dendritic elaboration of output neurons. It is this dendritic substrate through which much of the cortico-collicular influence is expressed. Double-labeling experiments showed that the dendritic and axonal processes of nitrergic interneurons already apposed the somata and dendrites of SMI-32 labeled neurons even at the earliest age examined. The results suggest that nitrergic interneurons play a role in refining the cortico-collicular projection patterns that are believed to be essential for SC output neurons to engage in multisensory integration and to support normal orientation responses to cross-modal stimuli.

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A critical survey on nitric oxide synthase expression and nitric oxide function in the retinotectal system

Cited by 7 publications

References 267 publications

NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus

NMDA receptor blockade alters the intracellular distribution of neuronal nitric oxide synthase in the superficial layers of the rat superior colliculus

Hypothermia translocates nitric oxide synthase from cytosol to membrane in snail neurons

Maturation of multisensory integration in the superior colliculus: Expression of nitric oxide synthase and neurofilament SMI-32

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