Nitric oxide signaling modulates synaptic inhibition in the superior paraolivary nucleus (SPN) via cGMP-dependent suppression of KCC2

Yassin, Lina; Radtke‐Schuller, Susanne; Asraf, Hila; Grothe, Benedikt; Hershfinkel, Michal; Forsythe, Ian D.; Kopp-Scheinpflug, Cornelia

doi:10.3389/fncir.2014.00065

Cited by 34 publications

(40 citation statements)

References 60 publications

(98 reference statements)

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“…A similar finding in human listeners has been reported by Roberts and Lister (2004), showing that binaural presentation of the noise carriers for the gap provided significantly lower gap thresholds than monaural presentation. Recent work suggested neurons in the superior paraolivary nucleus (SPN) in the auditory brainstem are reliable detectors of gaps in noise (Kadner et al, 2008; Kadner et al, 2006; Kopp-Scheinpflug et al, 2011; Kulesza et al, 2003; Yassin et al, 2014). The broad frequency tuning in wild type SPN neurons (Dehmel et al, 2002) enables across frequency integration to the benefit of better temporal resolution.…”

Section: Discussionmentioning

confidence: 99%

Auditory deficits of Kcna1 deletion are similar to those of a monaural hearing impairment

et al. 2015

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Kv1.1 subunits of low voltage-activated (Kv) potassium channels are encoded by the Kcna1 gene and crucially determine the synaptic integration window to control the number and temporal precision of action potentials in the auditory brainstem of mammals and birds. Prior electrophysiological studies showed that auditory signaling is compromised in monaural as well as in binaural neurons of the auditory brainstem in Kv1.1 knockout mice (Kcna1−/−). Here we examine the behavioral effects of Kcna1 deletion on sensory tasks dependent on either binaural processing (detecting the movement of a sound source across the azimuth), monaural processing (detecting a gap in noise), as well as binaural summation of the acoustic startle reflex (ASR). Hearing thresholds measured by auditory brainstem responses (ABR) do not differ between genotypes, but our data show a much stronger performance of wild type mice (+/+) in each test during binaural hearing which was lost by temporarily inducing a unilateral hearing loss (through short term blocking of one ear) thus remarkably, leaving no significant difference between binaural and monaural hearing in Kcna1−/− mice. These data suggest that the behavioral effect of Kv1.1 deletion is primarily to impede binaural integration and thus to mimic monaural hearing.

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Section: Discussionmentioning

confidence: 99%

Auditory deficits of Kcna1 deletion are similar to those of a monaural hearing impairment

et al. 2015

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“…Thus, the NO-mediated signal can modulate glutamatergic [Garthwaite, 1991;Lawrence and Jarrott, 1993;Rudkouskaya et al, 2010;Neitz et al, 2011;Raju et al, 2015] and dopaminergic [Zhu and Luo, 1992;Bugnon et al, 1994;Chaparro-Huerta et al, 1997;Kiss et al, 2004] neurotransmission, via presynaptic regulation of neurotransmitter release and/or postsynaptic regulation of signal action. In addition, NO also acts on GABAergic synaptic transmission [Yang et al, 2007;Maggesissi et al, 2009;Tarasenko et al, 2014;Gasulla and Calvo, 2015;Yamamoto et al, 2015] by reducing the strength of inhibition, which allows the fine tuning of information processing [Yassin et al, 2014]. Therefore, NO plays a key role in synaptic plasticity, being involved in long-term potentiation and long-term depression, and in the regulation of the sleep-wake cycle.…”

Section: Introductionmentioning

confidence: 99%

Pattern of Nitrergic Neuronal System Organization in the Brain of Two Holostean Fishes (Actinopterygii: Ginglymodi)

et al. 2017

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The study of the nitrergic system, formed by the networks of neurons containing the enzyme nitric oxide synthase (NOS), has been extremely useful in unraveling neuroanatomical features of the organization of the central nervous system of vertebrates. Thus, data are available for representatives of most vertebrate classes and, in particular, several studies have detailed the organization of this system in teleosts. In contrast, no information is available regarding this neurotransmission system in the brains of holosteans, an early diverged and poorly understood group of actinopterygian fishes, currently considered a sister group of teleosts that contains only 8 species. The present study provides the first detailed information on the distribution of nitrergic cell bodies and fibers in 2 holostean species of the genus Lepisosteus, the spotted gar L. oculatus and the Florida gar L. platyrhincus. NOS immunohistochemistry and the NADPH diaphorase (NADPH-d) histochemical reaction were used, and both techniques yielded identical results, with the exception of the primary olfactory and terminal nerve fibers, which only labeled for NADPH-d exclusively in L. oculatus. Double immunohistochemistry was conducted for the simultaneous detection of NOS with tyrosine hydroxylase, choline acetyltransferase, calbindin, calretinin, and serotonin to accurately establish the localization of the nitrergic neurons and fibers in the brain of holosteans, the neuroanatomy of which has been mostly neglected, and to assess possible interactions between these neuroactive substances. Distinct groups of nitrergic cells were located in subpallial areas, the basal hypothalamus, posterior tubercle, optic tectum and mesencephalic tegmentum, reticular formation, solitary tract nucleus, spinal cord, and amacrine cells in the retina. In addition, low numbers of nitrergic cells were observed in the pallium, suprachiasmatic nucleus, prethalamic and thalamic areas, torus lateralis and torus semicircularis, cerebellar and laterodorsal tegmental nuclei, and the ventral octavolateral area. Comparison of these results with those from other classes of vertebrates, and including a segmental analysis to correlate cell populations, reveals that the pattern of the nitrergic system in holosteans is very close to that in ancestral actinopterygian fishes and highlights conserved and derived traits.

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“…Numerous functions of this regulatory molecule have been identified in the CNS, in the process of endothelium-dependent vasodilatation [5][6][7][8], in neurotransmission [9,10], and in host-defense mechanisms [11,12].…”

Section: Introductionmentioning

confidence: 99%

Role of Nitric Oxide Synthase in the Function of the Central Nervous System under Normal and Infectious Conditions

Reis¹,

Gonçalves-de-Albuquerque²,

Maron‐Gutierrez³

et al. 2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Nitric oxide (NO) was discovered as an endothelium-derived relaxing factor more than two decades ago. Since then, it has been shown to participate in many pathways. NO has been described as a key mediator of different pathways in the central nervous system (CNS) in both healthy and diseased processes. The three isoforms of nitric oxide synthase differ in their activity patterns and expression in different cells. Neuronal nitric oxide synthase (nNOS) is localized in synaptic spines, astrocytes, and the loose connective tissue surrounding blood vessels in the brain; eNOS is present in both cerebral vascular endothelial cells and motor neurons; and iNOS is induced in astrocytes and microglia under pathological conditions. During physiological processes, NO produced by eNOS/nNOS, respectively, controls blood flow activation, and act as a messenger during long-term potentiation (LTP). However, under pathological conditions, eNOS appears to be impaired, leading to a reduction in blood flow and, consequently, low oxygen/metabolites delivery, efflux of toxicological agents from the brain tissue and disturbance in the blood-brain barrier. The NO produced by iNOS in glial cells and nNOS, which triggers the NMDA-excitotoxic pathway, combines with superoxide anion and results in peroxynitrite synthesis, a potent free radical that contributes to tissue damage in the brain. Here, we intend to show the controversial role of the nitric oxide delivered by the three isoforms of the nitric oxide synthase in the CNS, assess its impact under healthy/pathological conditions and speculate on its possible sequela, particularly in long-term cognitive decline.

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Nitric oxide signaling modulates synaptic inhibition in the superior paraolivary nucleus (SPN) via cGMP-dependent suppression of KCC2

Cited by 34 publications

References 60 publications

Auditory deficits of Kcna1 deletion are similar to those of a monaural hearing impairment

Auditory deficits of Kcna1 deletion are similar to those of a monaural hearing impairment

Pattern of Nitrergic Neuronal System Organization in the Brain of Two Holostean Fishes (Actinopterygii: Ginglymodi)

Role of Nitric Oxide Synthase in the Function of the Central Nervous System under Normal and Infectious Conditions

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