Preferential Potentiation by Nitric Oxide of Spontaneous Inhibitory Postsynaptic Currents in Rat Supraoptic Neurones

Ozaki, Masayuki; Shibuya, Izumi; Kabashima,; Noguchi,; Ueta,; Inoue,; Shigematsu,; Yamashita,

doi:10.1046/j.1365-2826.2000.00448.x

Cited by 72 publications

(64 citation statements)

References 29 publications

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“…In support of our findings, Ozaki et al (26) observed that SNAP, a donor of NO, increases the frequency of inhibitory postsynaptic potentials in hypothalamic slices containing the SON by a mechanism independent of cGMP. Similarly, Cui et al (25) have demonstrated that the inhibitory effects of NO on NMDA-induced depolarization of membrane potentials in SON neurons of hypothalamic slices are independent of cGMP.…”

Section: No and Signal-transduction Pathwaysupporting

confidence: 92%

“…SNP also reduces the depolarization of supraoptic neurons elicited by NMDA in vitro (25). Moreover, S-nitroso-N-acetylpenicillamine (SNAP), a donor of NO, increases the frequency of spontaneous inhibitory postsynaptic current (IPSC) from supraoptic neurons in slice preparations, without affecting its amplitude (26). This indicates that NO potentiates IPSCs via a pre-synaptic mechanism, possibly through NO's action on GABA terminals.…”

Section: No's Influence On Electrical Activity Of Magnocellular Neuronsmentioning

confidence: 99%

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Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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Nitric oxide (NO), a free radical gas produced endogenously from the amino acid L-arginine by NO synthase (NOS), has important functions in modulating vasopressin and oxytocin secretion from the hypothalamo-neurohypophyseal system. NO production is stimulated during increased functional activity of magnocellular neurons, in parallel with plastic changes of the supraoptic nucleus (SON) and paraventricular nucleus. Electrophysiological data recorded from the SON of hypothalamic slices indicate that NO inhibits firing of phasic and non-phasic neurons, while L-NAME, an NOS inhibitor, increases their activity. Results from measurement of neurohypophyseal hormones are more variable. Overall, however, it appears that NO, tonically produced in the forebrain, inhibits vasopressin and oxytocin secretion during normovolemic, isosmotic conditions. During osmotic stimulation, dehydration, hypovolemia and hemorrhage, as well as high plasma levels of angiotensin II, NO inhibition of vasopressin neurons is removed, while that of oxytocin neurons is enhanced. This produces a preferential release of vasopressin over oxytocin important for correction of fluid imbalance. During late pregnancy and throughout lactation, fluid homeostasis is altered and expression of NOS in the SON is down-and up-regulated, respectively, in parallel with plastic changes of the magnocellular system. NO inhibition of magnocellular neurons involves GABA and prostaglandin synthesis and the signal-transduction mechanism is independent of the cGMP-pathway. Plasma hormone levels are unaffected by icv 1H-[1, 2, 4]oxadiazolo-[4,3-a]quinoxalin-1-one (a soluble guanylyl cyclase inhibitor) or 8-Br-cGMP administered to conscious rats. Moreover, cGMP does not increase in homogenates of the neural lobe and in microdialysates of the SON when NO synthesis is enhanced during osmotic stimulation. Among alternative signal-transduction pathways, nitrosylation of target proteins affecting activity of ion channels is considered.

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Section: No and Signal-transduction Pathwaysupporting

confidence: 92%

Section: No's Influence On Electrical Activity Of Magnocellular Neuronsmentioning

confidence: 99%

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Kadekaro

2004

Braz J Med Biol Res

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“…In the present study, an in vitro PAG slice preparation allowed us to determine the modulatory actions of NO on inhibitory GABAergic and excitatory glutamatergic synaptic activity in the dl-PAG (Kabashima et al, 1997;Ozaki et al, 2000;Sulzer and Pothos, 2000). Our results demonstrated that bath application of an NO donor, SNAP as well as the NO precursor, Larginine, increased the frequency of mIPSCs in dl-PAG neurons but did not significantly affect their amplitude (Fig.…”

Section: Discussionsupporting

confidence: 47%

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

Xing

2008

Neuropharmacology

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Nitric oxide (NO) affects neuronal activity of the midbrain periaqueductal gray (PAG). The purpose of this report was to investigate the role of GABA receptors in NO modulation of neuronal activity through inhibitory and excitatory synaptic inputs within the dorsolateral PAG (dl-PAG). First, spontaneous miniature inhibitory postsynaptic currents (mIPSCs) and excitatory postsynaptic currents (mEPSCs) were recorded using whole cell voltage-clamp methods. Increased NO by either S-nitroso-N-acetyl-penicillamine (SNAP, 100 μM) or L-arginine (50 μM) significantly augmented the frequency of mIPSCs of the dl-PAG neurons without altering their amplitudes or decay time constants. The effects were eliminated after bath application of carboxy-PTIO (NO scavenger), and 1-(2-trifluorom-ethylphenyl) imidazole (NO synthase inhibitor). In contrast, SNAP and L-arginine did not alter mEPSCs in dl-PAG neurons. However the frequency of mEPSCs was significantly increased with prior application of the GABA B receptors antagonist, CGP55845. In addition, NO significantly decreased the discharge rate of spontaneous action potentials in the dl-PAG neurons and the effect was reduced in the presence of the GABA A receptor antagonist, bicuculline. Our data show that within the dl-PAG NO potentiates the synaptic release of GABA, while NO-induced GABA presynaptically inhibits glutamate release through GABA B receptors. Overall, NO suppresses neuronal activity of the dl-PAG via a potentiation of GABAergic synaptic inputs and via GABA A receptors.

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“…In subcortical areas, several studies demonstrated that the NO-NOsGC-cGMP pathway can either facilitate (Klyachko et al, 2001;Kraus and Prast, 2002;Li et al, 2004) or inhibit (Ozaki et al, 2000) GABAergic neurotransmission. There are at least three molecular targets that can mediate the action of cGMP in the brain.…”

Section: Both Perisomatic and Dendrite Targeting Gabaergic Neurons Comentioning

confidence: 99%

Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling

Szabadits¹,

Cserép²,

Ludányi³

et al. 2007

J. Neurosci.

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Nitric oxide (NO) plays an important role in synaptic plasticity as a retrograde messenger at glutamatergic synapses. Here we describe that, in hippocampal pyramidal cells, neuronal nitric oxide synthase (nNOS) is also associated with the postsynaptic active zones of GABAergic symmetrical synapses terminating on their somata, dendrites, and axon initial segments in both mice and rats. The NO receptor nitric oxide-sensitive guanylyl cyclase (NOsGC) is present in the brain in two functional subunit compositions: ␣ 1 ␤ 1 and ␣ 2 ␤ 1 . The ␤ 1 subunit is expressed in both pyramidal cells and interneurons in the hippocampus. Using immunohistochemistry and in situ hybridization methods, we describe that the ␣ 1 subunit is detectable only in interneurons, which are always positive for ␤ 1 subunit as well; however, pyramidal cells are labeled only for ␤ 1 and ␣ 2 subunits. With double-immunofluorescent staining, we also found that most cholecystokinin-and parvalbumin-positive and smaller proportion of the somatostatin-and nNOS-positive interneurons are ␣ 1 subunit positive. We also found that the ␣ 1 subunit is present in parvalbumin-and cholecystokinin-positive interneuron terminals that establish synapses on somata, dendrites, or axon initial segments. Our results demonstrate that NOsGC, composed of ␣ 1 ␤ 1 subunits, is selectively expressed in different types of interneurons and is present in their presynaptic GABAergic terminals, in which it may serve as a receptor for NO produced postsynaptically by nNOS in the very same synapse.

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Preferential Potentiation by Nitric Oxide of Spontaneous Inhibitory Postsynaptic Currents in Rat Supraoptic Neurones

Cited by 72 publications

References 29 publications

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Nitric oxide modulation of the hypothalamo-neurohypophyseal system

Role of GABA receptors in nitric oxide inhibition of dorsolateral periaqueductal gray neurons

Hippocampal GABAergic Synapses Possess the Molecular Machinery for Retrograde Nitric Oxide Signaling

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