Nitric oxide controls oscillatory activity in thalamocortical neurons

Pape, Hans‐Christian; Mager, Ralph

doi:10.1016/0896-6273(92)90182-d

Cited by 216 publications

(123 citation statements)

References 38 publications

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“…Evidence that the identified neurons actually generate NO is supported by the coexpression of NADPH-d and NOS by cells in virtually all regions examined both in the PNS and CNS . Moreover, NADPH-d staining in the nondiscriminative nuclei, particularly in the n.Pvt and central media1 intralaminar nucleus, was remarkably well circumscribed and equivalent in concentration to that in the LGN where NO was recently shown to dampen oscillatory activities of thalamocortical neurons (Pape and Mager, 1992). The functional significance of the especially high density in n.Pvt is unknown, although a role in behavioral expression seems likely.…”

Section: Discussionmentioning

confidence: 97%

“…We have focused our work on the paraventricular thalamic nucleus (n.Pvt) enriched in an NO synthase and recently classified as a constituent of the nondiscriminative thalamus and viscerallimbic system (Berendse and Groenewegen, 1991;Otake et al, 1994). This experimental series was designed based on recent compelling evidence that NO acts in the LGN, encouraging a functional state of activity conducive to wakefulness (Pape and Mager, 1992).…”

mentioning

confidence: 99%

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Monoamines and nitric oxide are employed by afferents engaged in midline thalamic regulation

Otake

Ruggiero

1995

J. Neurosci.

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The neurochemical identities of afferents to the midline thalamus were investigated in chloral hydrate-anesthetized adult Sprague-Dawley rats. The retrograde tracers, FluoroGold or cholera toxin B subunit, were centered on the paraventricular thalamic nucleus (n.Pvt), a periventricular member of the diffuse thalamocortical projection system that is reciprocally linked with visceral areas of cerebral cortex and implicated in food intake and addictive behavior. Tissues were processed with antisera raised against 5-HT, the catecholamine- synthesizing enzymes, tyrosine hydroxylase or phenylethanolamine N- methyltransferase or the cholinergic anabolic enzyme, ChAT. Serotonergic afferents principally derive from dorsal and median constituents of the mesopontine raphe. Previously unrecognized sources of catecholaminergic afferents were detected. Adrenergic afferents were traced to neurons in the C1 and C3 areas of rostral medullary reticular formation and periventricular gray, respectively, and the C2 area corresponding to the dorsal general viscerosensory field of nucleus tractus solitarii. Noradrenergic afferents arise principally from neurons in the locus ceruleus and A5 area. Dopaminergic projections to the n.Pvt derive from the A14, A13 and A11 cell groups in diencephalon. Afferents presumed to generate nitric oxide (NO) as a diffusible membrane-permeant transcellular signal were detected by processing retrogradely labeled tissues histochemically for NADPH-diaphorase, a molecule associated with nitric oxide synthase. NO in the n.Pvt is generated predominantly by noncholinergic neurons in the lateral hypothalamic area and mesopontine tegmentum. In striking contrast, extensive interactions were predicted between NO and ACh in the central medial and other loci in the nondiscriminative thalamus. We conclude that the n.Pvt is a site of interaction of NO and monoaminergic afferents derived from nuclei implicated in sensory gating, regulation of electrocortical neural activity and behavior. Taken collectively, our data predict that the labile transcellular messenger NO may enable structurally differentiated subnuclei of the diffuse thalamocortical projection system to act in concert as a functionally unified unit.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

Monoamines and nitric oxide are employed by afferents engaged in midline thalamic regulation

Otake

Ruggiero

1995

J. Neurosci.

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“…Because of its rapid membrane-permeating characteristics and short half-life in biological tissues, NO is typically used to transmit information between closely juxtaposed cells. For example, NO serves as a local modulator of blood pressure (Shesely et al, 1996;Hanafy et al, 2001), cardiac function (Balligand et al, 1993;Keaney et al, 1996;Zahradnikova et al, 1997;Gyurko et al, 2000), neuronal development (Cramer et al, 1998;Scholz et al, 1998;Champlin and Truman, 2000), synaptic transmission (Schuman and Madison, 1994;Huang, 1997), and oscillatory behavior in patterngenerating networks of neurons (Pape and Mager, 1992;Moroz et al, 1993;Gelperin, 1994;Elphick et al, 1995;Hedrick and Morales, 1999;Scholz et al, 2001;Newcomb and Watson, 2002;McLean and Sillar, 2000).…”

Section: Introductionmentioning

confidence: 99%

Nitric Oxide Inhibits the Rate and Strength of Cardiac Contractions in the LobsterHomarus americanusby Acting on the Cardiac Ganglion

et al. 2004

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The lobster heart is synaptically driven by the cardiac ganglion, a spontaneously bursting neural network residing within the cardiac lumen. Here, we present evidence that nitric oxide (NO) plays an inhibitory role in lobster cardiac physiology. (1) NO decreases heartbeat frequency and amplitude. Decreased frequency is a direct consequence of a decreased ganglionic burst rate. Decreased amplitude is an indirect consequence of decreased burst frequency, attributable to the highly facilitating nature of the synapses between cardiac ganglion neurons and muscle fibers (although, during prolonged exposure to NO, amplitude recovers to the original level by a frequencyindependent adaptation mechanism). NO does not alter burst duration, spikes per burst, heart muscle contractility, or amplitudes of synaptic potentials evoked by stimulating postganglionic motor nerves. Thus, NO acts on the ganglion, but not on heart muscle. (2) Two observations suggest that NO is produced within the lobster heart. First, immunoblot analysis shows that nitric oxide synthase (NOS) is strongly expressed in heart muscle relative to other muscles. Second, L-nitroarginine (L-NA), an NOS inhibitor, increases the rate of the heartbeat (opposite to the effects of NO). In contrast, the isolated ganglion is insensitive to L-NA, suggesting that heart muscle (but not the ganglion) produces endogenous NO. Basal heart rate varies from animal to animal, and L-NA has the greatest effect on the slowest hearts, presumably because these hearts are producing the most NO. Thus, because the musculature is a site of NOS expression, whereas the ganglion is the only intracardiac target of NO, we hypothesize that NO serves as an inhibitory retrograde transmitter.

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“…Interestingly, HCN channel had already been reported to be an important downstream target for NO signaling in many brain areas. For example, exogenous NO modified oscillatory activity in thalamocortical relay neurons by acting on HCN channels (Pape and Mager, 1992); in mesencephalic neurons, NO reversibly depolarized the membrane and reduced the firing threshold by a presumed action on HCN channels (Pose et al, 2003); and in deep cerebellar nuclei neurons, NO enhanced HCN currents (Wilson and Garthwaite, 2010). In hippocampus CA1 region, it was recently reported that presynaptic NO/cGMP signaling facilitated glutamate release via HCN channels (Neitz et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Role of HCN Channels in Neuronal Hyperexcitability after Subarachnoid Hemorrhage in Rats

Luo²,

Tang³

et al. 2012

J. Neurosci.

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Disruption of ionic homeostasis and neuronal hyperexcitability contribute to early brain injury after subarachnoid hemorrhage (SAH).The hyperpolarization-activated/cyclic nucleotide (HCN)-gated channels play critical role in the regulation of neuronal excitability in hippocampus CA1 region and neocortex, in which the abnormal neuronal activities are more readily provoked. This study was to investigate the interactions between HCN channels and hyperneuronal activity after experimental SAH. The present results from wholecell recordings in rat brain slices indicated that (1)

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Nitric oxide controls oscillatory activity in thalamocortical neurons

Cited by 216 publications

References 38 publications

Monoamines and nitric oxide are employed by afferents engaged in midline thalamic regulation

Monoamines and nitric oxide are employed by afferents engaged in midline thalamic regulation

Nitric Oxide Inhibits the Rate and Strength of Cardiac Contractions in the LobsterHomarus americanusby Acting on the Cardiac Ganglion

Role of HCN Channels in Neuronal Hyperexcitability after Subarachnoid Hemorrhage in Rats

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