Cholinergic basal forebrain projections to nitric oxide synthase-containing neurons in the rat cerebral cortex

Vaucher, Elvire; Linville, Donald G.; Hamel, Edith

doi:10.1016/s0306-4522(97)00033-x

Cited by 76 publications

(54 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…NOS neurons were the most frequently contacted by ACh afferents (ϳ70%), followed by SOM (57%), VIP/ ChAT (35-40%), small NPY neurons not colocalized with NOS (30%), and, finally, VIP cells not colocalized with . Consistent with ACh and 5-HT innervations of the cerebral cortex acting mainly through diffuse transmission (Descarries and Mechawar, 2000), the ACh input to NOS neurons has previously been found to be mainly nonjunctional (Vaucher et al, 1997). A larger proportion (ϳ30%) of NOS neurons also received both ACh and 5-HT innervations compared with other interneurons (10 -19%).…”

Section: Afferent Inputs To Different Subsets Of Gaba Neurons and Funsupporting

confidence: 54%

“…A larger proportion of NOS cells received somatic basal forebrain (Vaucher et al, 1997) ACh compared with brainstem 5-HT afferents (69.0 vs 40.9%; p Ͻ 0.05) (Fig. 6 A), with 30 -35% of their somata or dendrites receiving both types of afferents (Fig.…”

Section: Nos Npy and Sommentioning

confidence: 98%

“…They are highly diverse in morphology, connectivity, and firing patterns as well as in the substances they express (Cauli et al, 1997;Kawaguchi and Kubota, 1997), many of which being vasoactive. As well, apart from specific subsets of GABA interneurons identified as anatomical or functional targets for (basal forebrain) cholinergic (ACh) and/or brainstem raphe nucleus serotonergic (5-HT) neurons (Vaucher et al, 1997;Porter et al, 1999;Ferezou et al, 2002), two subcortical systems known to elicit changes in cortical perfusion after stimulation (for review, see Hamel, 2004) (Cohen et al, 1996;Iadecola, 2004), little is known about the input to cortical interneurons by both ACh and 5-HT afferent systems.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Cortical GABA Interneurons in Neurovascular Coupling: Relays for Subcortical Vasoactive Pathways

Cauli¹,

Tong²,

Rancillac³

et al. 2004

J. Neurosci.

511

530

View full text Add to dashboard Cite

show abstract

Section: Afferent Inputs To Different Subsets Of Gaba Neurons and Funsupporting

confidence: 54%

Section: Nos Npy and Sommentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Cortical GABA Interneurons in Neurovascular Coupling: Relays for Subcortical Vasoactive Pathways

Cauli¹,

Tong²,

Rancillac³

et al. 2004

J. Neurosci.

511

530

View full text Add to dashboard Cite

show abstract

“…Because GABAergic nNOS-ir neurons send long-range projections within the cortex (19,33), form exclusively axodendritic connections with other neurons, and probably widely arborize in the layers in which their cell bodies are located (34), nNOS-ir neurons appear to be well suited to synchronize cortical EEG activity over large brain areas. In this regard, it is noteworthy that nNOS-ir cell bodies and their proximal dendrites receive both cholinergic (35) and serotonin inputs (36), neurotransmitters that have historically been implicated in arousal state control.…”

Section: Discussionmentioning

confidence: 99%

Identification of a population of sleep-active cerebral cortex neurons

Gerashchenko

Wisor

Burns

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

180

162

View full text Add to dashboard Cite

The presence of large-amplitude, slow waves in the EEG is a primary characteristic that distinguishes cerebral activity during sleep from that which occurs during wakefulness. Although sleepactive neurons have been identified in other brain areas, neurons that are specifically activated during slow-wave sleep have not previously been described in the cerebral cortex. We have identified a population of cells in the cortex that is activated during sleep in three mammalian species. These cortical neurons are a subset of GABAergic interneurons that express neuronal NOS (nNOS). Because Fos expression in these sleep-active, nNOS-immunoreactive (nNOS-ir) neurons parallels changes in the intensity of slow-wave activity in the EEG, and these neurons are innvervated by neurotransmitter systems previously implicated in sleep/wake control, cortical nNOS-ir neurons may be part of the neurobiological substrate that underlies homeostatic sleep regulation.Fos ͉ interneuron ͉ neuronal NOS ͉ sleep deprivation ͉ wakefulness S leep is well known to have recuperative properties (1) and to facilitate performance of learned behaviors (2, 3); conversely, sleep deprivation results in cognitive and performance deficits (4). The presence of large-amplitude, slow waves in the EEG is the hallmark that distinguishes cerebral activity during sleep from wakefulness. Because the intensity of slow waves measured in the delta range of the EEG (1.0-4.0 Hz) appears to be homeostatically regulated and proportional to prior wake duration (5), slow-wave activity (SWA) has been hypothesized to be associated with the restorative function of sleep and with synaptic plasticity (2, 3, 6).The neural circuitry underlying SWA involves a corticothalamocortical loop and interplay between a hyperpolarizationactivated cation current (I h ) and a low-threshold Ca 2ϩ current (I t ) in thalamocortical neurons (7,8). It is currently unknown whether the cerebral cortex is an active participant or simply a passive conveyor of sleep history-dependent SWA dynamics. Identification of a discrete sleep-active population of cortical neurons, such as those in the basal forebrain (BF) (9) and the preoptic-anterior hypothalamus (POAH) (10-13), would help distinguish between these alternatives.In experiments conducted in three mammalian species, we found that GABAergic interneurons expressing the enzyme neuronal NOS (nNOS) are activated both during spontaneous sleep and during recovery sleep (RS) after sleep deprivation (SD). The proportion of nNOS-immunoreactive (nNOS-ir) neurons that are activated during sleep is correlated with a measure of SWA intensity known as ''delta energy' ' (14, 15). Because sleep-active, nNOS-ir neurons are innervated by neurotransmitter systems previously implicated in sleep/wake control, cortical nNOS-ir neurons may be a previously unrecognized cell type involved in SWA and part of the neurobiological substrate that underlies homeostatic sleep regulation. Results Fos Expression Is Increased in Cortical nNOS Neurons During RS.Fos expression has previ...

show abstract

“…Cortical nNOS neurons receive cholinergic (12), monoaminergic (13), and peptidergic (14,15) inputs. Sleep-active nNOS cells correspond to type I nNOS neurons, which are larger and less numerous than type II cells, express the neurokinin-1 receptor (NK1; 14,15), and are likely projection neurons (16,17).…”

mentioning

confidence: 99%

A role for cortical nNOS/NK1 neurons in coupling homeostatic sleep drive to EEG slow wave activity

Morairty

Dittrich

Pasumarthi

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

122

View full text Add to dashboard Cite

Although the neural circuitry underlying homeostatic sleep regulation is little understood, cortical neurons immunoreactive for neuronal nitric oxide synthase (nNOS) and the neurokinin-1 receptor (NK1) have been proposed to be involved in this physiological process. By systematically manipulating the durations of sleep deprivation and subsequent recovery sleep, we show that activation of cortical nNOS/NK1 neurons is directly related to non-rapid eye movement (NREM) sleep time, NREM bout duration, and EEG δ power during NREM sleep, an index of preexisting homeostatic sleep drive. Conversely, nNOS knockout mice show reduced NREM sleep time, shorter NREM bouts, and decreased power in the low δ range during NREM sleep, despite constitutively elevated sleep drive. Cortical NK1 neurons are still activated in response to sleep deprivation in these mice but, in the absence of nNOS, they are unable to up-regulate NREM δ power appropriately. These findings support the hypothesis that cortical nNOS/NK1 neurons translate homeostatic sleep drive into up-regulation of NREM δ power through an NO-dependent mechanism.T he electrical activity of the cerebral cortex has been used to distinguish sleep vs. wakefulness since the earliest EEG studies of sleep (1). Several neural circuits have been implicated in the synchronization and desynchronization of cortical activity that distinguish non-rapid eye movement sleep (NREM) from wakefulness and rapid eye movement sleep (REM). Input from the basal forebrain (BF), likely from both cholinergic and noncholinergic neurons, is critical for the desynchronized EEG characteristic of wakefulness and REM (2, 3). Synchronization of the EEG during NREM depends on thalamic as well as intrinsic cortical oscillators (4).The firing rate of cortical neurons has generally been reported to be reduced during NREM relative to wakefulness and REM (5, 6). A few studies have reported cortical neurons with the opposite pattern. For example, 4 of 177 neurons in the monkey orbitofrontal cortex increased their firing rates during NREM (7). In the cat parietal cortex, 25% of neurons discharged in phase with NREM slow waves during up states but ceased firing during quiet wakefulness (8).Using Fos immunohistochemistry as a marker of cellular activity, we described a population of cortical GABAergic interneurons that are activated during sleep in three species (9, 10). These neurons express neuronal nitric oxide synthase (nNOS) and thus likely release nitric oxide (NO) as well as GABA (11). The percentage of activated cortical nNOS neurons was proportional to NREM δ energy (NRDE), the product of NREM time and NREM EEG δ power. Because NREM time and δ power increase in response to prolonged wakefulness through a regulated process referred to as sleep homeostasis, NRDE is an electrophysiological marker of homeostatic sleep "drive." Consequently, activation of cortical nNOS neurons during sleep seems to be related to the sleep need that accrues during wakefulness.Cortical nNOS neurons receive cholinergic (12), monoamin...

show abstract

Cholinergic basal forebrain projections to nitric oxide synthase-containing neurons in the rat cerebral cortex

Cited by 76 publications

References 50 publications

Cortical GABA Interneurons in Neurovascular Coupling: Relays for Subcortical Vasoactive Pathways

Cortical GABA Interneurons in Neurovascular Coupling: Relays for Subcortical Vasoactive Pathways

Identification of a population of sleep-active cerebral cortex neurons

A role for cortical nNOS/NK1 neurons in coupling homeostatic sleep drive to EEG slow wave activity

Contact Info

Product

Resources

About