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ABSTRACT: Trigeminal sensory nuclei that give rise to ascending pathways of vibrissal information are heavily linked by intersubnuclear connections. This is the case, for instance, of the principal trigeminal nucleus, which receives strong inhibitory input from the caudal sector of the interpolaris subnucleus. Because this inhibitory input can gate the relay of sensory messages through the lemniscal pathway, a central issue in vibrissal physiology is how brain regions that project to the interpolaris control the activity of inhibitory cells. In the present study, we examined how corticotrigeminal neurons of the primary and second somatosensory cortical areas control the excitability of interpolaris cells. Results show that these two cortical areas exert a differential control over the excitability of projection cells and intersubnuclear interneurons, and that this control also involves the recruitment of inhibitory cells in the caudalis subnucleus. These results provide a basic circuitry for a mechanism of disinhibition through which the cerebral cortex can control the relay of sensory messages in the lemniscal pathway. It is proposed that top-down control of brainstem circuits is prompted by motor strategies, expectations, and motivational states of the animal.
Journal of Neuroscience 02/2010; 30(5):1832-8. · 7.11 Impact Factor
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ABSTRACT: Higher-order thalamic nuclei receive input from both the cerebral cortex and prethalamic sensory pathways. However, at rest these nuclei appear silent due to inhibitory input from extrathalamic regions, and it has therefore remained unclear how sensory gating of these nuclei takes place. In the rodent, the ventral division of the zona incerta (ZIv) serves as a relay station within the paralemniscal thalamocortical projection pathway for whisker-driven motor activity. Most, perhaps all, ZIv neurons are GABAergic, and recent studies have shown that these cells participate in a feedforward inhibitory circuit that blocks sensory transmission in the thalamus. The present study provides evidence that the stimulation of the vibrissa motor cortex suppresses vibrissal responses in ZIv via an intra-incertal GABAergic circuit. These results provide support for the proposal that sensory transmission operates via a top-down disinhibitory mechanism that is contingent on motor activity.
Neuron 12/2007; 56(4):714-25. · 14.74 Impact Factor
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ABSTRACT: Three ascending pathways of information processing have been identified so far in the vibrissal system of rodents. In the ventral posterior medial nucleus of the thalamus, two of these pathways convey information through the core and tail of barrel-associated structures, called barreloids. The other pathway transits through the posterior group nucleus. The present study provides anatomical and electrophysiological evidence for the existence of an additional pathway that passes through the head of the barreloids. This pathway arises from multiwhisker-responsive cells in the principal trigeminal nucleus and differs from the classic lemniscal pathway, in that constituent thalamic cells have multiwhisker receptive field and receive corticothalamic input from lamina 6 of the vibrissa motor cortex. It is suggested that this pathway might be involved in relaying signals encoding phase of whisker motion during free whisking.
Journal of Neuroscience 12/2007; 27(45):12407-12. · 7.11 Impact Factor
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ABSTRACT: Dopamine is involved in motivation, memory, and reward processing. However, it is not clear whether the activity of dopamine neurons is related or not to vigilance states. Using unit recordings in unanesthetized head restrained rats we measured the firing pattern of dopamine neurons of the ventral tegmental area across the sleep-wake cycle. We found these cells were activated during paradoxical sleep (PS) via a clear switch to a prominent bursting pattern, which is known to induce large synaptic dopamine release. This activation during PS was similar to the activity measured during the consumption of palatable food. Thus, as it does during waking in response to novelty and reward, dopamine could modulate brain plasticity and thus participate in memory consolidation during PS. By challenging the traditional view that dopamine is the only aminergic group not involved in sleep physiology, this study provides an alternative perspective that may be crucial for understanding the physiological function of PS and dream mentation.
Neuropsychopharmacology 07/2007; 32(6):1232-41. · 7.99 Impact Factor
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ABSTRACT: Through their widespread projections to the entire brain, dorsal raphe cells participate in many physiological functions and are associated with neuropsychiatric disorders. In previous studies, the width of action potentials was used as a criterion to identify putative serotonergic neurons, and to demonstrate that cells with broad spikes were more active in wakefulness, slowed down their activity in slow wave sleep and became virtually silent during paradoxical sleep. However, recent studies reported that about half of these presumed serotonergic cells were not immunoreactive for tyrosine hydroxylase. Here, we re-examine the electrophysiological properties of dorsal raphe cells across the sleep-wake cycle in rats by the extracellular recording of a large sample of single units (n = 770). We identified two major types of cells, which differ in spike waveform: a first population characterized by broad, mostly positive spikes, and a second one displaying symmetrical positive-negative spikes with a large distribution of spike durations (0.6-3.2 ms). Although we found classical broad-spike cells that were more active in wakefulness, we also found that about one-third of these cells increased or did not change their firing rate during sleep compared with wakefulness. Moreover, 62% of the latter cells were active in paradoxical sleep when most of raphe cells were silent. Such a diversity in the neuronal firing behaviour is important in the light of the recent controversy regarding the neurochemical identity of dorsal raphe cells exhibiting broad spikes. Our results also suggest that the dorsal raphe contains subpopulations of neurons with reciprocal activity across the sleep-wake cycle.
The Journal of Physiology 07/2006; 573(Pt 3):679-95. · 4.72 Impact Factor
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ABSTRACT: Sensory stimuli evoke strong responses in thalamic relay cells, which ensure a faithful relay of information to the neocortex. However, relay cells of the posterior thalamic nuclear group in rodents, despite receiving significant trigeminal input, respond poorly to vibrissa deflection. Here we show that sensory transmission in this nucleus is impeded by fast feedforward inhibition mediated by GABAergic neurons of the zona incerta. Intracellular recordings of posterior group neurons revealed that the first synaptic event after whisker deflection is a prominent inhibition. Whisker-evoked EPSPs with fast rise time and longer onset latency are unveiled only after lesioning the zona incerta. Excitation survives barrel cortex lesion, demonstrating its peripheral origin. Electron microscopic data confirm that trigeminal axons make large synaptic terminals on the proximal dendrites of posterior group cells and on the somata of incertal neurons. Thus, the connectivity of the system allows an unusual situation in which inhibition precedes ascending excitation resulting in efficient shunting of the responses. The dominance of inhibition over excitation strongly suggests that the paralemniscal pathway is not designed to relay inputs triggered by passive whisker deflection. Instead, we propose that this pathway operates through disinhibition, and that the posterior group forwards to the cerebral cortex sensory information that is contingent on motor instructions.
Journal of Neuroscience 09/2005; 25(33):7489-98. · 7.11 Impact Factor
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ABSTRACT: The subthalamic nucleus (STN) has been implicated in movement disorders observed in Parkinson's disease because of its pathological mixed burst firing mode and hyperactivity. In physiological conditions, STN bursty pattern has been shown to be dependent on slow wave cortical activity. Indeed, cortical ablation abolished STN bursting activity in urethane-anaesthetized intact or dopamine depleted rats. Thus, glutamate afferents might be involved in STN bursting activity during slow wave sleep (SWS) when thalamic and cortical cells oscillate in a low-frequency range. The present work was aimed to test, on non-anaesthetized rats, if it was possible to regularize the SWS STN bursty pattern by microiontophoresis of kynurenate, a broad-spectrum glutamate ionotropic receptors antagonist. As glutamatergic effects might be masked by GABAergic inputs arriving tonically and during the entire sleep-wake cycle on STN neurons, kynurenate was also co-iontophoresed with bicuculline, a GABA(A) receptors antagonist. Kynurenate iontophoretic applications had a weak inhibitory effect on the discharge rate of STN neurons whatever the vigilance state, and did not regularize the SWS STN bursty pattern. But, the robust bursty bicuculline-induced pattern was impaired by kynurenate, which elicited the emergence of single spikes between remaining bursts. These data indicate that the bursty pattern exhibited by STN neurons specifically in SWS, does not seem to exclusively depend on glutamatergic inputs to STN cells. Furthermore, GABA(A) receptors may play a critical role in regulating the influence of excitatory inputs on STN cells.
European Journal of Neuroscience 08/2004; 20(2):392-402. · 3.63 Impact Factor
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Bernadette Astier,
Laura Lambás Señas,
Fabienne Soulière,
Patricia Schmitt, Nadia Urbain,
Nicolas Rentero,
Lionel Bert,
Luc Denoroy,
Bernard Renaud,
Monique Lesourd,
Carmen Muñoz,
Guy Chouvet
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ABSTRACT: The aim of the present study was to compare, in chloral-hydrate anaesthetized rats, the alpha(2)-adrenergic properties of the selective 5-HT(1A) receptor agonist, alnespirone (S-20499), with those of buspirone, a 5-HT(1A) receptor agonist exhibiting potent alpha(2)-adrenoceptor antagonist properties via its principal metabolite, 1-(2-pyrimidinyl)-piperazine. Both locus coeruleus spontaneous firing activity and noradrenaline release in the medial prefrontal cortex were potently inhibited by the alpha(2)-adrenoceptor agonist clonidine, at a dose of 40 microg/kg (i.p.). Such an inhibition was neither prevented nor reversed by alnespirone (10 mg/kg, i.p.), while buspirone, at the same dose, potently antagonized the locus coeruleus inhibitory effects of clonidine. These data demonstrate that, in contrast with some aryl-piperazine compounds (such as buspirone), alnespirone, either on its own or via a possible metabolite such as buspirone, is devoid in vivo of significant alpha(2)-adrenoceptor antagonist properties.
European Journal of Pharmacology 02/2003; 459(1):17-26. · 2.52 Impact Factor
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ABSTRACT: The subthalamic nucleus (STN) powerfully controls basal ganglia outputs and has been implicated in movement disorders observed in Parkinson's disease because of its pathological mixed burst firing mode and hyperactivity. A recent study suggested that reciprocally connected glutamatergic STN and GABAergic globus pallidus (GP) neurons act in vitro as a generator of bursting activity in basal ganglia. In vivo, we reported that GP neurons increased their firing rate in wakefulness (W) compared with slow-wave sleep (SWS) without any change in their random pattern. In contrast, STN neurons exhibited similar firing rates in W and SWS, with an irregular pattern in W and a bursty one in SWS. Thus, the pallidal GABAergic tone might control the STN pattern. This hypothesis was tested by mimicking such variations with microiontophoresis of GABA receptor ligands. GABA agonists specifically decreased the STN firing rate but did not affect its firing pattern. GABA(A) (but not GABA(B)) antagonists strongly enhanced the STN mean discharge rate during all vigilance states up to three to five times its basal activity. However, such applications did not change the typical W random pattern. When applied during SWS, GABA(A) antagonists strongly reinforced the spontaneous bursty pattern into a particularly marked one with instantaneous frequencies reaching 500-600 Hz. SWS-W transitions occurring during ongoing antagonist iontophoresis invariably disrupted the bursty pattern into a random one. Thus GABA(A) receptors play a critical, but not exclusive, role in regulating the excitatory STN influence on basal ganglia outputs.
Journal of Neuroscience 11/2002; 22(19):8665-75. · 7.11 Impact Factor
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Nadia Urbain,
Damien Gervasoni,
Fabienne Soulière,
Letícia Lobo,
Nicolas Rentéro,
François Windels,
Bernadette Astier,
Marc Savasta,
Patrice Fort,
Bernard Renaud,
Pierre-Hervé Luppi,
Guy Chouvet
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ABSTRACT: The pallido-subthalamic pathway powerfully controls the output of the basal ganglia circuitry and has been implicated in movement disorders observed in Parkinson's disease (PD). To investigate the normal functioning of this pathway across the sleep–wake cycle, single-unit activities of subthalamic nucleus (STN) and globus pallidus (GP) neurons were examined, together with cortical electroencephalogram and nuchal muscular activity, in non-anaesthetized head-restrained rats. STN neurons shifted from a random discharge in wakefulness (W) to a bursting pattern in slow wave sleep (SWS), without any change in their mean firing rate. This burst discharge occurred in the 1–2 Hz range, but was not correlated with cortical slow wave activity. In contrast, GP neurons, with a mean firing rate higher in W than in SWS, exhibited a relatively regular discharge whatever the state of vigilance. During paradoxical sleep, both STN and GP neurons increased markedly their mean firing rate relative to W and SWS. Our results are not in agreement with the classical ‘direct/indirect’ model of the basal ganglia organization, as an inverse relationship between STN and GP activities is not observed under normal physiological conditions. Actually, because the STN discharge pattern appears dependent on coincident cortical activity, this nucleus can hardly be viewed as a relay along the indirect pathway, but might rather be considered as an input stage conveying corticothalamic information to the basal ganglia.
European Journal of Neuroscience 12/2001; 12(9):3361 - 3374. · 3.63 Impact Factor
