Distribution and synaptic contacts of the cortical terminals arising from neurons in the rat ventromedial thalamic nucleus

Arbuthnott, G.W.; Macleod, Neil; Maxwell, David; Wright, Angela

doi:10.1016/0306-4522(90)90373-c

Cited by 63 publications

(58 citation statements)

References 43 publications

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“…Local connections lead to correlated dendritic activity, which is then desynchronized by excitatory input to L1 as the animal wakes up. Although L1 is subject to arousal-dependent cholinergic modulation (33,37,38), the fact that blocking AMPA/kainate receptors removes state-dependent synchrony argues against acetylcholine as a mechanism.…”

Section: Discussionmentioning

confidence: 99%

In vivo two-photon voltage-sensitive dye imaging reveals top-down control of cortical layers 1 and 2 during wakefulness

Kühn

Denk

Bruno

2008

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

105

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Conventional methods of imaging membrane potential changes have limited spatial resolution, particularly along the axis perpendicular to the cortical surface. The laminar organization of the cortex suggests, however, that the distribution of activity in depth is not uniform. We developed a technique to resolve network activity of different cortical layers in vivo using two-photon microscopy of the voltage-sensitive dye (VSD) ANNINE-6. We imaged spontaneous voltage changes in the barrel field of the somatosensory cortex of head-restrained mice and analyzed their spatiotemporal correlations during anesthesia and wakefulness. EEG recordings always correlated more strongly with VSD signals in layer (L) 2 than in L1. Nearby (<200 m) cortical areas were correlated with one another during anesthesia. Waking the mouse strongly desynchronized neighboring cortical areas in L1 in the 4-to 10-Hz frequency band. Wakefulness also slightly increased synchrony of neighboring territories in L2 in the 0.5-to 4.0-Hz range. Our observations are consistent with the idea that, in the awake animal, long-range inputs to L1 of the sensory cortex from various cortical and thalamic areas exert top-down control on sensory processing.ayer (L) 1 has been least investigated of all the cortical layers despite its potentially prominent role in cortical processing. Although largely acellular, except for a sparse population of inhibitory neurons (1), L1 is the main target of axons originating in distant cortical and subcortical regions. This dense plexus of axons makes excitatory synapses on apical dendritic tufts of L2/3 and L5 pyramidal neurons. Dendritic tufts contain powerful active conductances that cause electrical changes that can propagate to their relatively distant somata and influence the integration of synaptic inputs there (2). L1 is therefore ideally positioned to mediate communication between brain regions.In the primary somatosensory cortex, long-range input to L1 consists of corticocortical synapses from primary motor cortex and the secondary somatosensory area (3). In contrast, synapses in other cortical layers, such as L2, originate from a mixture of excitatory and inhibitory cells located mainly in that specific cortical column (4). A major source of thalamocortical synapses in L1 is the second-order sensory nucleus, also called the ''posterior medial'' (POm) nucleus (5), whose activity appears to be strongly modulated by arousal (6). This finding suggests that synaptic inputs in L1 also should be modulated by arousal. Synaptic inputs can be studied by recording membrane-voltage (V m ) changes, but L1 is relatively inaccessible using conventional methods.Wide-field imaging of voltage-sensitive dyes (VSDs) has been used successfully to sample V m in neurites of isolated neurons and across large populations of cortical cells (7). Although such imaging allows high frame rates (Ͼ1 kHz), scattering and limited depth discrimination result in poor spatial resolution. Thus, when imaging in vivo, the signal at any point in the image co...

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Section: Discussionmentioning

confidence: 99%

In vivo two-photon voltage-sensitive dye imaging reveals top-down control of cortical layers 1 and 2 during wakefulness

Kühn

Denk

Bruno

2008

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

105

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“…However, it is known for the rat that there are less neurons in the frontal cortex than in the posterior areas (Beaulieu, 1993). On the other hand, frontal areas receive a massive input from the contralateral cortical areas via the corpus callosum (Ozaki and Wahlsten, 1993), from the thalamus (Arbuthnott et al, 1990) and from the brainstem (Lamour et al, 1982;Woolf et al, 1983). Therefore, the relative number of synaptic connections formed in the frontal cortex may be higher compared with other areas.…”

Section: Introductionmentioning

confidence: 93%

Running Wheel Accessibility Affects the Regional Electroencephalogram during Sleep in Mice

Vyazovskiy¹,

Ruijgrok²,

Deboer³

et al. 2005

Cerebral Cortex

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Regional aspects of sleep homeostasis were investigated in mice provided with a running wheel for several weeks. Electroencephalogram (EEG) spectra of the primary motor (frontal) and somatosensory cortex (parietal) were recorded for three consecutive days. On a single day (day 2) the wheel was locked to prevent running. Wheel running correlated negatively with the frontal--parietal ratio of slow-wave activity (EEG power between 0.75 and 4.0 Hz) in the first 2 h after sleep onset (r 5 20.60; P < 0.01). On day 2 frontal EEG power (2.25--8.0 Hz) in non-rapid eye movement sleep exceeded the level of the previous day, indicating that the diverse behaviors replacing wheel-running elicited more pronounced regional EEG differences. The frontal--parietal power ratio of the lower frequency bin (0.75--1.0 Hz) in the first 2 h of sleep after dark onset correlated positively with the duration of the preceding waking (r 5 0.64; P < 0.001), whereas the power ratio in the remaining frequencies of the delta band (1.25--4.0 Hz) was unrelated to waking. The data suggest that in mice EEG power in the lower frequency, corresponding to the slow oscillations described in cats and humans, is related to local sleep homeostasis.

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“…However, we cannot exclude the contribution of a rebound response in corticothalamic neurons Timofeev et al, 2002) and/or of an intrinsic postinhibitory excitation attributable to I h and/or I T . The increase in firing of VM thalamic neurons associated with the termination of the seizure, could be responsible for the postictal rebound of depolarization in striatal output neurons (Arbuthnott et al, 1990;Slaght et al, 2004), which, in turn, might contribute to the transient interruption of firing in SNR neurons at the end of cortical paroxysms (Deransart et al, 2003).…”

Section: Membrane Oscillations and Bursting Of Vm Thalamic Neurons Dumentioning

confidence: 99%

Activity of Ventral Medial Thalamic Neurons during Absence Seizures and Modulation of Cortical Paroxysms by the Nigrothalamic Pathway

Paz

Chávez²,

Saillet³

et al. 2007

J. Neurosci.

132

112

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Absence seizures are characterized by bilaterally synchronous spike-and-wave discharges (SWDs) in the electroencephalogram, which reflect abnormal oscillations in corticothalamic networks. Although it was suggested that basal ganglia could modulate, via their feedback circuits to the cerebral cortex, the occurrence of SWDs, the cellular and network mechanisms underlying such a subcortical control of absence seizures remain unknown. The GABAergic projections from substantia nigra pars reticulata (SNR) to thalamocortical neurons of the ventral medial (VM) thalamic nucleus provide a potent network for the control of absence seizures by basal ganglia. The present in vivo study provides the first description of the activity of VM thalamic neurons during seizures in the genetic absence epilepsy rats from Strasbourg, a well established model of absence epilepsy. Cortical paroxysms were accompanied in VM thalamic neurons by rhythmic bursts of action potentials. Pharmacological blockade of excitatory inputs of nigrothalamic neurons led to a transient interruption of SWDs, correlated with a change in the activity of thalamic cells, which was increased in frequency and converted into a sustained arrhythmic firing pattern. Simultaneously, cortical neurons exhibited a decrease in their firing rate that was associated with an increase in membrane polarization and a decrease in input resistance. These new findings demonstrate that an inhibition of SNR neurons changes the activity of their thalamic targets, which in turn could affect cortical neurons excitability and, consequently, the generation of cortical epileptic discharges. Thus, the nigro-thalamo-cortical pathway may provide an on-line system control of absence seizures.

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Distribution and synaptic contacts of the cortical terminals arising from neurons in the rat ventromedial thalamic nucleus

Cited by 63 publications

References 43 publications

In vivo two-photon voltage-sensitive dye imaging reveals top-down control of cortical layers 1 and 2 during wakefulness

In vivo two-photon voltage-sensitive dye imaging reveals top-down control of cortical layers 1 and 2 during wakefulness

Running Wheel Accessibility Affects the Regional Electroencephalogram during Sleep in Mice

Activity of Ventral Medial Thalamic Neurons during Absence Seizures and Modulation of Cortical Paroxysms by the Nigrothalamic Pathway

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