Differential participation of some ‘specific’ and ‘non-specific’ thalamic nuclei in generalized spike and wave discharges of feline generalized penicillin epilepsy

Extracellular single unit and electroencephalographic (EEG) activity during generalized spike and wave discharges (SW) induced by i.m. penicillin was recorded simultaneously in the cortex, in a ‘specific’ thalamic nucleus (n. lateralis posterior, LP) and in some ‘non-specific’ thalamic nuclei (n. centralis medialis, NCM; n. centrum medianum, CM; n. centralis lateralis, CL) Computer-generated EEG averages and histograms of single unit activity were triggered by either peaks of EEG transients or action potentials. The time at which cortical neurons (66/66) were most likely to fire was during the ‘spike’ of the SW complex while absence of firing was the rule during the ‘wave’. Most LP neurons (23/26) showed a similar pattern, 3 cells firing preferentially during the ‘wave’. In NCM only 17 of 39 neurons fired during the ‘spike’, 8 of 39 neurons during the ‘wave’ while the others showed no change in their firing pattern during SWs. Twenty-six of 30 CM and 20 of 24 CL neurons fired during the ‘spike’ of SW; the other cells in these nuclei did not change their firing pattern during SWs. When present, rhythmic fluctuations in firing linked to SW discharge were less prominent in these ‘non-specific’ thalamic nuclei than in cortex and LP. Furthermore, participation of NCM, CM and CL neurons in the SW rhythm occurred only after neurons in cortex and LP had become involved in it. Thus, as is the case for cortical neurons, the main firing pattern of thalamic cells during SWs consists of an oscillation between ‘excitation’ during the ‘spike’ and ‘inhibition’ during the ‘wave’ of the SW complex. However, the coupling between cortical and thalamic neuronal firing is less intimate for cells of the ‘non-specific’ thalamic nuclei than for a ‘specific’ nucleus such as LP. Thus, at least some ‘specific’ thalamic nuclei are more intimately involved in the mechanism of SW discharge than the midline intralaminar nuclei.     

Interaction of cortex and thalamus in spike and wave discharges of feline generalized penicillin epilepsy

The transition from spindles to spike and wave (SW) discharges of feline generalized penicillin epilepsy was studied using simultaneous EEG recordings from mutually related cortical and thalamic sites after i.m. injection (350,000 IU/kg) or diffuse cortical application of a weak solution (100–300 IU/hemisphere) of penicillin. Both procedures induced similar changes at cortical and thalamic levels, those in the thalamus developing at the same time or slightly later but nerver earlier than in the cortex. These changes consisted of: (i) amplitude increase of spindles, development of positive phases, and decrease in amplitude, followed by disappearance of every second spindle wave as SW discharges developed; (ii) facilitation, progressive amplitude increase, and increase or development of positive phases of recruiting responses to midline thalamic stimulation. Once SW had developed, a decrease in cortical excitability by cortical application of 15% KCl caused the cortical and thalamic SW discharges to disappear and to be replaced by spindles. These results demonstrate that important changes in thalamic activity occur during the development of cortical SW discharge whether induced by i.m. penicillin or by diffuse cortical application of a weak penicillin solution. Changes in thalamic activity appear to be secondary to changes in cortical activity. Thus, although cortical SWs are triggered by thalamocortical inputs which originally were spindle-inducing, these inputs change after penicillin, and reflect an alteration in thalamic activity imposed by the cortex through corticothalamic volleys. In their turn, they modify the cortical response.     

Role of the thalamus in generalized penicillin epilepsy: Observations on decorticated cats

Experiments in bilaterally and unilaterally decorticated cats determined whether or not the thalamus plays a primary role in the production of spike and wave (SW) discharge in feline generalized penicillin epilepsy (FGPE). In bilaterally decorticated cats an i.m. dose of penicillin sufficient to induce FGPE in intact cats did not change thalamic spindles appreciably; it failed to induce thalamic SWs or any other form of epileptic activity in the decorticated thalamus. Low-frequency spindles bearing some resemblance to SWs were often seen in the nucleus lateralis posterior (LP) before penicillin administration and showed some slight increase thereafter. This may have some bearing on earlier evidence suggesting that the thalamocortical sector comprising the LP and suprasylvian gyrus plays a leading role in the elaboration of SWs in FGPE. In unilaterally decorticated cats the SW discharges in the intact hemisphere were associated with lower voltage synchronous discharges in the decorticated thalamus which persisted after transection of the massa intermedia or of the mesencephalic reticular formation, but disappeared after section of the anterior commissure. This pathway thus seemed to be responsible for transmitting rhythmic activity at the SW frequency from the intact hemisphere to the decorticated thalamus. These findings support earlier conclusions that the development of generalized SW discharge in FGPE primarily depends on a change in cortical excitability, even though a thalamic trigger is essential. Thalamic SW activity appearing in intact animals after penicillin thus seems to be imposed upon the thalamus by the cortex.     

Frontal cortex leads other brain structures in generalised spike-and-wave spindles and seizure spikes induced by picrotoxin

Generalised spike-and-wave (SW) spindles (5–7 Hz) associated with myoclonic jerks precede the occurrence of regular spikes (2–3 Hz) associated with convulsive seizure induced by picrotoxin. SW spindles occur spontaneously in rodent and cat under some experimental conditions and are considered to be models of human generalised epilepsy. These spindles have been proposed as being led by a thalamic pacemaker. To examine this possibility in picrotoxin-induced SW spindles and seizure spikes, we recorded EEG using chronically implanted unipolar electrodes during intravenous picrotoxin infusion in freely behaving rat. The 6 EEG signals were digitally sampled at 1000 Hz. Linear correlation, spectral, coherence and phase analyses were undertaken to determine time differences (TDs) between EEG channels and the brain structure leading seizure activity.One frontal cortex led all other structures during SW spindles. TD between SW spindles in the leading frontal cortex (Frl) and the contralateral Frl was 3.6 ± 0.5 msec. All ipsilateral structures (hippocampus, thalamus, amygdala, caudate nucleus and occipital cortex) were delayed by more than 3 msec from Frl (intralaminar thalamic nuclei − by 6.3 ± 0.9 msec). TDs of SW spindles between subcortical regions were less than 1.5 msec. Similar relationships with slightly smaller TDs were found with spikes during convulsive seizure except TDs between frontal cortices did not significantly differ from zero.We suggest that seizure activity induced by picrotoxin is led by one Frl during SW spindles and by both frontal cortices working as one system during convulsive seizure.     

Sleep Oscillations Developing into Seizures in Corticothalamic Systems

Summary:  Purpose: The aim of this article is to discuss the neuronal substrates of sleep oscillations leading to seizures consisting of spike–wave (SW) complexes at 2–4 Hz, mimicking those seen in absence epilepsy, or SW and polyspike–wave (PSW) complexes at 1.5–2.5 Hz, often associated with fast runs at 10–15 Hz, as in the Lennox–Gastaut syndrome.
Methods: Extracellular recordings were done in permanently implanted animals during the natural waking–sleep cycle. Single and dual simultaneous recordings from cortical neurons, cortical and thalamic neurons, or cortical neurons and glial cells were performed in cats under ketamine–xylazine anesthesia.
Results: (a) The minimal substrate of SW seizures is the neocortex because such seizures may occur in thalamectomized animals, in which spindles are absent. In intact-brain animals, SW seizures are initiated in neocortex and spread to the thalamus after a few seconds. The majority of thalamocortical (TC) neurons are steadily hyperpolarized throughout the cortical SW seizures. (b) In the Lennox–Gastaut syndrome, the paroxysmal depolarizing shifts (PDSs) associated with the EEG "spike" of SW/PSW complexes contain an important inhibitory component, whereas the hyperpolarization during the EEG "wave" component is not due to γ-aminobutryic acid (GABA)ergic inhibitory postsynaptic potentials (IPSPs) but is ascribed to a mixture of disfacilitation and K⁺ currents. As is also the case with seizures consisting of pure SW complexes, the majority of TC neurons are hyperpolarized during the cortical paroxysms and disinhibited after the cessation of cortical seizures.
Conclusions: Seizures with SW complexes and of the Lennox–Gastaut type preferentially evolve from sleep oscillations. They are initiated in neocortex and spread to the thalamus after a few seconds. The majority of TC neurons are inhibited during these seizures.     

Contribution of intralaminar thalamic nuclei to spike-and-wave-discharges during spontaneous seizures in a genetic rat model of absence epilepsy

In an epileptic rat model of generalized absence epilepsies, the genetic absence epilepsy rats from Strasbourg (GAERS), simultaneous recordings of bilateral epidural electroencephalogram (EEG) of the prefrontal cortex and unit activity of neurons in the intralaminar centrolateral (CL) and paracentral thalamic nucleus (PC) were performed under neurolept-anaesthesia (fentanyl-dehydrobenzperidol analgesia). Spike-and-wave (SW) seizures in these rats are characterized by generalized 7-10 Hz spike-and-wave discharges (SWDs) on the EEG. All neurons recorded in intralaminar thalamic nuclei during spontaneous SWDs showed high-frequency (average 368 Hz, range 200-500 Hz), burst-like activity, which occurred in a highly synchronized fashion with every SWD or with alternating SWD-complexes. Burst discharges in intralaminar neurons were delayed by 13.1 ms (CL) and 12.7 ms (PC), with respect to the spike component of a given SWD on the EEG, whereas burst discharges in the ventrobasal thalamus (VB) and in the rostral nucleus reticularis thalami (rRT) preceded the spike component by 17.8 ms and 8.3 ms, respectively. The onset of SWDs on the EEG was preceded by a tonic firing pattern (20-50 Hz) in about one third of CL and PC neurons. Microiontophoretic application of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline aggravated, whereas, the glutamate receptor antagonists DNQX and APV dampened, SWD-related discharges in PC and CL; the GABAB receptor antagonist CGP 35347 had no measurable effect. These data indicate that intrathalamic nuclei are recruited rhythmically during SWDs, through mechanisms that seem to rely on a delayed glutamatergic excitation modulated by GABAergic influences, rather than a GABA-mediated rebound burst activity typical of relay cells. The finding of a temporal delay of SWD-related activity in intrathalamic, compared with "specific" thalamic relay nuclei, does not support the notion of a leading or pacemaker role in SWD generation. It is, however, rather suggestive of a function of intrathalamic neurons during synchronization and maintenance of neuronal oscillations, and these intrathalamic neurons may be recruited through glutamatergic corticofugal inputs.     

Relations between cortical and thalamic cellular activities during absence seizures in rats

In a rat model of generalized absence epilepsies (Genetic Absence Epilepsy Rats from Strasbourg, GAERS), multiunit activity was recorded simultaneously at different sites of the thalamocortical system under neurolept anaesthesia (fentanyl-droperidol). Under these conditions, bilaterally synchronized spike-and-wave-discharges (SWDs) occurred spontaneously on the electroencephalogram (EEG) that were in principle identical to those reported earlier from unanaesthetized preparations. The generation of SWDs on the EEG was associated with spike-concurrent, rhythmic burst-like activity in (mono-)synaptically connected regions of specific (somatosensory) thalamic regions and layers IV/V of the somatosensory cortex, and the reticular thalamic nucleus. Precursor activity was typically recorded in cortical units, concomitant with ‘embryonic’ SW seizures on the EEG, before the paroxysm was evident on the gross EEG and in the thalamus. On average, SWD-correlated activity in layers IV/V of the somatosensory cortex started significantly earlier than correlated burst-like firing in reticular and in ventrobasal thalamic neurons. Cellular peak firing in thalamus and cortex during bilaterally synchronized SWDs was related to the spike component on the gross EEG with the temporal rank order ventroposteromedial > ventrolateral ≥ ventroposterolateral thalamic > > rostral reticular thalamic nuclei ≥ cortex (layers IV/V) = caudal reticular thalamic nucleus. A spike-related depression and wave-related increase in firing was recorded in anteroventral ventrolateral thalamic areas, presumably reflecting their peculiar anatomical arrangement within the thalamus. These results from an in vivo preparation with intact synaptic connections that spontaneously produces SWDs indicate that SWDs spread within the thalamocortical network, involving short and long delays. The order of concurrent rhythmic firing observed in thalamocortical circuits during SW seizures are supportive of the hypothesis that the processes of rhythmogenesis recruit local thalamic networks, while cortical mechanisms appear to synchronize rhythmic activities on a larger spatiotemporal scale, thereby providing an important contribution to the generalization of epileptiform activity and expression of SWDs on the EEG.     

Coupling between the prelimbic cortex,nucleus reuniens,and hippocampus during NREM sleep remains stable under cognitive and homeostatic demands

The interplay between the medial prefrontal cortex and hippocampus during non-rapid eye movement (NREM) sleep contributes to the consolidation of contextual memories. To assess the role of the thalamic nucleus reuniens (Nre) in this interaction, we investigated the coupling of neuro-oscillatory activities among prelimbic cortex, Nre, and hippocampus across sleep states and their role in the consolidation of contextual memories using multi-site electrophysiological recordings and optogenetic manipulations. We showed that ripples are time-locked to the Up state of cortical slow waves, the transition from UP to DOWN state in thalamic slow waves, the troughs of cortical spindles, and the peaks of thalamic spindles during spontaneous sleep, rebound sleep and sleep following a fear conditioning task. In addition, spiking activity in Nre increased before hippocampal ripples, and the phase-locking of hippocampal ripples and thalamic spindles during NREM sleep was stronger after acquisition of a fear memory. We showed that optogenetic inhibition of Nre neurons reduced phase-locking of ripples to cortical slow waves in the ventral hippocampus whilst their activation altered the preferred phase of ripples to slow waves in ventral and dorsal hippocampi. However, none of these optogenetic manipulations of Nre during sleep after acquisition of fear conditioning did alter sleep-dependent memory consolidation. Collectively, these results showed that Nre is central in modulating hippocampus and cortical rhythms during NREM sleep.     

Basic mechanism for generation of brain rhythms

Study of the basic mechanism of brain rhythms adds to our understanding of the underlying processes of neuronal network within the human brain. Electroencephalography (EEG) records summated extracellular field potentials from large pyramidal neurons in the cerebral cortex. The characteristic rhythmic oscillation of brain rhythms are beststudied by sleep spindles, which are generated within the thalamus through a network of thalamic reticular cells, thalamocortical projection cells and cortical pyramidal cells. Fast rhythms including beta and gammaare present during arousal and focused attention. Besides a reflection of activation from the brainstem reticular activating system, fast rhythms also represent an activated state of the underlying neuronal network. Alpha waves are readily recognized brain waves during relaxed wakefulness; however, the origins of alpha rhythm are not well understood. It is presumed that alpha rhythms are generated by contingent pyramidal cell, and by intracortical connections, spread in the cortical layers. Rhythmic alpha spindles probably represent a de-activated state.     

Firing pattern of neurons in the rostral and ventral part of nucleus reticularis thalami during EEG spindles

The firing pattern of neurons in the rostral and ventral part of nucleus reticularis thalami during cortical EEG spindles was investigated in unanesthetized encéphale isolé cats. Spontaneous spindles as well as those induced by a single thalamic shock were accompanied by an increase in discharge frequency in 97% of the neurons in the rostral pole of the nucleus. In most cases the enhanced firing rate was tonically sustained throughout the duration of the spindles, although phasic bursts at EEG wave frequency were sometimes superimposed on the tonic cellular activation. Suppression of triggered spindles by conditioning fast-frequency stimulation in the mesencephalic reticular formation also abolished the rostral reticularis response. Intracellular recordings revealed a depolarizing shift of small amplitude which was sustained throughout the duration of triggered spindies. The majority of neurons in the ventral part of nucleus reticularis, in contrast, underwent a prolonged hyperpolarizing shift in membrane potential during cortical spindles, sustained for as long as 2 sec and interrupted by depolarizing waves. Both the prolonged membrane hyperpolarization and the depolarizing waves were reduced during the intracellular passage of polarizing currents, suggesting that the former was an inhibitory postsynaptic potential and the latter were disinhibitory potentials. Since neurons in dorsal thalamic nuclei, to which the reticularis axons project, are hyperpolarized concomitantly with cortical spindles, the results are viewed as being in agreement with the hypothesis that, during EEG spindles, neurons in the rostral pole but not in the ventral part of nucleus reticularis exert a tonic inhibitory influence on cells throughout the thalamus.     

Emergence of synchronous EEG spindles from asynchronous MEG spindles

Sleep spindles are bursts of rhythmic 10-15 Hz activity, lasting ～0.5-2 s, that occur during Stage 2 sleep. They are coherent across multiple cortical and thalamic locations in animals, and across scalp EEG sites in humans, suggesting simultaneous generation across the cortical mantle. However, reports of MEG spindles occurring without EEG spindles, and vice versa, are inconsistent with synchronous distributed generation. We objectively determined the frequency of MEG-only, EEG-only, and combined MEG-EEG spindles in high density recordings of natural sleep in humans. About 50% of MEG spindles occur without EEG spindles, but the converse is rare (～15%). Compared to spindles that occur in MEG only, those that occur in both MEG and EEG have ～1% more MEG coherence and ～15% more MEG power, insufficient to account for the ～55% increase in EEG power. However, these combined spindles involve ～66% more MEG channels, especially over frontocentral cortex. Furthermore, when both MEG and EEG are involved in a given spindle, the MEG spindle begins ～150 ms before the EEG spindle and ends ～250 ms after. Our findings suggest that spindles begin in focal cortical locations which are better recorded with MEG gradiometers than referential EEG due to the biophysics of their propagation. For some spindles, only these regions remain active. For other spindles, these locations may recruit other areas over the next 200 ms, until a critical mass is achieved, including especially frontal cortex, resulting in activation of a diffuse and/or multifocal generator that is best recorded by referential EEG derivations due to their larger leadfields.     

Collateral projections of single neurons in the posterior thalamic region to both the temporal cortex and the amygdala: a fluorescent retrograde double-labeling study in the rat

It has been reported that the acoustic thalamus of the rat sends projection fibers to both the temporal cortical areas and the lateral amygdaloid nucleus to mediate conditioned emotional responses to an acoustic stimulus. In the present study, fluorescent retrograde double labeling with Fast Blue and Diamidino Yellow has been used in the rat to examine whether single neurons in the posterior thalamic region send axon collaterals to both the temporal cortical areas and lateral amygdaloid nucleus. One of the tracers was injected into the lateral amygdaloid nucleus and the other into the temporal cortical areas close to the rhinal sulcus. Neurons double-labeled with both tracers were found mainly in the posterior intralaminar nucleus and suprageniculate nucleus, and to a lesser extent in the subparafascicular nucleus and medial division of the medial geniculate nucleus. No double-labeled neurons were seen in either the dorsal or ventral division of the medial geniculate nucleus. When one of the tracers was injected into the lateral amygdaloid nucleus and the other into either the dorsal portion of the temporal cortex, the dorsal portion of the entorhinal cortex, or the posterior agranular insular cortex, no double-labeled neurons were found in the posterior thalamic region. The present results indicate that a substantial number of single neurons in the acoustic thalamus project to both the limbic cortical areas and lateral amygdaloid nucleus by way of axon collaterals. These neurons may be implicated in affective and autonomic components of responses to multi-sensory stimuli, including acoustic ones. J. Comp. Neurol. 384:59-70, 1997. © 1997 Wiley-Liss, Inc.     

Thalamic afferents of the rat infralimbic and lateral agranular cortices

The infralimbic cortex is a visceromotor area of the cortex. To define the thalamic afferents of this area, contrast them with those of the lateral agranular cortex, a somatic motor region, and assess the degree to which the thalamus might coordinate the activity of these cortical areas through axon collaterals, we conducted a retrograde fluorescent double labeling study using bisbenzimide and Fast Blue. Injections into infralimbic cortex resulted in labeling in the mediodorsal, intralaminar, and midline nuclei. Injections into lateral agranular cortex resulted in labeling in the ventrolateral, ventrobasal, ventromedial, and intralaminar nuclei. There was almost no overlap in the thalamic labeling following injections into these two cortical areas. The pattern of labeling following infralimbic injections is discussed in terms of the possible function of the midline thalamic nuclei as a relay for visceral sensory information. The labeling in mediodorsal nucleus following infralimbic cortex argues for including this area in the definition of rodent prefrontal cortex. In addition, the results suggest that the role of the thalamus in coordinating the activity of these cortical areas is minimal.     

Neural damage in the rat thalamus after cortical infarcts.

Histopathologic changes in the thalamus of 23 rats after somatosensory cortical infarction produced by middle cerebral artery occlusion were examined using the Fink-Heimer silver staining method, immunohistochemistry with antibodies against glial fibrillary acidic protein and laminin, and conventional stains. Middle cerebral artery occlusion produced cortical infarcts in the lateral parietal region, with variable involvement of the frontoparietal parasagittal sensorimotor cortex. Within 3 days after occlusion, massive terminal degeneration but no neuronal changes were apparent in the ipsilateral thalamus. By 1 week after occlusion, abnormal neurons with darkly stained, shrunken nuclei and atrophic perikarya were present in the ipsilateral thalamic nuclei. These neurons were densely argyrophilic in Fink-Heimer sections. Rats with small lateral parietal cortical lesions had degenerating neurons limited to the medial ventroposteromedial nucleus. Large lesions involving the parasagittal sensorimotor cortex resulted in widespread neuronal damage in the ventroposteromedial, ventroposterolateral, intralaminar, and posterior nuclear regions but nowhere else. Immunoreactivity to laminin antibody decreased, and astrocytic proliferation was abundant in affected thalamic areas. These findings are consistent with retrograde neuronal degeneration due to thalamocortical fiber damage in ischemic cortical regions. Such lesions remote from the infarct may influence functional recovery in patients with stroke.     

Thalamic projections to the anterior suprasylvian and posterior sigmoid cortex: An HRP study of the “vestibular areas” of the cerebral cortex in the cat

We have confirmed electrophysiologically the existence of an oligosynaptic vestibular projection to the cortex surrounding the rostral end of the anterior suprasylvian sulcus (ASsS). However, we failed to confirm a similar projection to area 3a in the posterior sigmoid gyros. We studied the thalamic projections to each of these cortical regions by injecting small amounts of HRP in the cortex and looking for neurons retrogradely labeled throughout the thalamus. The exact location of the cortical injections was assessed cytoarchitectonically. The heaviest neuronal labeling after injections in the banks of ASsS was obtained in Po (including in this complex GMmc). A moderate number of projections was found from VPi. VPm and VP1 (the labeling in the latter being particularly prominent in a case injected in the lower bank of ASsS), and also from VL. Occasional labeled neurons were found in the rostro-ventral part of LP. After injections in area 3a in the posterior sigmoid gyrus, which affected to a minor degree either area 3b or 4, many labeled cells appeared in the rostral and dorsal part of VP1, and in the central and lateral parts of VL. Fewer labeled cells were found in VPi, Po and LP. In most cases some occasional labeled cell was observed also in the intralaminar nuclei and in Vm.     

Thalamic projections to areas 3a, 3b,and 4 in the sensorimotor cortex of the mature and infant macaque monkey

Area 3a in the macaque monkey, located in the fundus of the central sulcus, separates motor and somatosensory cortical areas 4 and 3b. The known connections of areas 4 and 3b differ substantially, as does the information which they receive, process, and transfer to other parts of the central nervous system. In this analysis the thalamic projections to each of these three cortical fields were examined and compared by using retrogradely transported fluorescent dyes (Fast Blue, Diamidino Yellow, Rhodamine and Green latex microspheres) as neuron labels. Coincident labeling of projections to 2–3 cortical sites in each monkey allowed the direct comparison of the soma distributions within the thalamic space of the different neuron populations projecting to areas 3a, 3b, and 4, as well as to boundary zones between these cortical fields. The soma distribution ofthalamic neurons projecting to a small circumscribed zone (diameter = 0.5–1.0 mm) strictly within cortical area 3a (in region of hand representation) filled out a “territory” traversing the dorsal half of the cytoarchitectonically defined thalamic nucleus, VPLc (abbreviations as in Olszewski [1952] The Thalamus of the Macaca mulatta. Basel: Karger). This elongate, rather cylindrical, territory extended caudally into the anterior pulvinar nucleus, but not forward into VPLo. The rostrocaudal extent of the thalamic territory defining the soma distribution of neurons projecting to small zones of cortical area 3b was similar, but typically extended into the ventral part of VPLc, filling out a medially concavo-convex laminar space. Two such territories projecting to adjacent zones of areas 3a and 3b, respectively, overlapped and shared thalamic space, but not thalamic neurons. Contrasting with the 3a and 3b thalamic territories, the soma distribution of thalamic neurons projecting to a circumscribed zone in the nearby motor cortex (area 4) did not penetrate into VPLc, but instead filled out a mediolaterally flattened territory extending from rostral VLo, VLm, VPLo to caudal and dorsal VLc, LP, and Pulo. These territories skirted around VPLc. All three cortical areas (4, 3a, and 3b) also received input from distinctive clusters of cells in the intralaminar Cn.Md. It is inferred that, in combination, the thalamic territories in areas 3a, 3b, and 4 (and also area 1 and 2), which would be coactive during the execution of a manual task, constituted a lamellar space extending from VLo rostrally to Pul.o caudally. How Pul.o neuron populations relate to the more rostral populations within the same thalamic territory projecting to a localized cortical zone remains uncertain. Within the medially located territories the distribution of the neuron population in Pul.o was spatially continuous with the more rostral thalamic cells projecting to the same localized cortex, but in lateral thalamic territories these 2 populations were usually spatially discontinous. In the newborn macaque an orderly change in the territorial projections to localized zones in area 4, 3a, and 3b was also demonstable. However, thalamic nuclear projections were more expansive than in the mature animal. As well as the VPLc input, a third of the thalamic input to area 3a was now from VLo, VPLo, and VLm. Area 4 also had a significant input from VPLc, an input not observed in the mature macaque. © 1993 Wiley-Liss, Inc.     

Participation of corticothalamic cells in penicillin-induced generalized spike and wave discharges

Single unit extracellular recordings were performed in the cortex of awake painlessly immobilized unanesthetized cats during generalized spike and wave discharges (SW) induced by i.m. penicillin. Corticothalamic cells were identified in cortical areas 3a and 4γ by stimulating n. ventralis lateralis (VL) and in cortical areas 5 and 7 by stimulating n. lateralis posterior (LP). Twelve of 24 neurons antidromically invaded from VL were also pyramidal tract cells. Two of 11 neurons antidromically invaded from LP also displayed orthodromic responses. Corticothalamic cells fired bursts of action potentials in association with the ‘spike’ whereas a period of inhibition was associated with the ‘wave’ of the SW complex. The data suggest that in this experimental model the appearance of SW in the thalamus is due to secondary activation of thalamic neurons by volleys arising from the cortex and mediated through corticothalamic connections.     

Dynamic neuronal responses in cortical and thalamic areas during different phases of formalin test in rats

Although formalin-induced activity in primary afferent fibers and spinal dorsal horn is well described, the forebrain neural basis underlying each phase of behavior in formalin test has not yet been clarified. The present study was designed to investigate the cortical and thalamic neuronal responses and interactions among forebrain areas during different phases after subcutaneous injection of formalin. Formalin-induced neuronal activities were simultaneously recorded from primary somatosensory cortex (SI), anterior cingulate cortex (ACC) and medial dorsal (MD) and ventral posterior (VP) thalamus during different phases (i.e., first phase, interphase, second phase and third recovery phase starting from 70 min after injection) of formalin test, using a multi-channel, single-unit recording technique. Our results showed that, (i) unlike the responses in primary afferent fibers and spinal dorsal horn, many forebrain neurons displayed monophasic excitatory responses in the first hour after formalin injection, except a small portion of neurons which exhibited biphasic responses; (ii) the response patterns of many cortical and thalamic neurons changed from excitatory to inhibitory at the end of the second phase; (iii) the direction of information flow also changed dramatically, i.e., from cortex to thalamus and from the medial to the lateral pathway in the first hour, but reversed in phase 3. These results indicate that the changes of activity pattern in forebrain networks may underlie the emerging and subsiding of central sensitization-induced pain behavior in the second phase of formalin test.     

The functional connectivity of intralaminar thalamic nuclei in the human basal ganglia

Projections of the centromedian‐parafasicularis neurons of the intralaminar thalamus are major inputs of the striatum. Their functional role in the activity of human basal ganglia (BG) is not well known. The aim of this work was to study the functional connectivity of intralaminar thalamic nuclei with other BG by using the correlations of the BOLD signal recorded during “resting” and a motor task. Intralaminar nuclei showed a marked functional connectivity with all the tested BG, which was observed during “resting” and did not change with the motor task. As regards the intralaminar nuclei, BG connectivity was much lower for the medial dorsal nucleus (a thalamic nucleus bordering the intralaminar nuclei) and for the default mode network (although intralaminar nuclei showed a negative correlation with the default mode network). After the “regression” of intralaminar nuclei activity (partial correlation), the functional connectivity of the caudate and putamen nuclei with other BG decreased (but not with the primary sensorimotor cortex). Present data provide evidence that intralaminar nuclei are not only critical for striatal activity but also for the global performance of human BG, an action involving subcortical BG loops more than cortico‐subcortical loops. The high correlation found between BG suggest that, similarly to that reported in other brain centers, the very‐slow frequency fluctuations are relevant for the functional activity of these centers. Hum Brain Mapp 36:1335–1347, 2015. © 2014 Wiley Periodicals, Inc .     

Thalamic and cortical spindles during early ontogenesis in kittens

On birth, focal thalamic recordings show sporadic sequences of spindle waves whereas EEG cortical recordings show no trace of spindles. Thalamic spindles are occasionally transferred to the cortex beginning with the 3rd–4th day. On the 8th–9th day, clear-cut spindle sequences, with the same patterns as in the adult animal, appear simultaneously in the thalamus and cortex.