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Brainstem stimulation during sleep evokes abnormal rhythmic activity in thalamic neurons in feline penicillin epilepsy.

Some periods in the sleep-waking cycle are more seizure prone than others. In absence epilepsy, transition periods between nonrapid-eye-movement (nonREM) sleep and waking or REM sleep can be more seizure prone that stable states. One feature of transition periods that is hypothesized to promote seizure activity is the presence of coincident activity in ascending brainstem reticular formation (RF) arousal systems with synchronized thalamo-cortical activity. To evaluate this hypothesis we examined the state-dependent effects of low intensity RF stimulation on thalamic single unit activity in control conditions and following systemic penicillin-G administration to adult cats. In control conditions, RF stimulation during waking and REM sleep typically evoked a short-latency action potential in thalamic neurons. The same stimulation during nonREM sleep commonly evoked a high frequency burst of action potentials followed by a period of suppressed discharge. In 16/26 neurons, a second rebound burst of action potentials followed the period of discharge suppression. The average interval between the initial and rebound bursts was 75.1 +/- 6.0 ms, which was similar to the interburst interval recorded in these same cells during spontaneous EEG spindles. Following administration of penicillin-G, RF stimulation during nonREM sleep evoked high frequency burst firing, followed by 1-2 rebound bursts in 21/22 thalamic neurons. The average evoked interburst interval was 152.5 +/- 7.3 ms, a value comparable to the interburst interval displayed by these same cells during spontaneous spike-wave seizure activity (157.8 +/- 8.7 ms). RF-evoked rhythmic discharges were dependent upon the presence of thalamocortical synchronization, as responses evoked during waking and REM sleep in penicillin treated cats were similar to those observed in control conditions.

Animals↗

The neurophysiology of concussion.

Cerebral concussion is both the most common and most puzzling type of traumatic brain injury (TBI). It is normally produced by acceleration (or deceleration) of the head and is characterized by a sudden brief impairment of consciousness, paralysis of reflex activity and loss of memory. It has long been acknowledged that one of the most worthwhile techniques for studying the acute pathophysiology of concussion is by the recording of neurophysiological activity such as the electroencephalogram (EEG) and sensory evoked potentials (EPs) from experimental animals. In the first parts of this review, the majority of such studies conducted during the past half century are critically reviewed. When potential methodological flaws and limitations such as anesthetic protocols, infliction of multiple blows and delay in onset of recordings were taken into account, two general principles could be adduced. First, the immediate post-concussive EEG was excitatory or epileptiform in nature. Second, the cortical EP waveform was totally lost during this period. In the second parts of this review, five theories of concussion which have been prominent during the past century are summarized and supportive evidence assessed. These are the vascular, reticular, centripetal, pontine cholinergic and convulsive hypotheses. It is concluded that only the convulsive theory is readily compatible with the neurophysiological data and can provide a totally viable explanation for concussion. The chief tenet of the convulsive theory is that since the symptoms of concussion bear a strong resemblance to those of a generalized epileptic seizure, then it is a reasonable assumption that similar pathobiological processes underlie them both. Further, it is demonstrated that EPs and EEGs recorded acutely following concussive trauma are indeed the same or similar to those obtained following the induction of a state of generalized seizure activity (GSA). According to the present incarnation of the convulsive theory, the energy imparted to the brain by the sudden mechanical loading of the head may generate turbulent rotatory and other movements of the cerebral hemispheres and so increase the chances of a tissue-deforming collision or impact between the cortex and the boney walls of the skull. In this conception, loss of consciousness is not orchestrated by disruption or interference with the function of the brainstem reticular activating system. Rather, it is due to functional deafferentation of the cortex as a consequence of diffuse mechanically-induced depolarization and synchronized discharge of cortical neurons. A convulsive theory can also explain traumatic amnesia, autonomic disturbances and the miscellaneous collection of symptoms of the post-concussion syndrome more adequately than any of its rivals. In addition, the symptoms of minor concussion (a.k.a. being stunned, dinged, or dazed) are often strikingly similar to minor epilepsy such as petit mal. The relevance of the convulsive theory to a number of associated problems is also discussed. These include the relationship between concussion and more serious types of closed head injury, the utility of animal models of severe brain trauma, the etiology of the cognitive deficits which may linger long after a concussive injury, the use of concussive (captive bolt) techniques to stun farm animals prior to slaughter and the question of why some animals (such as the woodpecker) can tolerate massive accelerative forces without being knocked out.

Animals↗

Multiple-unit recordings during slow field-potential shifts in low-[Ca2+]0 solutions in rat hippocampal and cortical slices.

Multiple-unit and field-potential recordings in low-[Ca2+]0 solutions were used to study epileptiform bursts generated in hippocampal region CA1 and medial entorhinal cortex, a cortical region that is not as densely packed or highly laminated as the hippocampus. As expected in CA1, multiple-unit activity appeared as large spikes that corresponded one-to-one with population spikes in the field-potential recordings. During the negative field-potential shifts that lacked large population spikes, the multiple-unit recordings showed an increase in baseline activity. Initiation of the negative field-potential shift always coincided with increased multiple-unit activity. Slices displaying a post-burst positive overshoot showed a corresponding decrease in multiple-unit activity. In addition to the large ictal-like events in CA1, small-amplitude field-potential shifts were also observed, these events were associated with increases in baseline spike activity in the multiple-unit recording. These small-amplitude field-potential shifts appeared to precede the occurrence of the ictal-like events, but they decreased in frequency during low-[Ca2+]0 exposure. Recordings in normal artificial cerebrospinal fluid (nominally 1.3 mM [Ca2+]0) showed rhythmic, multiple-unit bursts of action potentials and corresponding negative small-amplitude field-potential shifts in the medial entorhinal cortex of immature rats (two-to three-weeks old), but not of adult rats. Rhythmic, spontaneous bursts of activity in low-[Ca2+]0 solution were found in both immature and adult medial entorhinal cortex, and were similar in amplitude to the small field-potential events generated in CA1. The probability of burst generation was higher in the immature than the adult medial entorhinal cortex, and the bursts in the immature cortex had more robust multiple-unit activity and an increased burst frequency compared with adult. These results indicate that the medial entorhinal cortex can also generate spontaneous synchronous bursts of activity in low-[Ca2+]0 solutions, and they suggest that the increased susceptibility of medial entorhinal cortex from immature versus adult rats to generate intense bursts of electrical activity does not require active chemical synaptic transmission. The various forms of epileptiform activity in low-[Ca2+]0 solutions probably arise from different contributions of electrical and ionic mechanisms of synchronization in these neuronal populations. The data suggest the hypothesis that ionic mechanisms (i.e. changes in [K+]0) may synchronize neurons in cortical regions (e.g. entorhinal cortex) that are not as densely packed and highly laminated as the hippocampus and dentate gyrus. The data also support the hypothesis that these mechanisms contribute significantly to the increased seizure susceptibility of the immature brain.

Animals↗

Precisely correlated firing in cells of the lateral geniculate nucleus.

Simple cells within layer IV of the cat primary visual cortex are selective for lines of a specific orientation. It has been proposed that their receptive-field properties are established by the pattern of connections that they receive from the lateral geniculate nucleus (LGN) of the thalamus. Thalamic inputs, however, represent only a small proportion of the synapses made onto simple cells, and others have argued that corticocortical connections are likely to be important in shaping simple-cell response properties. Here we describe a mechanism that might be involved in selectively strengthening the effect of thalamic inputs. We show that neighbouring geniculate neurons with overlapping receptive fields of the same type (on-centre or off-centre) often fire spikes that are synchronized to within 1 millisecond. Moreover, these neurons often project to a common cortical target neuron where synchronous spikes are more effective in evoking a postsynaptic response. We propose that precisely correlated firing within a group of geniculate neurons could serve to reinforce the thalamic input to cortical simple cells.

Action Potentials↗

Representation of a species-specific vocalization in the primary auditory cortex of the common marmoset: temporal and spectral characteristics.

1. The temporal and spectral characteristics of neural representations of a behaviorally important species-specific vocalization were studied in neuronal populations of the primary auditory cortex (A1) of barbiturate-anesthetized adult common marmosets (Callithrix jacchus), using both natural and synthetic vocalizations. The natural vocalizations used in electrophysiological experiments were recorded from the animals under study or from their conspecifics. These calls were frequently produced in vocal exchanges between members of our marmoset colony and are part of the well-defined and highly stereotyped vocal repertoire of this species. 2. The spectrotemporal discharge pattern of spatially distributed neuron populations in cortical field A1 was found to be correlated with the spectrotemporal acoustic pattern of a complex natural vocalization. However, the A1 discharge pattern was not a faithful replication of the acoustic parameters of a vocalization stimulus, but had been transformed into a more abstract representation than that in the auditory periphery. 3. Subpopulations of A1 neurons were found to respond selectively to natural vocalizations as compared with synthetic variations that had the same spectral but different temporal characteristics. A subpopulation responding selectively to a given monkey's call shared some but not all of its neuronal memberships with other individual-call-specific neuronal subpopulations. 4. In the time domain, responses of individual A1 units were phase-locked to the envelope of a portion of a complex vocalization, which was centered around a unit's characteristic frequency (CF). As a whole, discharges of A1 neuronal populations were phase-locked to discrete stimulus events but not to their rapidly changing spectral contents. The consequence was a reduction in temporal complexity and an increase in cross-population response synchronization. 5. In the frequency domain, major features of the stimulus spectrum were reflected in rate-CF profiles. The spectral features of a natural call were equally or more strongly represented by a subpopulation of A1 neurons that responded selectively to that call as compared with the entire responding A1 population. 6. Neuronal responses to a complex call were distributed very widely across cortical field A1. At the same time, the responses evoked by a vocalization scattered in discrete cortical patches were strongly synchronized to stimulus events and to each other. As a result, at any given time during the course of a vocalization, a coherent representation of the integrated spectrotemporal characteristics of a particular vocalization was present in a specific neuronal population. 7. These results suggest that the representation of behaviorally important and spectrotemporally complex species-specific vocalizations in A1 is 1) temporally integrated and 2) spectrally distributed in nature, and that the representation is carried by spatially dispersed and synchronized cortical cell assemblies that correspond to each individual's vocalizations in a specific and abstracted way.

Acoustic Stimulation↗

Chemical sympathectomy-induced changes in TH-, VIP-, and CGRP-immunoreactive fibers in the rat mandible periosteum: influence on bone resorption.

The expression of neurotransmitter receptors by bone cells supports the concept that the nervous system is a regulator of bone metabolism. The discrimination of the respective roles of the sensory and sympathetic nervous systems requires evidence of topographic relationships between the corresponding fibers and the cells involved in bone turnover, in vivo. In this study, the influence of the sympathetic system on bone resorption was assessed by using a synchronized model of cortical resorption along the mandible. The sympathetic system was destroyed by daily injections of guanethidine (40 mg/kg) for 25 days; a resorption wave was induced on day 21. The distribution of periosteal tyrosine-hydroxylase (TH)-, vasoactive intestinal polypeptide (VIP)-, and calcitonin gene-related peptide (CGRP)-immunoreactive (IR) fibers was studied by compartmentalizing the periosteum. Most fibers were located in the distal, non-osteogenic compartment. TH-IR fibers were located perivascularly, VIP-IR fibers were gathered at the boundary with the osteogenic compartment, and CGRP-IR fibers were scattered. Sympathectomy decreased the number of TH- and VIP-IR fibers and increased the number of CGRP-IR fibers, without changing their topography. After the injection of Fast blue, a retrograde fluorescent marker, over the periosteum, fluorescent neuronal cell bodies were found in the superior cervical ganglion (SCG). Many neurons were TH-IR and very few were VIP-IR. Sympathectomy decreased the numbers of fluorescent and TH-IR cell bodies. It also decreased the number of preosteoclasts and osteoclasts, which had a drastic effect on the cortical bone surface, as assessed by scanning electron microscopy. These data indicate that VIP-IR fibers have a strategic position close to the most peripheral and less differentiated, osteogenic cells, pointing to a functional relationship. As poorly differentiated osteogenic cells support preosteoclast differentiation, VIP-IR fibers may be involved in this process, as suggested by the smaller number of preosteoclasts in sympathectomized rats. Although VIP is predominantly a parasympathetic mediator, it seemed to be conveyed by sympathetic fibers, as shown by the marked effect of guanethidine treatment. Nevertheless, these fibers did not originate from the SCG, contrary to TH-IR fibers.

Adrenergic Fibers↗

Thalamocaudate projection neurons with a branching axon to the cerebral motor cortex.

Sixty-nine thalamocaudate projection neurons in ventroanterior (VA: 32 cells), centrolateral (CL: 12 cells) and centrum medianum or parafascicular (CM-Pf: 25 cells) nuclei of the cat were identified by antidromic response to stimulation of the caudate nucleus (CD). Twenty-two VA and 3 CL neurons in this sample were proved to have a branching axon projecting on both CD and the cerebral motor cortex (Mcx). Most of the branching VA neurons showed repetitive discharges synchronous with the cortical recruiting response elicited by repetitive stimulation (6-10/sec) of the pallidum. Such activities of the VA neuron which would induce the motor cortical recruiting response, were proved to be conveyed to CD.

Animals↗

Expression of intrinsic bursting properties in neurons of maturing sensorimotor cortex.

Intrinsically bursting (IB) neurons, responding with a burst of action potentials to just threshold intracellular depolarizing current pulses, are encountered in layer V of mature rodent sensorimotor cortex. We report the results of intracellular recordings performed on neocortical slices obtained from immature rats between postnatal day (P) 7 and P21, as compared to adult animals (above P60). The bursting properties are here reported to mature abruptly around P14. After this time a subpopulation of IB neurons was recognizable on the basis of both physiological and morphological characteristics (i.e. extensive apical and basal dendrites arborization, axon collaterals limited to layers V-VI). Maturational changes in number and distribution of Ca2+/K+ channels may account for this developmental step. The immaturity of IB neurons may be correlated with the poorly synchronized character of cortical activities in the very young animals.

Action Potentials↗

gamma-Hydroxybutyric acid induced spike and wave discharges in rats: relation to high-affinity [3H]gamma-hydroxybutyric acid binding sites in the thalamus and cortex.

gamma-Hydroxybutyric acid is a naturally occurring compound which induces bilaterally synchronous spike and wave discharges in rats. The gamma-hydroxybutyric acid model of absence seizures simulates clinical absence seizures behaviorally as well as electrographically. The present study was undertaken in order to establish the role of the high-affinity gamma-hydroxybutyric acid binding sites in the generation of gamma-hydroxybutyric acid-induced spike and wave discharges. Spike and wave discharges induced by gamma-hydroxybutyric acid were recorded with the aid of bipolar depth electrodes implanted in discrete regions of thalamus, cortex and hippocampus. In the present study we found that ventroposterolateral, ventroposteromedial, medial and the reticular nuclei of the thalamus discharged synchronously with the cortical generation of spike and wave discharges. In the cortex, the superficial layers (I-IV) of frontoparietal cortex generated spike and wave discharges, whereas no spike and wave discharges were recorded from deeper layers (V-VI) of frontoparietal cortex. At the onset of spike and wave discharges induced by gamma-hydroxybutyric acid, a rapid but reversible upregulation of gamma-hydroxybutyric acid binding sites was observed. This increased [3H]gamma-hydroxybutyric acid binding was characterized by an increase in the number of gamma-hydroxybutyric acid sites with no significant change in their affinity for gamma-hydroxybutyric acid. Moreover, the change in [3H]gamma-hydroxybutyric acid binding was observed only in those thalamic structures and cortical layers which were found to be involved in the generation of spike and wave discharges induced by gamma-hydroxybutyric acid. The CA3 field or dorsal hippocampus possesses the highest density of [3H]gamma-hydroxybutyric acid binding sites of all brain regions. However, no significant change in [3H]gamma-hydroxybutyric acid binding was observed in this region nor was the CA3 field involved in the generation of spike and wave discharges during gamma-hydroxybutyric acid-induced absence-like seizures. These findings confirm that gamma-hydroxybutyric acid-induced absence-like seizures originate from thalamocortical pathways and that the onset of gamma-hydroxybutyric acid-induced spike and wave discharges is directly related to the regulation of gamma-hydroxybutyric acid binding sites in those regions which constitute the involved thalamocortical loop.

Animals↗

Motor and electrocorticographic epileptic activity induced by 3-mercaptopropionic acid in immature rats.

The convulsant action of 3-mercaptopropionic acid (3-MPA), a known inhibitor of glutamate decarboxylase activity, was studied in 7-, 12-, 18- and 25-day-old rats and in adult animals. 3-MPA elicited predominantly clonic, minimal seizures as well as generalized tonic-clonic (major) seizures at all developmental stages studied. The CD50 for major seizures did not change during development; CD50 for minimal seizures was significantly lower in 18-day-old rats than in older animals. Latency to the onset of seizures was shortest in 18-day-old rats and extremely long in 12- and, especially, in 7-day-old rats. This long latency might signify either changing molecular properties of glutamate decarboxylase during development or slow turnover of GABA at early postnatal stages. Electrocorticographic recordings demonstrated sharp EEG components in the frontal region as a first sign of 3-MPA action, and seizure patterns exhibited similar developmental changes as found with other seizure models (a decrease in duration of individual graphoelements and an increase in synchronization among various cortical regions). This indicates the primary importance of brain maturation in the expression of epileptic EEG phenomena. The correlation between EEG and motor phenomena was poor in the youngest animals and it ameliorated with age, but it never became perfectly coincidental.

3-Mercaptopropionic Acid↗

Increased neocortical spiking and surgical outcome after selective amygdalo-hippocampectomy.

We studied the electrocorticogram (ECoG) before and immediately after transcortical selective amygdalo-hippocampectomy, prospectively in 13 consecutive patients and retrospectively in three others. ECoG was performed with surface and two depth electrodes inserted through T2 aimed at the amygdala and anterior hippocampus. Before resection the ECoG showed a variable amount of interictal spiking, recorded either independently from the depth and surface, or synchronously. A small cortical incision (2-3 cm) was made in T2. The hippocampus, amygdala and parahippocampal gyrus were removed subpially. After the resection, increased epileptiform abnormality was observed in all 16 patients and a different ECoG pattern emerged. It consisted of repetitive, high amplitude spikes and polyspikes, separated by attenuated background, recorded from the most anterior temporal area. Similar observations were reported by Niemeyer in 1958. The outcome was comparable to that of standard anterior temporal resection: 62.5% class I and 25% class II (Engel's scale). ECoG is often used to tailor the amount of resection, and the persistence of epileptic abnormalities correlates with worse outcome. This is not the case in selective amygdalo-hippocampectomy, suggesting that a different underlying mechanism is responsible for the increased interictal spiking following this procedure.

Adolescent↗

Mast cell activation and degranulation occur early during induction of periosteal bone resorption.

We have previously postulated that mast cells participate in the cellular network involved in osteoclastic resorption, probably through histamine release. In this study, we examined mast cell activation and histamine release during origination of resorption. Groups of 10 rats were killed 0, 0.5, 1, 1.5, 3, 6, 9, 12 and 18 h after induction of resorption in a synchronized model of cortical resorption along the mandible. The total number of mast cells was transiently decreased by about one-third at 1 and 9 h. Mast cell activation was monitored by Alcian blue-safranin staining. Early after induction, mast cells started to release their mediator stores; complete release led to the apparent disappearance of the cells with the staining technique used. Histamine immunostaining confirmed the release of histamine and its diffusion in the extracellular environment. Massive degranulation was observed at 1.5 and 9 h with toluidine blue staining. Cell recovery, assessed in terms of histidine decarboxylase expression, occurred gradually. The number of ED1+ osteoclast precursors strongly increased from 12 h up to 18 h. Most parameters had returned to baseline at 18 h, except the ED1+ cells. H2 receptor inhibition with famotidine strongly decreased ED1+ osteoclast precursors at 12 h and subsequently osteoclasts at the peak of resorption. These data support a role of mast cells in resorption origination. They show an early and transient intervention of mast cells in the events regulating the recruitment of circulating osteoclast precursors and ultimately of resorption. Mast cell activation and degranulation induce the release of mediators, particularly histamine acting through its H2 receptors, which are likely involved in these reactions.

Animals↗

Changes in cerebral and autonomic activity heralding periodic limb movements in sleep.

BACKGROUND AND PURPOSE: Periodic limb movement disorder (PLMD) is frequently accompanied by awakenings or signs of EEG arousal. However, it is matter of debate whether EEG arousals trigger leg movements or both EEG arousal and leg movements are separate expressions of a common pathophysiological mechanism. Previous studies showed that cardiac and cerebral changes occur in association with periodic limb movements (PLMs), and that a combining increase in delta activity and in heart rate (HR) occurs before the onset of PLMs. PATIENTS AND METHODS: This paper presents some preliminary data, obtained from a sample of 5 subjects with PLMD not associated to restless legs syndrome. To describe the temporal pattern of cardiac and EEG activities changes concomitant with PLMs in NREM sleep we used time frequency analysis technique. RESULTS: PLM onset is heralded by a significant activation of HR and delta activity power, beginning 4.25 and 3 s respectively before PLMs onset, with PLMs onset and arousal onset falling together. DISCUSSION: Delta and HR variations herald PLMs and activation of fast EEG frequencies. Such a stereotyped pattern is common in PLMs and in spontaneous or stimuli-induced arousals. Moreover a similar pattern seems to encompass the CAP phenomenon. The whole of these phenomena can be linked to the activity of a common brainstem system, which receives peripheral inputs, regulating the vascular, cardiac and respiratory activities and synchronizing them to cortical oscillations of EEG.

Adult↗

[Event-related desynchronization and synchronization. Reactivity of electrocortical rhythms in relation to the planning and execution of voluntary movement].

Cortical electroencephalographic rhythms reactivity may be quantified using event-related desynchronization (ERD) and synchronization (ERS) methods. We therefore studied cortical activation occurring during programming and performance of voluntary movement in healthy subjects. EEG power evolution within the reactive frequency bands (mu and beta central rhythms) was averaged before, during and after a minimum of 50 self-paced flexions of the thumb. Recordings in 18 normal adults showed that ERD (decrease in power) of mu rhythm started 2,000 ms before movement onset, while ERD of beta rhythm started 1,500 ms before movement onset. Early ERD of mu and beta rhythms were located over the contralateral central region covering primary motor cortex. They were followed by bilateral ERD occurring over ipsilateral and contralateral central regions during performance of the movement. At the end of the movement, an ERS (increase in power) of beta rhythm occurred. These results suggest that programming of voluntary movement induces early activation in contralateral sensorimotor areas, while performance of the movement induces bilateral activation in sensorimotor areas. ERS of beta rhythm occurring at the end of the movement could correspond to inactivation of motor areas activated by movement. Based on EEG activity, ERD and ERS prove to be useful methods to analyze cortical activation during programming and performance of voluntary movements with good spatial and temporal resolution.

Adult↗

Benzo- and pyrido-1,4-oxazepin-5-ones and -thiones: synthesis and structure-activity relationships of a new series of H1 antihistamines.

A series of novel benzo- and pyrido-1,4-oxazepinones and -thiones which represents a new structural class of compounds possessing H1 antihistaminic activity was synthesized, and the SARs were evaluated. The antihistaminic activity was determined by blockade of histamine-induced lethality in guinea pigs. The sedative potential was determined by comparison of the EEG profiles of the compounds with those of known sedating and nonsedating antihistamines. Several of the compounds were shown to possess potent H1 antihistaminic activity and to be free of the cortical slowing with synchronized waves and spindling activity found in the EEG of sedative antihistamines. One compound, 2-[2-(dimethylamino)ethyl]-3,4-dihydro-4-methylpyrido[3,2-f]-1,4- oxazepine-5(2H)-thione (rocastine) is currently undergoing clinical evaluation as a nonsedating H1 antihistamine.

Animals↗

Simulated electrocortical activity at microscopic, mesoscopic, and global scales.

Simulation of electrocortical activity requires (a) determination of the most crucial features to be modelled, (b) specification of state equations with parameters that can be determined against independent measurements, and (c) explanation of electrical events in the brain at several scales. We report our attempts to address these problems, and show that mutually consistent explanations, and simulation of experimental data can be achieved for cortical gamma activity, synchronous oscillation, and the main features of the EEG power spectrum including the cerebral rhythms and evoked potentials. These simulations include consideration of dendritic and synaptic dynamics, AMPA, NMDA, and GABA receptors, and intracortical and cortical/subcortical interactions. We speculate on the way in which Hebbian learning and intrinsic reinforcement processes might complement the brain dynamics thus explained, to produce elementary cognitive operations.

Animals↗

The functional significance of K-complexes.

This paper summarizes the present knowledge about the cellular bases of the sleep K-complex (KC). The KC has two phases: the initial surface-positive wave is due to the synchronous excitation of cortical neurones, while the subsequent surface-negative wave represents neuronal hyperpolarization. These variations of membrane potential occur within a slow (<1 Hz) oscillation that characterizes all sleep stages. Therefore, KCs are periodic, and their shape and frequency are modulated by the increasing degree of deafferentation attained by the corticothalamic network with the deepening of the sleep. Within this network, the rhythmic KCs recurring at the frequency of the slow oscillation play a leading role by triggering and grouping other sleep oscillations, such as spindles (7-14 Hz) and delta (1-4 Hz). The KC is mainly a spontaneous event generated in cortical networks. During nocturnal epileptic seizures, the KCs are precursors of paroxysmal spike-wave complexes.

Brain↗

Utilizing latency for object recognition in real and artificial neural networks.

A consistent analysis of a visual scene requires the recognition of different objects. In vertebrate brains this could be achieved by synchronization of the activity of disjunct nerve cell assemblies. During such a process cross-talk between spatially adjacent image parts occurs, preventing efficient synchronization. Temporal differences, naturally introduced by stimulus latencies in every sensory system, were utilized in this study to counteract this effect and strongly improve network performance. To this end in our model the image is 'spread out' in time as a function of contrast-dependent visual latencies, and synchronization of cell assemblies occurs without mutual disturbance. The network model requires a direct link between visual latencies and the onset of synchronous oscillations in cortical cells. This was confirmed experimentally.

Cognition↗