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PubMed2002

Bridging rate coding and temporal spike coding by effect of noise.

It is controversial whether temporal spike coding or rate coding is dominant in the information processing of the brain. We show by a two-layered neural network model with noise that, when noise is small, cortical neurons fire synchronously and intervals of synchronous firing robustly encode the signal information, but that the neurons desynchronize with moderately strong noise to encode waveforms of the signal more accurately. Further increase of noise just deteriorates the encoding. A positive role of noise in the brain is suggested in a meaning different from stochastic resonance, coherence resonance, and deterministic chaos.

Action Potentials↗
PubMed2005

Consequences of partial and severe dopaminergic lesion on basal ganglia oscillatory activity and akinesia.

Severe chronic dopamine (DA) depletion increases the proportion of neurons in the basal ganglia that fire rhythmic bursts of action potential (LFO units) synchronously with the cortical oscillations. Here we report on how different levels of mesencephalic DA denervation affect substantia nigra pars reticulata (SNpr) neuronal activity in the rat and its relationship to akinesia (stepping test). Chronic nigrostriatal lesion induced with 0 (control group), 4, 6 or 8 microg of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle resulted in a dose-dependent decrease of tyrosine hydroxylase positive (TH+) neurons in the SN and ventral tegmental area (VTA). Although 4 microg of 6-OHDA reduced the number of TH+ neurons in the SN by approximately 60%, both stepping test performance and SNpr neuronal activity remained indistinguishable from control animals. By contrast, animals that received 6 microg of 6-OHDA showed a marked reduction of TH+ cells in the SN ( approximately 75%) and VTA ( approximately 55%), a significant stepping test deficit and an increased proportion of LFO units. These changes were not dramatically enhanced with 8 microg 6-OHDA, a dose that induced an extensive DA lesion (> 95%) in the SN and approximately 70% reduction of DA neurons in the VTA. These results suggest a threshold level of DA denervation for both the appearance of motor deficits and LFO units. Thus, the presence of LFO activity in the SNpr is not related to a complete nigrostriatal DA neuron depletion (ultimate stage parkinsonism); instead, it may reflect a functional disruption of cortico-basal ganglia dynamics associated with clinically relevant stages of the disease.

Animals↗
PubMed1970

Calcium, magnesium and the electrical activity of guinea-pig olfactory coex in vitro.

1. Evoked electrical activity was observed in slices from guinea-pig olfactory cortex maintained in vitro. This evoked activity was studied in saline solutions containing various concentrations of Ca(2+) and Mg(2+).2. The evoked potentials recorded from the surface of the prepiriform cortex comprised a negative wave (N-wave) of about 10-15 msec duration upon which a variable number of short duration positive notches were superimposed. The N-wave was identified as a population excitatory post-synaptic potential (EPSP) of the olfactory cortex neurones and the positive notches were identified with synchronous discharge of cortical neurones.3. The relation between the EPSP amplitude and saline Ca(2+) concentration was sigmoid. The N-wave amplitude (EPSP) was proportional to [Ca(2+)](o) (n). When saline Ca(2+) was between 0.4 and 1 mMn averaged 2.5 (range 1.5-4.3).4. The EPSP amplitude was reduced by increasing saline [Mg(2+)]. High Mg(2+) salines (about 10 mM) abolished the EPSP.5. Both Ca(2+) and Mg(2+) in high concentrations depressed the positive notches.6. Salines containing little or no Ca(2+) and Mg(2+) caused the preparation to show signs of hyperexcitability. Under these conditions the evoked potentials were very variable and unstable. ;Ca(2+)-free' salines caused a reversible loss of excitability.7. The results indicated that Ca(2+) and Mg(2+) had antagonistic effects on the release of the transmitter substance(s). Increased Ca(2+) concentrations increased the output of transmitter, increased Mg(2+) concentrations reduced the output of transmitter. Both Ca(2+) and Mg(2+) in increasing concentration increased the threshold for action potential generation.

Action Potentials↗
PubMed2006

Retinoic acid signaling in the functioning brain.

Retinoic acid, an active form of vitamin A, regulates gene expression throughout the body, and many components of the signaling system through which it acts are present in the brain. Very little is known, however, about how retinoic acid functions in neurobiological systems. Several studies have provided evidence that retinoic acid plays a role in sleep, learning, and memory, but the precise mechanisms through which it influences these processes remain unclear. All of these processes involve local or long-range inhibition and synchronized neuronal activity between separate locations in the brain. A critical component in the generation of the synchronized firing of cortical neurons (cortical synchrony) is a network of inhibitory interneurons containing parvalbumin, a cell population affected by retinoid perturbations, such as exposure to a vitamin A overdose. An understanding of the role of retinoids in normal brain function would provide clues to the long-standing question of whether abnormalities in retinoic acid signaling contribute to the pathogenesis of some brain diseases with uncertain etiologies that involve both genetic and environmental factors.

Animals↗
PubMed1998

Mechanisms underlying the synchronizing action of corticothalamic feedback through inhibition of thalamic relay cells.

Early studies have shown that spindle oscillations are generated in the thalamus and are synchronized over wide cortical territories. More recent experiments have shown that this large-scale synchrony depends on the integrity of corticothalamic feedback. Previously proposed mechanisms emphasized exclusively intrathalamic mechanisms to generate the synchrony of these oscillations. In the present paper, we propose a cellular mechanism in which the synchrony is dependent of a mutual interaction between cortex and thalamus. This cellular mechanism is tested by computational models consisting of pyramidal cells, interneurons, thalamic reticular (RE) and thalamocortical (TC) relay cells, on the basis of voltage-clamp data on intrinsic currents and synaptic receptors present in the circuitry. The model suggests that corticothalamic feedback must operate on the thalamus mainly through excitation of GABAergic RE neurons, therefore recruiting relay cells essentially through inhibition and rebound. We provide experimental evidence for such dominant inhibition in the lateral posterior nucleus. In these conditions, the model shows that cortical discharges optimally evoked thalamic oscillations. This feature is essential to the present cellular mechanism and is also consistently observed experimentally. The model further shows that, with this type of corticothalamic feedback, cortical discharges recruited large areas of the thalamus because of the divergent cortex-to-RE and RE-to-TC axonal projections. Consequently, the thalamocortical network generated patterns of oscillations and synchrony similar to in vivo recordings. The model also emphasizes the important role of the modulation of the Ih current by calcium in TC cells. This property conferred a relative refractoriness to the entire network, a feature also observed experimentally, as we show here. Further, the same property accounted for various spatiotemporal features of oscillations, such as systematic propagation after low-intensity cortical stimulation, local oscillations, and more generally, a high variability in the patterns of spontaneous oscillations, similar to in vivo recordings. We propose that the large-scale synchrony of spindle oscillations in vivo is the result of thalamocortical interactions in which the corticothalamic feedback acts predominantly through the RE nucleus. Several predictions are suggested to test the validity of this model.

Animals↗
PubMed1999

Temporal encoding of the voice onset time phonetic parameter by field potentials recorded directly from human auditory cortex.

Voice onset time (VOT) is an important parameter of speech that denotes the time interval between consonant onset and the onset of low-frequency periodicity generated by rhythmic vocal cord vibration. Voiced stop consonants (/b/, /g/, and /d/) in syllable initial position are characterized by short VOTs, whereas unvoiced stop consonants (/p/, /k/, and t/) contain prolonged VOTs. As the VOT is increased in incremental steps, perception rapidly changes from a voiced stop consonant to an unvoiced consonant at an interval of 20-40 ms. This abrupt change in consonant identification is an example of categorical speech perception and is a central feature of phonetic discrimination. This study tested the hypothesis that VOT is represented within auditory cortex by transient responses time-locked to consonant and voicing onset. Auditory evoked potentials (AEPs) elicited by stop consonant-vowel (CV) syllables were recorded directly from Heschl's gyrus, the planum temporale, and the superior temporal gyrus in three patients undergoing evaluation for surgical remediation of medically intractable epilepsy. Voiced CV syllables elicited a triphasic sequence of field potentials within Heschl's gyrus. AEPs evoked by unvoiced CV syllables contained additional response components time-locked to voicing onset. Syllables with a VOT of 40, 60, or 80 ms evoked components time-locked to consonant release and voicing onset. In contrast, the syllable with a VOT of 20 ms evoked a markedly diminished response to voicing onset and elicited an AEP very similar in morphology to that evoked by the syllable with a 0-ms VOT. Similar response features were observed in the AEPs evoked by click trains. In this case, there was a marked decrease in amplitude of the transient response to the second click in trains with interpulse intervals of 20-25 ms. Speech-evoked AEPs recorded from the posterior superior temporal gyrus lateral to Heschl's gyrus displayed comparable response features, whereas field potentials recorded from three locations in the planum temporale did not contain components time-locked to voicing onset. This study demonstrates that VOT at least partially is represented in primary and specific secondary auditory cortical fields by synchronized activity time-locked to consonant release and voicing onset. Furthermore, AEPs exhibit features that may facilitate categorical perception of stop consonants, and these response patterns appear to be based on temporal processing limitations within auditory cortex. Demonstrations of similar speech-evoked response patterns in animals support a role for these experimental models in clarifying selected features of speech encoding.

Auditory Cortex↗
PubMed1978

Thalamic control of spontaneous alpha-rhythm and evoked responses.

EEG, depth recordings from the thalamus, visual-evoked potentials, and readiness motor potentials were analyzed with a computer in 40 patients with involuntary movements and intractable pain who underwent stereotactic thalamotomy. It was demonstrated that there were significant correlations in alpha-rhythms between the ventrolateral (VL) nucleus and the frontocentral cortex, and also between the centromedian nucleus and the centroparietal cortex, with the phase difference of the cortex lagging behind the thalamus. Relationships between the thalamic VL nucleus and the frontocentral cortex were significant not only in alpha-rhythms, but also in evoked responses following photic stimulations, voluntary movements, and electrical thalamic stimulation. Thalamotomy produced a bilaterally decreased synchronization of the cortical alpha-rhythms, which recovered within 6 months.

Alpha Rhythm↗
PubMed2003

Neural synchrony, axonal path lengths, and general anesthesia: a hypothesis.

Despite decades of research, the mechanism by which general anesthetics produce loss of consciousness remains mysterious. A clue may be provided by the evidence that synchronous firing of cortical neurons underlies higher forms of neural processing. In order for these synchrony codes to be precise, transmission time must be independent of path length over all the connected sites between any two cortical areas. Because path lengths vary, developmental mechanisms must compensate for the resulting delay variations. Delay variations could be detected by spike-timing-dependent cues and compensation implemented by systematic changes in axon diameter, myelin thickness, or internodal distance. Anesthetics have been shown to increase conduction velocity in myelinated fibers and may therefore disrupt path-length compensation by changing velocities by different amounts in different types of axon. This simple and testable theory explains why anesthetics interfere selectively with higher cognitive functions but leave those dominated by rate-based firing relatively intact.

Anesthesia, General↗
PubMed1991

[Electroencephalographic study with rolipram (ME 3167), a selective inhibitor of adenosine 3',5'-monophosphate phosphodiesterase, in rabbits].

The electroencephalographic (EEG) effects of rolipram were investigated in rabbits with chronic electrode implants. Intravenous administration of rolipram at 10 to 100 micrograms/kg evoked an increase in the arousal EEG pattern period (low amplitude fast waves) in the cortical EEG and synchronization of the hippocampal theta waves with increased voltages. Rolipram at higher doses caused behavioral excitation in rabbits. Rolipram did not affect EEG arousal responses to both auditory stimulation (2000 Hz, monotone) and electrical stimulation (100 Hz, 0.1 msec, 3-6 V) of the midbrain reticular formation or the posterior hypothalamus. The recruiting response induced by centromedian thalamic stimulation at a low frequency (7 Hz, 0.1 msec, 4-8 V) was not altered by rolipram. Rolipram was without effect on the photic driving response to flash light (2 Hz) in the occipital cortex. Rolipram caused a slight increase in the duration of after discharges induced by electrical stimulation (50 Hz, 0.5 msec, 4-20 V) of the dorsal hippocampus. These results suggest that rolipram is a drug that causes the EEG arousal pattern.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2002

Activation of human cerebral and cerebellar cortex by auditory stimulation at 40 Hz.

We used functional brain imaging with positron emission tomography (PET)-H2 15O to study a remarkable neurophysiological finding in the normal brain. Auditory stimulation at various frequencies in the gamma range elicits a steady-state scalp electroencephalographic (EEG) response that peaks in amplitude at 40 Hz, with smaller amplitudes at lower and higher stimulation frequencies. We confirmed this finding in 28 healthy subjects, each studied with monaural trains of stimuli at 12 different stimulation rates (12, 20, 30, 32, 35, 37.5, 40, 42.5, 45, 47.5, 50, and 60 Hz). There is disagreement as to whether the peak in the amplitude of the EEG response at 40 Hz corresponds simply to a superimposition of middle latency auditory evoked potentials, neuronal synchronization, or increased cortical synaptic activity at this stimulation frequency. To clarify this issue, we measured regional cerebral blood flow (rCBF) with PET-H2 15O in nine normal subjects at rest and during auditory stimulation at four different frequencies (12, 32, 40, and 47 Hz) and analyzed the results with statistical parametric mapping. The behavior of the rCBF response was similar to the steady-state EEG response, reaching a peak at 40 Hz. This finding suggests that the steady-state amplitude peak is related to increased cortical synaptic activity. Additionally, we found that, compared with other stimulation frequencies, 40 Hz selectively activated the auditory region of the pontocerebellum, a brain structure with important roles in cortical inhibition and timing.

Acoustic Stimulation↗
PubMed2004

Pathological oscillatory coupling within the human motor system in different tremor syndromes as revealed by magnetoencephalography.

Whole-head MEG-systems and modern spatial-filter-based analysis tools recently provided new possibilities to analyze non-invasively cerebral networks of human tremor syndromes. We compared tremor syndromes in Parkinsonian patients with a typical resting tremor as well as in patients with hepatic encephalopathy (HE) with a postural tremor called "mini-asterixis". In 6 patients with idiopathic Parkinson's disease (PD) we found strong coherence between the electromyography (EMG) of forearm muscles and activity in the contralateral primary motor cortex (M1) at tremor frequency but also at double tremor frequency. Furthermore, significant coherences were observed between M1 and medial wall areas (CMA/SMA), lateral premotor cortex, diencephalon, SII cortex, posterior parietal cortex and the contralateral cerebellum at tremor and, stronger, at double tremor frequency. In contrast, in 6 patients with "mini-asterixis" and HE due to chronic liver cirrhosis excessive corticomuscular coherence occurred at the individual tremor frequency between EMG and M1 activity. Interestingly, thalamus-M1 coupling was significantly altered towards lower frequencies matching the individual frequency of the mini-asterixis. Cerebro-muscular or cerebro-cerebral coupling at double tremor frequency was not observed. Therefore, "mini-asterixis" reflects most likely a pathologically decelerated and augmented synchronized rhythmical motor cortical output. This could be due to functional alterations in the M1-basal-ganglia-thalamo-cortical loops in severe HE. In summary, tremor syndromes in PD as well as in patients with HE and "mini-asterixis" are characterized by pathological oscillatory activity within cerebral networks of motor areas. However, the present study shows different mechanisms of tremor generation in PD and HE patients.

Evoked Potentials, Motor↗
PubMed1977

[Acute liver damage due to thioacetamide. Morphology, biochemistry and neurophysiologic comparison with cerebrotoxic substances].

Morphology, biochemistry and neurophysiological comparisons with effects of brain-toxic substances. The acute damage of the liver by thioacetamide is characterized neurophysiologically by a far--reached synchronous beginning of cortical and subcortical alteration of activity, a retardation of cortical and subcortical EEG, threshold increase of the EEG--arousal reaction, reductions in amplitude of centrally evoked potentials and increase of acoustically evoked potentials. We impute that according to an acute "toxic" damage of the liver a "membrane hyperpolarisation" results in all or nearly all areas of the brain. A general decrease of excitability of the brain seems consequently plausible. In opposition to this results only activities of the cortex or structures nearby the cortex (areas above the midbrain reticular formation) will be affected by exogenous arterial hyperammoniemia up to 1700 mug/100 ml.

Acetamides↗
PubMedDate not supplied

[EEG slow components during human mental activity].

A study was made on 13 subjects in a state of rest and mental stress, of interconnection between the level of distant biopotential synchronization of separate cortical zones (which is a criterion of the rate of brain activation) and the spectral power of EEG frequencies. There is a statistically significant positive correlation between the first parameter and the energy of low frequency activity band (delta-theta). At the same time similar dependences for the alpha- and beta-rhythms are negative and topographically less spread. The coherence function likewise increases during mental stress for the low-frequency band alone. The data obtained point to the special role of low-frequency rhythms in the transmission of excitation over the cortex and support the significance of the alpha-rhythm in providing for the mechanisms involved in the control of homeostasis.

Adolescent↗
PubMed1997

[Control and development of breathing, pathophysiological aspects].

The respiratory control system guarantees acid-base-homeostasis as well as the rhythmic activities of the respiratory motor system in accordance with exercise and behavioural programmes of the human being. Cortical patterns and synchronized respiratory patterns with tracheal flow and pressure variations in the fetus indicate the common network of respiration and sleep-wake mechanisms in an early stage already. During fetal life acid-base-homeostasis is dependent on progesterone controlled mechanisms. CO2 partial pressure of the uterine artery reduces to 32 mmHg. The O2 Partial pressure of the umbilical vein is 25-30 mmHg only. The raise of PCO2 during delivery is accompanied by a shower of sensory input to the reticular formation causing arousal and the opening of the lungs. The continuation of postnatal breathing is the consequence of the integration of the central chemosensitive mechanism and the reticular activating system at an adequate threshold. Perinatal defense reflexes, functional patterns and strategies in early life may outline later pathophysiological mechanisms for sleep apnea, apparently life threatening event (ALTE), sudden infant death, and congenital central hypoventilation syndrome.

Acid-Base Equilibrium↗
PubMed1998

L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol stimulates ganglioside biosynthesis, neurite outgrowth and synapse formation in cultured cortical neurons, and ameliorates memory deficits in ischemic rats.

To address the role of brain gangliosides in synaptic plasticity, the synthetic ceramide analog, 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) was used to manipulate the biosynthesis of gangliosides in cultured cortical neurons. Spontaneous synchronized oscillatory activity of intracellular Ca2+ between the neurons, which represents synapse formation, was suppressed by the depletion of endogenous gangliosides by D-threo-PDMP, an inhibitor of glucosylceramide synthase. The decreased functional synapse formation was normalized by supplementation of GQ1b but not by the other gangliosides, suggesting that de novo synthesis of ganglioside GQ1b is essential for the synaptic activity (Mizutani A. et al., Biochem. Biophys. Res. Commun. 222, 494-498, 1996). On the other hand, the enantiomer of the inhibitor, L-threo-PDMP, could elevate cellular levels of glycosphingolipids including gangliosides. This paper presents our recent findings on the neurotrophic actions of L-threo-PDMP in vitro and in vivo. We found that L-PDMP could up-regulate neurite outgrowth, functional synapse formation and ganglioside biosynthesis through activating GM3, GD3 and GQ1b synthases. Simultaneously, the activity of p42 mitogen-activated protein kinase was also facilitated by L-PDMP. To evaluate the efficacy of this drug on long term memory, rats were trained for 2 weeks using an 8-arm radial maze task, and then forebrain ischemia was induced by 4-vessel occlusion (for 10 min x 2 with a 60 min interval). Repeated treatment of L-threo-PDMP (40 mg/kg, i.p. for 6 days, twice a day) starting 24 h after the ischemia, improved the deficit of the well-learned spatial memory, demonstrating the potential therapeutic use of the ceramide analog for treatment of neurodegenerative disorders.

Animals↗
PubMed1984

[Shifts in spatial synchronization potentials of the rabbit cortex evoked by the administration of noradrenaline to the visual area].

Application of noradrenaline to the visual cortex of alert rabbits led to a general brief increase of the distant potential synchronization in the visual and motor areas as well as to a local rather steady (5-10 min) synchronization between the processes in the visual cortical area. Later a similar and even more obvious increase occurred between bioelectrical processes in the sensorimotor cortex. The synchronization increase seems to be favourable for excitation transmission.

Animals↗
PubMed1999

Visual stimulus-dependent changes in interhemispheric EEG coherence in humans.

We analyzed the coherence of electroencephalographic (EEG) signals recorded symmetrically from the two hemispheres, while subjects (n = 9) were viewing visual stimuli. Considering the many common features of the callosal connectivity in mammals, we expected that, as in our animal studies, interhemispheric coherence (ICoh) would increase only with bilateral iso-oriented gratings located close to the vertical meridian of the visual field, or extending across it. Indeed, a single grating that extended across the vertical meridian significantly increased the EEG ICoh in normal adult subjects. These ICoh responses were obtained from occipital and parietal derivations and were restricted to the gamma frequency band. They were detectable with different EEG references and were robust across and within subjects. Other unilateral and bilateral stimuli, including identical gratings that were effective in anesthetized animals, did not affect ICoh in humans. This fact suggests the existence of regulatory influences, possibly of a top-down kind, on the pattern of callosal activation in conscious human subjects. In addition to establishing the validity of EEG coherence analysis for assaying cortico-cortical connectivity, this study extends to the human brain the finding that visual stimuli cause interhemispheric synchronization, particularly in frequencies of the gamma band. It also indicates that the synchronization is carried out by cortico-cortical connection and suggests similarities in the organization of visual callosal connections in animals and in man.

Adult↗
PubMed1986

Cellular basis of neuronal synchrony in epilepsy.

Synchronized discharge of populations of cortical neurons are often observed to underly both the interictal spikes and tonic seizures generated in experimental epilepsy studies. Recently it has been shown that similar synchronized discharges occur in cortical brain slices treated with convulsants such as penicillin, picrotoxin, or bicuculline. The favorable experimental conditions offered by the in vitro preparation have facilitated a detailed examination on the cellular basis for the generation of the epileptic neuronal synchrony. In this chapter we shall review some experimental observations on the neuronal synchronization and describe a mechanism for its generation based on the computer simulation approach. Three factors are considered to be essential for epileptic synchronization observation in vitro. First, cortical neurons may intrinsically generate bursts of action potentials. Second, recurrent excitatory connections exist that are sufficiently powerful that bursting activity may spread between synaptically connected neurons. Third, inhibition within the local neuronal circuit must be adequately attenuated to allow excitation to spread through the recurrent excitatory connections. Computer simulation studies have been based on these assumptions, using neuronal networks where each cell is connected to more than one postsynaptic neuron. Bursting initiated in one cell excites all its follower cells, and the sequential recruitment of an increasing number of cells eventually leads to a simultaneous discharge of the population. A number of recent experimental observations lend credence to the proposed scheme for neuronal synchrony. Simultaneous paired intracellular recordings provided direct evidence that a burst of action potentials in a presynaptic cell can activate action potentials postsynaptically. Furthermore, it is shown that the rhythm of spontaneous discharge in a neuronal population can be influenced by the activity of one neuron within the population.

Animals↗

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