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PubMedDate not supplied

Neurophysiological correlates of improvements in cognitive characteristics in monkeys during modification of NMDA-ergic structures of the prefrontal cortex.

The effects of modification of NMDA-ergic structures by microdialysis perfusion in the prefrontal cortex (field 8) with NMDA glutamate (2 mM) on visual recognition and short-term memory (STM) were studied in rhesus macaques, using methods based on the deferred differentiation of stimuli of different colors. Impulse activity of neurons in the prefrontal and visual cortex was measured during these experiments, both before and after administration of NMDA. NMDA increased (2-fold) the duration of short-term retention of information and significantly reduced the latent period of the motor response at all delay periods, and also produced significant changes in neuron activity in the prefrontal cortex: depending on the stage of behavior, activity decreased in 60-75% of neurons and increased in 8-26%. NMDA produced significant increases in the cross-correlation coefficients between the responses of neurons in the visual and prefrontal cortex. The results showed that glutaminergic structures in the prefrontal cortex are involved in processes of visual recognition and STM in monkeys. The effect of NMDA, which synchronized cortical neuronal processes, improved the short-term understanding of visual information.

Animals↗
PubMed1984

Antiepileptic action of the beta-carboline ZK 91296 in a genetic petit mal model in rats.

The anticonvulsant action of the benzodiazepine (BZ) receptor partial agonist, ethyl 5-benzyloxy-4-methoxymethyl-beta-carboline-3-carboxylate (ZK 91296) was studied in rats of Wistar origin exhibiting spontaneous bilateral cortical synchronous spike and wave discharges with a symptomatology paralleling that of human petit mal seizures. ZK 91296 1-16 mg/kg i.p.) attenuated the absence seizures without inducing signs of sedation or disorganized EEG patterns at any dose. Diazepam (1-8 mg/kg i.p.) suppressed seizures but also induced sedation and modified EEG background activity in a dose-related manner.

Animals↗
PubMed1989

Responses of VPL thalamic neurones to peripheral stimulation in wakefulness and sleep.

In unanaesthetized, undrugged, normally respiring cats extracellular recordings were obtained from ventroposterolateral thalamic units through different states of the sleep-waking cycle. An air-puff peripheral stimulation was used to activate the recorded neurones. State-dependent changes of the response of thalamic neurones were shown, comparing slow-wave sleep (SWS) to wakefulness (W). During SWS an increase was observed in the strength of the discharge suppression, which follows the excitatory peak in the typical response pattern. Also the cell excitability is further reduced in slow-wave sleep during the 150-200 ms period following an excitatory response, suggesting that an enhancement of the post-excitatory inhibition could be involved in the generation of the slow 5-6 Hz rhythms, observed during thalamic and cortical synchronization.

Action Potentials↗
PubMed1981

Phencyclidine-induced alterations of rat electrophysiology.

Phencyclidine (PCP) at high doses causes both excitation and depression in the rat. The visual evoked potential (VEP) was measured in rats following PCP administration in doses ranging from 1 mg/kg to 56 mg/kg. Consistent lengthening of VEP latencies suggests that PCP has an unusual inhibitory effect on visual function in the presence of the excitatory signs of bilaterally synchronous cortical spiking. The epileptogenic properties of PCP are quite evident in rats.

Animals↗
PubMed1985

Neural mechanisms distinguishing the neocortical EEG of C57BL/6 mice from that of DBA/2 mice.

C57BL/6 inbred mice lack the 1-5 sec bursts of 6-7 cps spindles characteristic of the neocortical EEG of DBA/2 mice during waking. C57BL/6 mice (1) may be unable to generate any synchronized cortical EEG activity, (2) may lack the thalamocortical circuitry required to generate these brief spindle episodes (BSEs), (3) may lack mechanisms that can activate this circuitry or (4) may possess a potent mechanism to suppress BSE initiation and generation. Possibilities 1 and 2 have been eliminated because C57BL/6 mice generate pentobarbital, rostropontine-induced and sleep spindles, and because certain C57BL/6 sleep spindles resembled the BSEs seen in DBA/2 mice. Possibilities 3 and 4 were examined in the experiments reported here. In DBA/2 mice, pentylenetetrazol activates BSEs at subconvulsant doses. In contrast, neither 20 nor 50 mg/kg, IP, pentylenetetrazol activated BSEs in C57BL/6 mice, although the higher dose provoked 4-5 cps slow waves and myoclonic jerks. In DBA/2 mice, the beta-noradrenergic antagonist propranolol has been reported to powerfully release BSEs. In C57BL/6 mice, 10 and 15 mg/kg propanolol weakly released BSEs; fewer than 3 per hour occurred. Hence neither possibilities 3 and 4 are sufficient in themselves to explain the lack of BSEs during waking in C57BL/6 mice. However, simultaneous administration of 10 mg/kg propranolol and 20 mg/kg pentylenetetrazol provoked numerous BSEs in C57BL/6 mice. This suggests that perhaps C57BL/6 mice, as compared to DBA/2 mice, possess both a more powerful noradrenergic mechanism to suppress spindles and a more weakly functioning mechanism to activate BSEs. Hence possibilities 3 and 4 may both be correct.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Electroencephalographic evidence for a dose-related biphasic effect of morphine on bicuculline-induced seizures in the rat.

The effects of systemic pretreatment with morphine sulfate (MS) on electroencephalographic (EEG) manifestations of seizures due to bicuculline (BIC) were studied in freely moving rats. Electrodes were placed on frontal and occipital cortices, into the hippocampus and into a region of the prepiriform cortex, area tempestas (AT). BIC (0.1-0.25 mg/kg i.v.) elicited dose-dependent changes in electrocortical activity, consisting of 3 stages: stage 1, slight increase in periods of desynchronization; stage 2, trains of 4-6 Hz spike-and-wave complexes and of 2-4 Hz slow waves; stage 3, 'grand mal' seizures. Isolated spikes and hypersynchronous high voltage spikes occurred in the hippocampus during stage 2 and stage 3, respectively. In the AT, EEG abnormalities were observed during stage 3 only. During the recovery period, cortical synchronization occurred associated with the presence of occasional synchronous spikes in both deep areas. After pretreatment with MS (2, 12, and 25 mg/kg), stage 3 EEG seizures occurred with doses of BIC (0.12 or 0.18 mg/kg i.v.) that in the absence of MS produced only stage 1 or 2. In contrast, after pretreatment with a low dose of MS(0.5 mg/kg) the seizures induced by a maximally effective dose of BIC (0.25 mg/kg) were markedly attenuated. Thus, the effect of MS on BIC-induced seizure activity appears to be biphasic, potentiating seizures at doses at or above 2 mg/kg and inhibiting seizures at lower doses.

Animals↗
PubMed2006

Electrocortical and behavioral responses elicited by acute electrical stimulation of inferior thalamic peduncle and nucleus reticularis thalami in a patient with major depression disorder.

OBJECTIVE: Our aim was to study electrocortical and behavioral responses elicited by 6, 60 and 3/s stimulation of the inferior thalamic peduncle (ITP) and nucleus reticularis thalami (Re) in a patient with of major depression disorder resistant to psychotherapy, pharmacotherapy and electroconvulsive therapy and candidate to be treated by electrical stimulation of the ITP. METHODS: In this patient, two multicontact electrodes were implanted bilaterally through frontal coronal parasagittal burr-holes with oblique trajectories aiming ITP and Re. Stimulation was performed through externalized systems. Referential scalp electroencephalographic (EEG) recordings were performed and subjective sensations and clinical symptoms reported by patient and changes in responsiveness in single response tasks during stimulation trials were systematically recorded. RESULTS: Unilateral, low (6/s) and high (60/s) frequency stimulation of either ITP or Re produced identical recruiting-like responses or desynchronization-DC shift changes predominant at frontopolar region, bilaterally. Billateral, high intensity 3/s stimulation or either ITP or Re produced electrocortical responses that consisted in generalized 3/s spike-wave complexes predominant at frontopolar, frontocentral and frontotemporal regions. However, while ITP responses were accompanied by all symptoms described for a spontaneous absence attack, Re responses were behaviorly accompanied only by delayed reaction time. CONCLUSION: These data suggests that in humans as in cats, ITP and Re are both part of a non-specific thalamo-orbitofrontal system normally engaged in cortical synchronization, selective attention and sleep. SIGNIFICANCE: Under abnormal conditions, ITP and RE may play a role in the physiopathology of typical absence attacks and depression disorders.

Brain Mapping↗
PubMed2006

Individual variability, end-point effects and possible biases in electrophysiological research.

Neocortical dynamics and signals reflect spatiotemporal cortical synchronization as well as functional condition and modulation by subcortical projecting structures that determine the brain state. However, neurotransmitters interact and neuronal function and signals also reflect non-neuronal factors that should (but not necessarily are, or can) be taken into proper consideration in neuroscience. Examples in this regard are the CNS modulation by spontaneous or induced changes in metabolism (e.g. glucose, ammonia), blood flow, pO(2), pCO(2), hormones (thyroxine; sexual hormones, ATCH) and neurohormonal interaction, maturation, aging, temperature, light-dark regulation of serotonine, histamine and dopamine/melatonin/vitamin B12 secretion and interaction, etc. Hormones also regulate the (functional) maturation and differentiation between sexes both during development and in adult life. These factors interact with each other and individually or collectively can account for unexplained or underestimated individual variability; on occasions, may become critical variables in animal or human research. In specific instances, variability is the information of interest. However, physiological variability due to neuronal or non-neuronal factors can interact with the experimental setups or affect electrophysiological signals to extents that can result in biased findings in otherwise controlled studies. An "inverse problem" difficult to approach may ensue in both animal and human research; in several instances, the specificity of brain signals for the investigated function may require experimental validation.

Analgesia↗
PubMed2005

NMDA receptor-mediated epileptiform persistent activity requires calcium release from intracellular stores in prefrontal neurons.

Various normal and pathological forms of synchronized population activity are generated by recurrent excitation among pyramidal neurons in the neocortex. However, the intracellular signaling mechanisms underlying this activity remain poorly understood. In this study, we have examined the cellular properties of synchronized epileptiform activity in the prefrontal cortex with particular emphasis on a potential role of intracellular calcium stores. We find that the zero-magnesium-induced synchronized activity is blocked by inhibition of sarco-endoplasmic reticulum Ca(2+)-ATPases, phospholipase C (PLC), the inositol 1,4,5-trisphosphate (IP3) receptor, and the ryanodine receptor. This same activity is, however, not affected by application of metabotropic glutamatergic receptor (mGluR) agonists, nor by introduction of an mGluR antagonist. These results suggest that persistent synchronized activity in vitro is dependent upon calcium release from internal calcium stores through the activation of PLC-IP3 receptor pathway. Our findings also raise the possibility that intracellular calcium release may be involved in the generation of pathologic synchronized activity in epilepsy in vivo and in physiological forms of synchronized cortical activity.

Action Potentials↗
PubMed2006

Candidate gene analysis of the succinic semialdehyde dehydrogenase gene (ALDH5A1) in patients with idiopathic generalized epilepsy and photosensitivity.

Succinic semialdehyde dehydrogenase (SSADH) is involved in the degradation of the inhibitory neurotransmitter GABA and about 50% of patients with SSADH deficiency suffer from seizures. The gene encoding SSADH (gene symbol: ALDH5A1) maps in proximity to susceptibility loci for juvenile myoclonic epilepsy (JME) and photosensitivity on chromosome 6p22. The present study tested whether variation of the ALDH5A1 gene confers susceptibility to common syndromes of idiopathic generalized epilepsy (IGE) and an abnormal photoparoxysmal response (PPR). Mutation screening of the ALDH5A1 coding sequence of 35IGE/PPR patients and four healthy control subjects identified 17 sequence variants, of which three resulted in an exchange of amino acids (H180Y, P182L, A237S). Association analysis was carried out for six single nucleotide polymorphisms (SNPs) and one trinucleotide repeat polymorphism (TNR, intron 1), covering the genomic ALDH5A1 sequence. The study sample comprised 566 unrelated German IGE patients, including 218 JME and 95 photosensitive IGE patients, 78 PPR probands without IGE, and 662 German population controls. None of the investigated ALDH5H1 polymorphisms showed evidence for an allelic or genotypic association with either IGE, JME, or PPR, when corrected for multiple tests. A tentative haplotypic association of the two-marker haplotype (rs1883415-TNR) covering the 5'-regulatory region in IGE patients (chi2=11.65, d.f.=3, P=0.009) warrants further replication studies. The present results do not provide evidence that any ALDH5A1 missense variant itself contributes a common and substantial susceptibility effect (RR>2) to IGE syndromes or an increased liability to visually-induced cortical synchronization.

Epilepsy, Generalized↗
PubMed2005

Gamma-band activity over early sensory areas predicts detection of changes in audiovisual speech stimuli.

Oscillatory activity in the gamma-band range in human magneto- and electroencephalogram is thought to reflect the oscillatory synchronization of cortical networks. Findings of enhanced gamma-band activity (GBA) during cognitive processes like gestalt perception, attention and memory have led to the notion that GBA may reflect the activation of internal object representations. However, there is little direct evidence suggesting that GBA is related to subjective perceptual experience. In the present study, magnetoencephalogram was recorded during an audiovisual oddball paradigm with infrequent visual (auditory /ta/ + visual /pa/) or acoustic deviants (auditory /pa/ + visual /ta/) interspersed in a sequence of frequent audiovisual standard stimuli (auditory /ta/ + visual /ta/). Sixteen human subjects had to respond to perceived acoustic changes which could be produced either by real acoustic or illusory (visual) deviants. Statistical probability mapping served to identify correlations between oscillatory activity in response to visual and acoustic deviants, respectively, and the detection rates for either type of deviant. The perception of illusory acoustic changes induced by visual deviants was closely associated with gamma-band amplitude at approximately 80 Hz between 250 and 350 ms over midline occipital cortex. In contrast, the detection of real acoustic deviants correlated positively with induced GBA at approximately 42 Hz between 200 and 300 ms over left superior temporal cortex and negatively with evoked gamma responses at approximately 41 Hz between 220 and 240 ms over occipital areas. These findings support the relevance of high-frequency oscillatory activity over early sensory areas for perceptual experience.

Adult↗
PubMed2006

Gamma-range corticomuscular coherence during dynamic force output.

The beta-range synchronization between cortical motor and muscular activity as revealed by EEG/MEG-EMG coherence has been extensively investigated for steady-state motor output. However, there is a lack of information on the modulation of the corticomuscular coherence in conjunction with dynamic force output. We addressed this question comparing the EEG-EMG coherence and the cortical motor spectral power in eight healthy subjects in a visuomotor task, in which the subjects exerted a steady-state or periodically modulated dynamic isometric force output with their right-index finger to keep a visual cursor within a target zone. In the static condition, significant coherence was confined to the beta-range. In the dynamic condition, the most distinct coherence occurred in the gamma-range and the significant beta-range coherence was strikingly reduced. The cortical motor power in the beta-range during dynamic force output was decreased, whereas the power in the gamma-range remained without significant change. We conclude that during dynamic force the corticospinal oscillation mode of the sensorimotor system shifts towards higher (principally gamma) frequencies for the rapid integration of the visual and somatosensory information required to produce the appropriate motor command.

Adult↗
PubMed2005

Inhibitory postsynaptic potentials carry synchronized frequency information in active cortical networks.

Temporal precision in spike timing is important in cortical function, interactions, and plasticity. We found that, during periods of recurrent network activity (UP states), cortical pyramidal cells in vivo and in vitro receive strong barrages of both excitatory and inhibitory postsynaptic potentials, with the inhibitory potentials showing much higher power at all frequencies above approximately 10 Hz and more synchrony between nearby neurons. Fast-spiking inhibitory interneurons discharged strongly in relation to higher-frequency oscillations in the field potential in vivo and possess membrane, synaptic, and action potential properties that are advantageous for transmission of higher-frequency activity. Intracellular injection of synaptic conductances having the characteristics of the recorded EPSPs and IPSPs reveal that IPSPs are important in controlling the timing and probability of action potential generation in pyramidal cells. Our results support the hypothesis that inhibitory networks are largely responsible for the dissemination of higher-frequency activity in cortex.

Action Potentials↗
PubMed2006

Enhancement of spike-timing precision by autaptic transmission in neocortical inhibitory interneurons.

In vivo studies suggest that precise firing of neurons is important for correct sensory representation. Principal neocortical neurons fire imprecisely when repeatedly activated by fixed sensory stimuli or current depolarizations. Here we show that in contrast to pyramidal neurons, firing in neocortical GABAergic fast-spiking (FS) interneurons is quite precise. FS interneurons are self-innervated by powerful GABAergic autaptic connections reliably activated after each spike, suggesting that autapses strongly regulate FS-cell spike timing. Indeed, blockade of autaptic transmission degraded temporal precision in multiple ways. Under these conditions, realistic dynamic-clamp hyperpolarizing autapses restored precision of spike timing, even in the presence of synaptic noise. Furthermore, firing precision was increased in pyramidal neurons by artificial GABAergic autaptic conductances, suggesting that tightly coupled synaptic feedback inhibition regulates spike timing in principal cells. Thus, well-timed inhibition, whether autaptic or synaptic, facilitates precise spike timing and promotes synchronized cortical network oscillations relevant to several behaviors.

Action Potentials↗
PubMed2002

Acute and long-term effects of the 5-HT2 receptor antagonist ritanserin on EEG power spectra, motor activity, and sleep: changes at the light-dark phase shift.

Parallel effects of a single injection of the 5-HT(2) receptor antagonist ritanserin on EEG power spectra, sleep and motor activity were measured for a 20-h period in freely moving Sprague-Dawley rats. Ritanserin (0.3 mg/kg, i.p.), administered at light onset (passive phase), caused an immediate transient increase in the EEG power density in the low frequency range (0.25-6 Hz, mainly delta activity) and a depression in the high frequency range (27-30 Hz) accompanied by a decrease in vigilance and light slow wave sleep (SWS-1), intermediate stage of sleep and increase in deep slow wave sleep (SWS-2) compared to control treatment. All these effects were over 8 h after the injection. Twelve hours after the injection, at dark onset (active phase), there was a marked increase in vigilance and motor activity and decrease in SWS-1 and spindle frequency activity in the control animals, but all these changes were diminished by ritanserin treatment. These effects resulted in a significant relative increase in the intermediate band (peak: 12-15 Hz) of the EEG power spectra and thus, a relative increase in thalamo-cortical synchronization caused by ritanserin at dark onset. Because ritanserin is a selective 5-HT(2) receptor antagonist, we conclude that under physiological conditions serotonin increases EEG desynchronization and produces an increase in vigilance level and motor activity by tonic activation of 5-HT(2) receptors. This regulatory mechanism plays an important role in the waking process, and the appearances of its effects in the light and dark phase are markedly different.

Animals↗
PubMed2003

Pyridostigmine enhances glutamatergic transmission in hippocampal CA1 neurons.

Pyridostigmine, a carbamate acetylcholinesterase (AChE) inhibitor, is routinely employed in the treatment of the autoimmune disease myasthenia gravis. Due to its positively charged ammonium group, under normal conditions pyridostigmine cannot cross the blood-brain barrier (BBB) and penetrate the brain. However, several studies have suggested that under conditions in which the BBB is disrupted, pyridostigmine enters the brain, changes cortical excitability, and leads to long-lasting alterations in gene expression. The aim of this study was to characterize the mechanisms underlying pyridostigmine-induced changes in the excitability of central neurons. Using whole cell intracellular recordings in hippocampal neurons we show that pyridostigmine decreases repetitive firing adaptation and increases the appearance of excitatory postsynaptic potentials. In voltage clamp recordings, both pyridostigmine and acetylcholine (ACh) increased the frequency but not the amplitude of excitatory postsynaptic currents. These effects were reversible upon the administration of the muscarinic receptor antagonist, atropine, and were not blocked by tetrodotoxin. We conclude that pyridostigmine, by increasing free ACh levels, causes muscarinic-dependent enhancement of excitatory transmission. This mechanism may explain central side effects previously attributed to this drug as well as the potency of AChE inhibitors, including nerve-gas agents and organophosphate pesticides, in the initiation of cortical synchronization, epileptic discharge, and excitotoxic damage.

Acetylcholine↗
PubMed2002

Role of onset asynchrony in contour integration.

Evidence that visual grouping is facilitated when elements comprising a foreground figure are presented simultaneously, and are temporally separated from elements comprising the background, has suggested cortical synchronous oscillations as a possible neural substrate. Supporting this theory, Usher and Donnelly (Nature 394 (1998) 179) showed in one of their experiments that contour integration is facilitated when path and background elements alternate with an asynchrony below the integration time of the visual system, suggesting that these flickering stimuli interact with this hypothetical binding mechanism. I replicated this experiment and report that the effect depends in fact on the order of asynchrony between path and background elements in the first cycle of stimuli presented for more than 100 ms: facilitation in visual grouping only occurs when path elements are presented before background elements. A second experiment, exploring the effect of onset delays between path and background elements, demonstrates a strong priming effect of path elements. I conclude that Usher and Donnelly's result is likely due to the high sensitivity of the visual system to stimulus onset, and that simple flickering stimuli are inadequate for revealing the neural code for binding in figure-ground segregation without controlling for the effect of stimulus onset.

Analysis of Variance↗
PubMed2000

Substantia nigra dopamine regulates synaptic plasticity and membrane potential fluctuations in the rat neostriatum, in vivo.

The spiny projection neurons of the neostriatum are a site at which dopamine inputs from the substantia nigra converge with excitatory inputs from the cerebral cortex. These two systems interact in certain learning and motor control mechanisms of the brain. We investigated these interactions using intracellular recording from spiny striatal neurons in urethane-anaesthetized rats. We found that acute dopamine depletion was associated with long-term depression of corticostriatal synaptic input. Electrical stimulation of the cortex which mimicked synchronous cortical input to striatal neurons also induced long-term depression of corticostriatal inputs. In intact control animals, but not in dopamine-depleted animals, this depression was prevented or reversed by concomitant stimulation of the substantia nigra. In agreement with previous in vitro studies, our in vivo findings show that long-term depression occurs in the corticostriatal pathway, and in addition show that it is regulated by dopaminergic inputs from the substantia nigra. This form of synaptic plasticity may therefore be important for understanding disturbances of the motor system seen in humans with Parkinson's disease.

Animals↗