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MeSH Review

Cortical Synchronization

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High impact information on Cortical Synchronization

  • Thus, NMDA receptor-based silent synapses are essential for paroxysmal corticothalamic activity during early postnatal development, and connections between layer VI neurons are sufficient for horizontal cortical synchronization [1].
  • Sleep-wake states and cortical synchronization control by pregnenolone sulfate into the pedunculopontine nucleus [2].
  • 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 [3].
  • In rats, both competitive and non-competitive NMDA antagonists induce three dose-dependent stages of EEG patterns: 1) increase in cortical desynchronization periods; 2) increase in amplitude of cortical high frequency (20-30 Hz), low voltage (30-50 microV) background activity; 3) appearance of cortical slow (2-3 Hz) wave-sharp wave complexes [4].
  • In rats, PCP produces three dose-dependent stages of EEG patterns: 1) increase of cortical desynchronization duration; 2) increase of the amplitude of the high-frequency (20-30 Hz) low-voltage (30-50 microV) cortical background activity; 3) appearance of cortical slow (2-3 Hz) wave-sharp wave complexes [5].

Anatomical context of Cortical Synchronization


Associations of Cortical Synchronization with chemical compounds

  • Agents known to inhibit serotonergic unit activity including serotonin, (+/-)-8-hydroxy-dipropylaminotetralin, fluoxetine and baclofen, when pressure ejected in the vicinity of the dorsal raphe, prevented cortical desynchronization as well as the suppression of focal epileptiform activity in response to noxious stimulation [7].
  • Recent evidence indicates that serotonin mediates both atropine-resistant cortical desynchronization and the suppression of focal epileptiform activity induced by noxious stimulation [7].
  • The NMDA competitive antagonist D,L-2-amino-5-phosphonovaleric acid (D,L-AP5), administered intracerebroventricularly (0.25-2 mumol), elicited phencyclidine-like stereotyped behaviour and cortical desynchronization, but failed to elicit/sigma typical cortical complexes [8].
  • The physiological effectiveness of NB stimulation was assessed later while subjects were anesthetized with urethane by noting whether stimulation produced cortical desynchronization [9].
  • Intravenous administration of methadone (0.2-0.5 mg/kg) markedly increased the threshold for cortical desynchronization by stimulation of the MRF [10].

Gene context of Cortical Synchronization

  • 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 [11].
  • Gamma band oscillatory activity mediates in sensory and cognitive operations, with a role in stimulus-related cortical synchronization, but is reportedly reduced in the time window of the P300 response [12].
  • Selective DA-receptor agonists induce biphasic effects, with low doses decreasing and large doses increasing cortical desynchronization and motility [13].
  • In rats, PCP (1.25-10 mg/kg i.p.) induced three dose-dependent EEG stages: 1) increase of the cortical desynchronization periods; 2) increase of the amplitude of cortical background activity; 3) appearance of cortical slow wave-spike complexes [14].

Analytical, diagnostic and therapeutic context of Cortical Synchronization


  1. Synchronized paroxysmal activity in the developing thalamocortical network mediated by corticothalamic projections and "silent" synapses. Golshani, P., Jones, E.G. J. Neurosci. (1999) [Pubmed]
  2. Sleep-wake states and cortical synchronization control by pregnenolone sulfate into the pedunculopontine nucleus. Darbra, S., George, O., Bouyer, J.J., Piazza, P.V., Le Moal, M., Mayo, W. J. Neurosci. Res. (2004) [Pubmed]
  3. Pyridostigmine enhances glutamatergic transmission in hippocampal CA1 neurons. Pavlovsky, L., Browne, R.O., Friedman, A. Exp. Neurol. (2003) [Pubmed]
  4. Diphenylhydantoin potentiates the EEG and behavioural effects induced by N-methyl-D-aspartate antagonists in rats. Popoli, P., Pèzzola, A., Sagratella, S. Psychopharmacology (Berl.) (1994) [Pubmed]
  5. Different capability of N-methyl-D-aspartate antagonists to elicit EEG and behavioural phencyclidine-like effects in rats. Sagratella, S., Pezzola, A., Popoli, P., Scotti de Carolis, A.S. Psychopharmacology (Berl.) (1992) [Pubmed]
  6. The effects of serotonin injections into the locus coeruleus on ponto geniculo occipital (PGO) waves and cortical EEG pattern in cats. Kostowski, W., Gumulka, W., Jerlicz, M. Polish journal of pharmacology and pharmacy. (1975) [Pubmed]
  7. Alteration of neocortical activity in response to noxious stimulation: participation of the dorsal raphe. Thompson, P.M., Zebrowski, G., Neuman, R.S. Neuropharmacology (1991) [Pubmed]
  8. Behavioural and electroencephalographic effects of excitatory amino acid antagonists and sigma opiate/phencyclidine-like compounds in rats. Sagratella, S., Benedetti, M., Pézzola, A., Scotti de Carolis, A. Neuropharmacology (1989) [Pubmed]
  9. Induction of long-term receptive field plasticity in the auditory cortex of the waking guinea pig by stimulation of the nucleus basalis. Bjordahl, T.S., Dimyan, M.A., Weinberger, N.M. Behav. Neurosci. (1998) [Pubmed]
  10. The effects of methadone on cortical and subcortical EEG in the rat. Mitra, J., O'Brien, C.P., Sloviter, H.A. Electroencephalography and clinical neurophysiology. (1981) [Pubmed]
  11. Candidate gene analysis of the succinic semialdehyde dehydrogenase gene (ALDH5A1) in patients with idiopathic generalized epilepsy and photosensitivity. Lorenz, S., Heils, A., Taylor, K.P., Gehrmann, A., Muhle, H., Gresch, M., Becker, T., Tauer, U., Stephani, U., Sander, T. Neurosci. Lett. (2006) [Pubmed]
  12. Time dynamics of stimulus- and event-related gamma band activity: contrast-VEPs and the visual P300 in man. Sannita, W.G., Bandini, F., Beelke, M., De Carli, F., Carozzo, S., Gesino, D., Mazzella, L., Ogliastro, C., Narici, L. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. (2001) [Pubmed]
  13. Catecholamines and the sleep-wake cycle. I. EEG and behavioral arousal. Monti, J.M. Life Sci. (1982) [Pubmed]
  14. Non-opioid antitussives potentiate some behavioural and EEG effects of N-methyl-D-aspartate channel blockers. Diana, G., Scotti de Carolis, A., Popoli, P., Pezzola, A., Sagratella, S. Life Sci. (1993) [Pubmed]
  15. EEG and behavioural effects of polyamines (spermine and spermidine) on rabbits. Bo, P., Giorgetti, A., Camana, C., Savoldi, F. Pharmacol. Res. (1990) [Pubmed]
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