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

• Both 5-HT and quipazine injected into the locus coeruleus decreased the frequency of reserpine-induced PGO waves and increased cortical synchronization [6].

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

• Spermine caused a dose-related cortical synchronization associated with a partial sedation; spermidine induced cortical synchronization at a low dose without any behavioural changes while at higher dose (after perfusion) cortical desychronization with an arousal behavioural pattern occurred [15].

References