Disease relevance of Photic Stimulation

• To separate these effects, we consecutively applied two different stimuli: visual stimulation (black/white checkerboard alternating with a frequency of 8 Hz) and hypercapnia (inspiration of 5% CO2) [1].
• METHODS: In 7 Senegalese baboons, we examined the effect of unilateral claustral lesioning on generalized convulsive seizures either kindled from the amygdaloid nucleus (AM) and cingulate cortex (CG) or induced by intermittent photic stimulation (IPS) after systemic administration of D,L-allylglycine (AG) [2].
• During rare target visual stimulation, P300 latency and reaction time in the patients with Parkinson's disease and reaction time in the normal subjects were gradually prolonged as the ISI increased [3].
• EEG abnormalities were activated by hyperventilation and modified neither by intermittent photic stimulation, nor by acetazolamide therapy [4].
• METHODS: We examined the functional blood flow response of the brain after visual stimulation (reversing checkerboard pattern), and cerebral vasoreactivity following acetazolamide (15 mg/kg) with [15O]H2O and positron emission tomography (PET) in Fabry disease [5].

Psychiatry related information on Photic Stimulation

• This study characterized brain energy metabolism in lithium-resistant bipolar disorder using the photic-stimulation paradigm [6].
• METHOD: Brain activation induced by periodic (monocular) 8 Hz visual stimulation was detected by fMRI in five patients with unexplained visual loss who fulfilled DSM-IV criteria for conversion disorder, and seven normal volunteers [7].
• The anticonvulsant actions of memantine (1,3-dimethyl-5-aminoadamantane) have been evaluated in mice (seizures induced by maximal electroshock, pentylenetetrazol, bicuculline, picrotoxin, 3-mercaptopropionic acid and N-methyl-D,L-aspartic acid) and in photosensitive baboons, Papio Papio (clonic responses to intermittent photic stimulation) [8].
• METHODS: EEG (with photic stimulation and hand/foot tapping) and median nerve somatosensory evoked potentials were recorded in a 8-year-old male patient with FRAXE mental retardation (diagnosis confirmed by molecular genetic analysis) and speech disturbances [9].
• AIM: An objective evaluation of the psychogenic cause of erectile dysfunction by performing the visual stimulation tumescence and rigidity (VSTR) test and sildenafil citrate test, together with the effectiveness of sildenafil citrate medication on impotence caused by different etiologies [10].

High impact information on Photic Stimulation

• Adult Drosophila were fed with tritium labeled deoxyglucose prior to a 5-hour period of visual stimulation [11].
• We identified candidate regulatory neurons by immunocytochemistry for immediate-early gene products, ZENK (zif268, Egr-1) and Fos, after appropriate visual stimulation [12].
• This differential plasticity may help explain the distinct roles of these receptors in shaping the relay neuron response to visual stimulation with the AMPA component being important for transient responses, while sustained high frequency responses rely more on the NMDA component [13].
• Four hours of visual stimulation or addition of intracellular spermine increased rectification in immature neurons [14].
• We studied CBF responses to bolus lactate injection at rest and in visual stimulation by using positron-emission tomography in seven healthy volunteers [15].

Chemical compound and disease context of Photic Stimulation

• EEG records of 408 consecutive patients, after a single epileptic seizure, were examined for evidence of a paroxysmal response to photic stimulation (PPD) [16].
• In the group of 37 patients with chronic carbon disulphide (CS2) intoxication manifested by encephalopathy, polyneuropathy or psycho-organic syndrome and complaining for vertigo, a statokinesiometric test was performed with open and closed eyes, and with visual stimulation [17].

Biological context of Photic Stimulation

• Moreover, eEF2 phosphorylation is induced by visual stimulation, and NMDAR blockade before stimulation eliminates this effect [18].
• In relation to the rhythms of GH secretion, recent studies have shown that nocturnal photic stimulation induces gene expression not only in the SCN but also in periventricular (PeN) somatostatin (SRIF) neurons [19].
• The representation of the visual field in the ventral lateral geniculate nucleus (LGNv) was studied in rats anesthetized with urethane by recording the response of single units to visual stimulation [20].
• The present study investigated reaction time (RT) and event-related potential (ERP) differences between gap and step conditions using visual stimulation and manual responses [21].
• Rapid visual stimulation induces N-methyl-D-aspartate receptor-dependent sensory long-term potentiation in the rat cortex [22].

Anatomical context of Photic Stimulation

• Bolus lactate injection augmented the CBF response to visual stimulation by 38-53% in regions of the visual cortex but had no effect on the resting CBF or the whole-brain CBF [15].
• Autonomic responsiveness to affective visual stimulation in temporal lobe epilepsy [23].
• In rats given increasing frequencies of photoflash visual stimulation, the two methods gave different results for glucose utilization within visual pathways [24].
• Fos expression in the suprachiasmatic nucleus of rats induced by photic stimulation (50 lux, 30 min) during the early subjective night was inhibited by treatment with nociceptin (0.5-10 nM, i.c.v.). The effect of nociceptin (10nM, i.c.v.) was blocked by pretreatment with compound B (30 mg/kg, i.p) [25].
• Somatostatin neurons in the periventricular nucleus which project to the external layer of the median eminence and are involved in regulation of growth hormone release showed NGFI-A gene expression corresponding to the duration of photic stimulation [26].

Associations of Photic Stimulation with chemical compounds

• Localized 1H NMR measurement of glucose consumption in the human brain during visual stimulation [27].
• When corrected by the global values, the magnitudes of the CBF and CMRO(2) responses to visual stimulation after acetazolamide administration were less than those before (20% vs 38% in CBF and -9% vs 3% in CMRO(2)) [28].
• Reversal appears possible by increasing melatonin levels with either appropriately timed exposure to photic stimulation and/or appropriately timed administration of exogenous melatonin [29].
• They used flow-sensitive alternating inversion recovery (FAIR) scan sequences to measure CBF and blood oxygen level-dependent (BOLD) sensitive T2* scan sequences during visual stimulation to measure neuronal activation before and after cocaine and saline infusions [30].
• As the fMRI baseline signal increased linearly with expired CO2 from hypocapnic to hypercapnic levels, the magnitude of the BOLD response to visual stimulation decreased linearly [31].

Gene context of Photic Stimulation

• In the absence of photic stimulation, inhibition of the MAPK pathway did not alter basal gene product expression levels [32].
• Immunohistochemical and Western analysis were used to show that photic stimulation during the early and late night triggered the phosphorylation of RSK-1 at two sites that are targeted by ERK [33].
• However, in contrast to the phase advance seen in wild-type mice, PAC1(-)/- mice responded with phase delays after photic stimulation [34].
• MSK1 phosphorylation was more responsive to late-night than early-night photic stimulation, indicating that MSK1 may differentially contribute to light-induced phase advancing and phase delaying of the clock [35].
• Here, we show that visual stimulation after a brief period of dark rearing caused a transient ERK activation in the visual cortex [36].

Analytical, diagnostic and therapeutic context of Photic Stimulation

• A technique to localize activation in the human brain with technetium-99m-HMPAO SPECT: a validation study using visual stimulation [37].
• The present study reports that such megadoses of vitamin C do significantly effect an objective electrophysiological measure, i.e., electroencephalogram (EEG) driving responses to photic stimulation [38].
• Corticosterone also caused an inhibition of paraventricular multiple-unit activity in response to acoustic stimulation, which was more effective than for photic stimulation, with complete blockade of response occurring with a dose of 1 mg corticosterone [39].
• The topographic organization of the orientation column system in the tree shrew striate cortex was examined by using 2-deoxyglucose autoradiography to map the cortical sites of increased metabolic activity produced by visual stimulation with stripes of a single orientation [40].
• The objective of this study was to test for evidence of alteration of BOLD signal response of occipital cortex, a region with a relatively low concentration of neuronal nicotine receptors, to photic stimulation during intravenous infusion of nicotine [41].

References