Alterations in flash evoked potentials (FEPs) in rats produced by 3,3′-iminodipropionitrile (IDPN),

Herr, David W.; King, Deborah; Barone, Stanley; Crofton, Kevin M.

doi:10.1016/0892-0362(95)02007-1

Cited by 27 publications

(14 citation statements)

References 51 publications

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“…VEP components found in our laboratory are in considerable agreement with those found in other laboratories regarding general trends in normative data (Dyer, Clark, & Boyes, 1987;Sisson & Siegel, 1998). The exact generators of the P1 peak have not been determined, but it is suggested that this component corresponds to the upper nasal portions of the visual field in areas 17 and 18a (Herr, King, Barone, & Crofton, 1995). P2 components of VEPs are believed to reflect the cortical response to the initial afferent volley from the retina through the lateral geniculate nucleus.…”

Section: Discussionsupporting

confidence: 78%

“…P2 and N2 peaks may represent hyperpolarization and depolarization of stellate cells in lamina IV, respectively (Herr et al, 1995;Kraut, Arezzo, & Vaughan, 1985). Even though the exact mechanism has not known, yet it is accepted that P3 reflects the excitatory postsynaptic response of pyramidal cells in the upper lamina (Herr et al, 1995), and is accepted as an early sign parameter in optic pathway (Celesia, 1984). HO activity was inhibited either by two protoporphyrin products to examine the specificity of HO inhibitors on VEPs.…”

Section: Discussionmentioning

confidence: 99%

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The Effect of Heme Oxygenase Inhibition on Visual Evoked Potentials

Savcioglu

Akpınar

Yargiçoğlu

et al. 2009

International Journal of Neuroscience

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This study investigated the effect of heme oxygenase (HO) inhibition on visual evoked potentials (VEPs). HO catalyzes the oxidative degradation of heme. Products of HO reaction are biliverdin, ferrous iron, and carbon monoxide (CO). CO is a signal molecule and is an endogenous modulator in the soluble guanylate cyclase/cyclic guanosine monophosphate signaling pathway. Rats were treated with HO inhibitors tin protoporphyrin IX (SnPP IX) or zinc protoporphyrin IX (ZnPP IX) or HO inducer sodium arsenite (Na-arsenite). Soluble guanylate cyclase is inhibited by 1H-[1,2,3]oxydiazolo[4,3-a]quinoxalin-1-one (ODQ) and induced by 3-(5'-hydroxymethyl-2'-furyl)-1-benzyl indazole (YC-1). VEPs were recorded under mild ether anesthesia with the help of stainless steel subdermal electrodes and a photic stimulator. SnPP IX, ODQ or SnPP IX + YC-1 injections significantly prolonged latencies of P3; however, Na-arsenite shortened latency of P3. It has been shown that HO affects VEPs.

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Section: Discussionsupporting

confidence: 78%

Section: Discussionmentioning

confidence: 99%

The Effect of Heme Oxygenase Inhibition on Visual Evoked Potentials

Savcioglu

Akpınar

Yargiçoğlu

et al. 2009

International Journal of Neuroscience

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“…Moreover, 3,3ø-iminodipropionitrile induces degeneration of the vestibular sensory hair cells (Llorens et al Author for correspondence: François Gagnaire, Department of Pollutants and Health, National Institute for Research and Safety, Avenue de Bourgogne, B. P. Nae 27, 54501 Vandoeuvre Cedex, France (fax π33 3 83 50 20 96, e-mail gagnaire/inrs.fr). 1993), visual system toxicity (Moser & Boyes 1993;Herr et al 1995;Seoane et al 1999) and deafness (Wolff et al 1977;Goldey et al 1993;Crofton et al 1994); the latter being caracterised by a broad-spectrum hearing loss ranging from 0.5 kHz to 80 kHz, a hair cell loss in all turns of the organ of Corti, with a basal-to-apical gradient at the lower dosages.…”

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confidence: 99%

The Ototoxic Effects Induced in Rats by Treatment for 12 Weeks with 2‐Butenenitrile, 3‐Butenenitrile and cis‐2‐Pentenenitrile

Gagnaire¹,

Marignac²,

Ban³

et al. 2001

Pharmacology & Toxicology

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Brainstem auditory and visual evoked-potentials were studied in male Sprague-Dawley rats during subchronic oral treatment with three unsaturated aliphatic nitriles. The rats were given, by gastric intubation, doses of 10, 20 and 40 mg ¡ kg ª1 3-butenenitrile (allyl cyanide) and 25, 50 and 100 mg ¡ kg ª1 of either cis/trans-2-butenenitrile (crotononitrile) or cis-2-pentenenitrile once a day, 5 days per week for 12 weeks. Oral administration of the three unsaturated nitriles produced deafness and absence of reaction when the animals were subject to droptest. Rats in the high dosage groups exhibited a complete disappearance of the five waves of the auditory evoked-potentials. There was a decrease in the amplitudes of the 2nd component of the auditory evoked-potentials. Those changes were not reversible at the 8th week of the recovery period. A dose-dependent effect on inner and outer hair cells was observed in the organ of Corti. The basal part of the cochlea was the most affected. Though no measurements were made of systemic exposure, a tentative ranking of decreasing ototoxicity of these three unsaturated nitriles might be proposed based on the electrophysiological deficiencies and histological losses observed: 3-butenenitrile Ͼcis-2-pentenenitrile Ͼcis/trans-2-butenenitrile. Moreover, rats treated with those nitriles showed a corneal opacity as well as a decrease in the amplitude and lengthening of the peak latencies of the visual evoked-potentials. These latter changes were reversible by the end of the 8th week of the recovery period and appeared to be related to the opacity of the cornea.

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“…Thus, changes in this portion of the VEP waveform suggest altered function in the 'front end' of the visual system. However, N 2 represents the initial excitatory response in the middle laminae to the visual stimulus, and the subsequent positive peak P 3 was reported to refl ect the excitatory post-synaptic response of pyramidal cells in the upper laminae (Herr et al 1995). P 2 and N 2 peaks may represent hyperpolarization and depolarization of stellate cells in laminae IV, respectively (Kraut et al 1985;Herr et al 1995).…”

Section: Discussionmentioning

confidence: 99%

“…However, N 2 represents the initial excitatory response in the middle laminae to the visual stimulus, and the subsequent positive peak P 3 was reported to refl ect the excitatory post-synaptic response of pyramidal cells in the upper laminae (Herr et al 1995). P 2 and N 2 peaks may represent hyperpolarization and depolarization of stellate cells in laminae IV, respectively (Kraut et al 1985;Herr et al 1995). It was previously shown that certain toxicological agents, such as carbon disulfi de (Graff and Herr 2003) and dichlo romethane, 1,3 dichloropropane and 1,2 dichlorobenzene (Herr and Boyes 1997), affect different VEP components via different neurotransmitter levels that generate and modulate VEP peaks.…”

Section: Discussionmentioning

confidence: 99%

Exercise Improves Visual Deficits Tested by Visual Evoked Potentials in Streptozotocin-Induced Diabetic Rats

Özkaya

Ağar

Hacioglu

et al. 2007

Tohoku J. Exp. Med.

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Visual evoked potentials (VEP) can be used as an objective non-invasive method to study the electrical activity of the visual system. Latency and amplitude measurements of VEP demonstrated that diabetes mellitus has been associated with increases in the latencies whereas the amplitude measurements revealed contradictory results. Although physical exercise has been reported to reduce the complications of diabetes mellitus, the effect of exercise on the visual system remains unknown. We investigated the effects of long-term moderate physical exercise on VEP in streptozotocin (STZ)-diabetic rats. We also measured brain thiobarbituric acid-reactive substances (TBARS) to explore the possible contribution of lipid peroxidation on the visual system. Animals were divided into four groups: control (C), control exercise (CE), diabetic (D) and diabetic exercise (DE) groups. Diabetes was induced by a single intraperitoneal injection of STZ (60 mg/kg). Three days after the confi rmation of diabetes, DE and CE groups were trained by running on a motor-driven treadmill with a progressive eightweek programme. The animals began running at 10 m/min, 0° slope, 10 min/day and reached a level of 28 m/min, 6° slope, 60 min/day by week 8. TBARS were elevated and VEP latencies were delayed in diabetic rats, indicating diabetes-induced defects in the optic pathway. These prolonged latencies were restored by exercise training. VEP amplitudes of the DE group were found unaltered with the exception of a decrement in P 2 N 2 which represents an early component of VEP, suggesting that exercise improves visual system defects in diabetic animals at different levels of the optic pathway. diabetes mellitus; visual evoked potentials; exercise; lipid peroxidation; rat © 2007 Tohoku University Medical PressPhysical exercise is well known to have many benefi cial effects on human health. Recently, attention has largely focused on the increase of free radicals generated during exercise, especially during aerobic activities. This increase is related to the elevation of electron transport fl ux, mitochondrial oxygen consumption, energy demand, oxygen supply and body

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Alterations in flash evoked potentials (FEPs) in rats produced by 3,3′-iminodipropionitrile (IDPN),

Cited by 27 publications

References 51 publications

The Effect of Heme Oxygenase Inhibition on Visual Evoked Potentials

The Effect of Heme Oxygenase Inhibition on Visual Evoked Potentials

The Ototoxic Effects Induced in Rats by Treatment for 12 Weeks with 2‐Butenenitrile, 3‐Butenenitrile and cis‐2‐Pentenenitrile

Exercise Improves Visual Deficits Tested by Visual Evoked Potentials in Streptozotocin-Induced Diabetic Rats

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