Differential effects of convulsants on visually evoked responses in the albino rat

Bigler, Erin D.; Shearer, Donald E.; Dustman, Robert E.; Fleming, Donovan E.

doi:10.1016/0091-3057(78)90273-3

Cited by 13 publications

(3 citation statements)

References 36 publications

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“…After 1 mg/kg of PHY in rats, an amplitude reduction in the middle component and an increase in the first component was shown [46]. 0.4 mg/kg of PHY in the rat at f-VEP [47,48] and 0.8 mg/kg in the cat at pattern reversal VEPs [49] suppressed all amplitude component; on the other hand, after 1 mg/kg Arakawa et al [50] showed only a reduction in the P1N1 component. In the superior colliculus of rats treated with 0.4 mg/kg of PHY, Hetzler and Melk [51] confirmed that the amplitudes of P1 and P3 components were depressed and the P4 component was enhanced.…”

Section: Discussionmentioning

confidence: 99%

“…antiamyloid agents, antioxidants, antiinflammatory drugs, estrogens) may interfere with specific steps of the disease. Although it was demonstrated that the cholinergic approach is not the only one, 48 Neuropsychobiology 1999;40: [47][48][49][50][51][52][53][54][55][56] Tebano/Luzi/Palazzesi/Pomponi/Loizzo the most promising therapy is the administration of acethylcholinesterase (AChE) inhibitors. These drugs represent the only primary treatment options approved by the Food and Drug Administration for Alzheimer disease [4].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Cholinergic Drugs on Neocortical EEG and Flash-Visual Evoked Potentials in the Mouse

Tebano

Luzi²,

Palazzesi³

et al. 1999

Neuropsychobiology

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The effects of single intraperitoneal injection of two cholinesterase inhibitors, physostigmine (PHY; 0.01, 0.025, 0.05, 0.1, 0.2 mg/kg) and heptylphysostigmine (HEP; 0.5, 2, 6 mg/kg) on electroencephalographic (EEG) activity and flash visual evoked potentials (f-VEP) in the occipital cortex were compared in DBA/2 mice. EEG spectral analysis of awake periods showed that PHY at all doses and HEP at 2 mg/kg induced an increase of power in the 4.25- to 7-Hz frequency band. Furthermore, PHY at the higher doses and HEP at all doses induced a decrease of power in the 7.25- to 12-Hz frequency band, while the lower doses of PHY (0.01, 0.025 mg/kg) produced an increase of this band. EEG effects elicited by the two drugs were similar, when doses displaying analogous biochemical effects (acetylcholinesterase inhibition) were used (i.e. 0.01 and 0.025 mg/kg of PHY versus 0.5 and 2 mg/kg of HEP). PHY and HEP induced similar changes in f-VEPs. Amplitudes of early and late components (P1N1, N1P2, P4N4 and particularly N1P3) were enhanced, while amplitudes of middle components were depressed after all doses. The peak latency measures were generally delayed, even though, after the lower doses, a trend to a latency reduction was evident in late components. This finding might indicate a possible effect on stimulus speed diffusion by ‘low therapeutic’ doses, analogous to the ones used in men. Our data show that both drugs are effective in modifying EEG and f-VEP parameters connected with brain cholinergic function, although in a very narrow dose range.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Cholinergic Drugs on Neocortical EEG and Flash-Visual Evoked Potentials in the Mouse

Tebano

Luzi²,

Palazzesi³

et al. 1999

Neuropsychobiology

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“…The amplitude of FEP peak N 166 is reported to be modified by pharmacologic agents reported to interact with non-monoamine-based neurotransmitter systems. Treatment of rats with physostigmine (a cholinesterase inhibitor) has been shown to decrease the amplitude of peak P3-N3 (P 102 N 166 ) and/or the PhAD (of which peak N 166 is the first portion) (Bigler and Fleming, 1976b;Bigler et al, 1978). Similarly, the amplitude of peak P3-N3 was reduced by the anticonvulsant trimethadione (Shearer et al, 1976).…”

Section: Figmentioning

confidence: 99%

Disassociation of Carbon Disulfide-Induced Depression of Flash-Evoked Potential Peak N166 Amplitude and Norepinephrine Levels

Graff

Herr²

2003

Toxicological Sciences

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Exposure to organic solvents frequently causes functional impairment of the central nervous system (CNS). One method to examine the effects of solvent exposure on visual function is flash-evoked potentials (FEPs). Greater knowledge of the role of various neurotransmitters in generating FEP peaks would be beneficial for understanding the basis of neurotoxicant-induced changes. FEP peak N166 is influenced by the psychological construct of arousal, which in turn is believed to be influenced by the function of neurons containing norepinephrine (NE). Because of its known effects on both NE and FEPs, we utilized carbon disulfide (CS2) as a means to examine the possible role of NE in modulating the amplitude of FEP peaks N36 and N166. Our hypothesis was that CS2-induced alterations in cortical NE levels would be correlated with changes in FEP peak N36 and N166 amplitudes. Adult male Long-Evans rats were implanted with electrodes over their visual cortex and allowed to recover. To develop peak N166, FEPs were recorded for two days prior to dosing. On the third day, FEPs were recorded prior to dosing, and one group of animals was sacrificed to serve as pretreatment controls. The remaining animals were dosed ip with 0 (corn oil vehicle; 2 ml/kg), 100, 200, or 400 mg/kg CS2. The treated animals were retested at 1, 4, 8, or 24 h after dosing, immediately sacrificed, and samples of the cortex, cerebellum, striatum, and brain stem were frozen for high performance liquid chromatography (HPLC) analysis of monoamine levels. Treatment with CS2 decreased peak N166 amplitude at 1 h, and peak N36 amplitude was depressed at 4 h, relative to the subject's pretreatment values. Peak latencies were increased, and colonic temperature was decreased by treatment with CS2. Exposure to CS2 depressed NE levels in the cortex, brain stem, and cerebellum 4 h after treatment. Conversely, at 4 h, levels of dopamine (DA) and its metabolite 3,4-dihydroxyphenylacetic acid were increased in the brain stem and cerebellum, and levels of the DA metabolite homovanillic acid were increased in the brain stem. Levels of serotonin were unaffected by CS2 treatment. There was a slight increase in striatal levels of the serotonin metabolite 5-hydroxyindole acetic acid at all times after treatment with CS2. There was no apparent association between the decreases in NE levels and the reductions in amplitudes for peaks N36 and N166. The neurochemical mechanism for CS2-induced reductions in FEP peak amplitudes remains to be determined.

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Effects of iontophoretic application of convulsants on the sensory responses of neurons in the brain-stem reticular formation

Faingold

Hoffmann

Caspary

1984

Electroencephalography and Clinical Neurophysiology

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Differential effects of convulsants on visually evoked responses in the albino rat

Cited by 13 publications

References 36 publications

Effects of Cholinergic Drugs on Neocortical EEG and Flash-Visual Evoked Potentials in the Mouse

Effects of Cholinergic Drugs on Neocortical EEG and Flash-Visual Evoked Potentials in the Mouse

Disassociation of Carbon Disulfide-Induced Depression of Flash-Evoked Potential Peak N166 Amplitude and Norepinephrine Levels

Effects of iontophoretic application of convulsants on the sensory responses of neurons in the brain-stem reticular formation

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