Visual Evoked Potentials Components Research Articles

Effect of ethanol on the visual-evoked potential in rat: dynamics of ON and OFF responses.

The effect of acute ethanol administration on the flash visual-evoked potential (VEP) was investigated in numerous studies. However, it is still unclear which brain structures are responsible for the differences observed in stimulus onset (ON) and offset (OFF) responses and how these responses are modulated by ethanol. The aim of our study was to investigate the pattern of ON and OFF responses in the visual system, measured as amplitude and latency of each VEP component following acute administration of ethanol. VEPs were recorded at the onset and offset of a 500 ms visual stimulus in anesthetized male Wistar rats. The effect of alcohol on VEP latency and amplitude was measured for one hour after injection of 2 g/kg ethanol dose. Three VEP components - N63, P89 and N143 - were analyzed. Our results showed that, except for component N143, ethanol increased the latency of both ON and OFF responses in a similar manner. The latency of N143 during OFF response was not affected by ethanol but its amplitude was reduced. Our study demonstrated that the activation of the visual system during the ON response to a 500 ms visual stimulus is qualitatively different from that during the OFF response. Ethanol interfered with processing of the stimulus duration at the level of the visual cortex and reduced the activation of cortical regions.

Rapid and Objective Assessment of Neural Function in Autism Spectrum Disorder Using Transient Visual Evoked Potentials.

ObjectiveThere is a critical need to identify biomarkers and objective outcome measures that can be used to understand underlying neural mechanisms in autism spectrum disorder (ASD). Visual evoked potentials (VEPs) offer a noninvasive technique to evaluate the functional integrity of neural mechanisms, specifically visual pathways, while probing for disease pathophysiology.MethodsTransient VEPs (tVEPs) were obtained from 96 unmedicated children, including 37 children with ASD, 36 typically developing (TD) children, and 23 unaffected siblings (SIBS). A conventional contrast-reversing checkerboard condition was compared to a novel short-duration condition, which was developed to enable objective data collection from severely affected populations who are often excluded from electroencephalographic (EEG) studies.ResultsChildren with ASD showed significantly smaller amplitudes compared to TD children at two of the earliest critical VEP components, P60-N75 and N75-P100. SIBS showed intermediate responses relative to ASD and TD groups. There were no group differences in response latency. Frequency band analyses indicated significantly weaker responses for the ASD group in bands encompassing gamma-wave activity. Ninety-two percent of children with ASD were able to complete the short-duration condition compared to 68% for the standard condition.ConclusionsThe current study establishes the utility of a short-duration tVEP test for use in children at varying levels of functioning and describes neural abnormalities in children with idiopathic ASD. Implications for excitatory/inhibitory balance as well as the potential application of VEP for use in clinical trials are discussed.

Effect of sodium tungstate on visual evoked potentials in diabetic rats

To evaluate the effect of sodium tungstate on visual evoked potentials (VEPs) in diabetic rats. Wistar rats were randomly divided into three groups as normal control, diabetic control and diabetic rats treated with sodium tungstate. Diabetes was induced by single intraperitoneal injection of streptozotocin (50 mg/kg). Sodium tungstate [40 mg/(kg·d)] was administered for 12wk and then VEPs were recorded. Additionally, thiobarbituric acid reactive substance (TBARS) levels were measured in brain tissues. The latencies of P1, N1, P2, N2 and P3 waves were significantly prolonged in diabetic rats compared with control group. Diabetes mellitus caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. However, prolonged latencies of VEPs for all components returned to control levels in sodium tungstate-treated group. The treatment of sodium tungstate significantly decreased brain TBARS levels and depleted the prolonged latencies of VEP components compared with diabetic control group. Sodium tungstate shows protective effects on visual pathway in diabetic rats, and it can be worthy of further study for potential use.

ID 197 – Altered recovery from inhibitory repetitive transcranial magnetic stimulation (rTMS) in subjects with photosensitive epilepsy

To investigate functional changes underlying photosensitivity, we studied the response of the visual cortex to low-frequency, inhibitory repetitive transcranial magnetic stimulation (rTMS) in patients with photosensitive seizures and healthy volunteers. Visual evoked potentials (VEPs) triggered by grating stimuli of different contrasts were recorded in both hemispheres before and after functional inactivation of the occipital cortex of one side via low-frequency rTMS (0.5 Hz for 20′). VEPs were recorded in before (T0), immediately after (T1) and 45′ following the completion of rTMS (T2). Baseline amplitudes of the early VEP components (N1 and P1) were enhanced in photosensitive subjects. At T1, rTMS produced an inhibitory effect on VEPs amplitudes at all contrasts in the targeted side, and a concurrent facilitation of responses in the contralateral hemisphere. While the relative variation with respect to pre-rTMS values was similar in photosensitive patients and controls at T1, robust changes appeared in the recovery phase (T2). Visual responses recovered more quickly in the stimulated hemisphere, and disinhibition persisted in the contralateral side of photosensitive subjects. The rapid recovery of excitability and the persistent transcallosal disinhibition following perturbation of cortical activity may play a role in the pathophysiology of photosensitive epilepsy.

2100-MHz electromagnetic fields have different effects on visual evoked potentials and oxidant/antioxidant status depending on exposure duration

The purpose of the present study was to investigate the duration effects of 2100-MHz electromagnetic field (EMF) on visual evoked potentials (VEPs) and to assess lipid peroxidation (LPO), nitric oxide (NO) production and antioxidant status of EMF exposed rats. Rats were randomized to following groups: Sham rats (S1 and S10) and rats exposed to 2100-MHz EMF (E1 and E10) for 2h/day for 1 or 10 weeks, respectively. At the end of experimental periods, VEPs were recorded under anesthesia. Brain thiobarbituric acid reactive substances (TBARS) and 4-hydroxy-2-nonenal (4-HNE) levels were significantly decreased in the E1 whereas increased in the E10 compared with their control groups. While brain catalase (CAT), glutathione peroxidase (GSH-Px) activities and NO and glutathione (GSH) levels were significantly increased in the E1, reduction of superoxide dismutase (SOD) activity was detected in the same group compared with the S1. Conversely, decreased CAT, GSH-Px activities and NO levels were observed in the E10 compared with the S10. Latencies of all VEP components were shortened in the E1 compared with the S1, whereas latencies of all VEP components, except P1, were prolonged in the E10 compared with the S10. There was a positive correlation between all VEP latencies and brain TBARS and 4-HNE values. Consequently, it could be concluded that different effects of EMFs on VEPs depend on exposure duration. In addition, our results indicated that short-term EMF could provide protective effects, while long-term EMF could have an adverse effect on VEPs and oxidant/antioxidant status.

Optic Nerve Dysfunction in Obstructive Sleep Apnea: An Electrophysiological Study.

The aim of this study was to evaluate the integrity of the visual system in patients affected by obstructive sleep apnea (OSA) by means of electroretinogram (ERG) and visual evoked potential (VEP). We performed electrophysiological study of the visual system in a population of severe OSA (apnea-hypopnea events/time in bed ≥ 30/h) patients without medical comorbidities compared to a group of healthy controls similar for age, sex, and body mass index. Patients and controls did not have visual impairment or systemic disorders with known influence on the visual system. ERG and VEP were elicited by a reversal pattern generated on a television monitor at low (55') and high (15') spatial frequencies stimulation. Daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS) in both patients and controls. In comparison with healthy controls (n = 27), patients with OSA (n = 27) showed a significant latency delay coupled with a significant amplitude reduction of P100 wave of VEP at all spatial frequencies in both eyes. No significant differences between groups were detected as concerning ERG components. No correlations were found between polygraphic parameters, ESS scores, or VEP and ERG components in OSA patients. This study documented that patients with OSA, without medical comorbidities, present VEP alteration as documented by lower amplitude and longer latency of the P100 component than healthy controls. These altered electrophysiological findings may be the expression of optic nerve dysfunction provoked by hypoxia, acidosis, hypercarbia and airway obstruction, frequently observed in patients with OSA. Hence, we hypothesize that OSA per se may impair optic nerve function.

LTP-like plasticity in the visual system and in the motor system appear related in young and healthy subjects.

LTP-like plasticity measured by visual evoked potentials (VEP) can be induced in the intact human brain by presenting checkerboard reversals. Also associated with LTP-like plasticity, around two third of participants respond to transcranial magnetic stimulation (TMS) with a paired-associate stimulation (PAS) protocol with a potentiation of their motor evoked potentials. LTP-like processes are also required for verbal and motor learning tasks. We compared effect sizes, responder rates and intercorrelations as well as the potential influence of attention between these four assessments in a group of 37 young and healthy volunteers. We observed a potentiation effect of the N75 and P100 VEP component which positively correlated with plasticity induced by PAS. Subjects with a better subjective alertness were more likely to show PAS and VEP potentiation. No correlation was found between the other assessments. Effect sizes and responder rates of VEP potentiation were higher compared to PAS. Our results indicate a high variability of LTP-like effects and no evidence for a system-specific nature. As a consequence, studies wishing to assess individual levels of LTP-like plasticity should employ a combination of multiple assessments.

Threat modulates neural responses to looming visual stimuli.

Objects on a collision course with an observer produce a specific pattern of optical expansion on the retina known as looming, which in theory exactly specifies the time-to-collision (TTC) of approaching objects. It was recently demonstrated that the affective content of looming stimuli influences perceived TTC, with threatening objects judged as approaching sooner than non-threatening objects. Here, the neural mechanisms by which perceived threat modulates spatiotemporal perception were investigated. Participants judged the TTC of threatening (snakes, spiders) or non-threatening (butterflies, rabbits) stimuli, which expanded in size at a rate indicating one of five TTCs. Visual-evoked potentials (VEPs) and oscillatory neural responses measured with electroencephalography were analysed. The arrival time of threatening stimuli was underestimated compared with non-threatening stimuli, though an interaction suggested that this underestimation was not constant across TTCs. Further, both speed of approach and threat modulated both VEPs and oscillatory responses. Speed of approach modulated the N1 parietal and oscillations in the beta band. Threat modulated several VEP components (P1, N1 frontal, N1 occipital, early posterior negativity and late positive potential) and oscillations in the alpha and high gamma band. The results for the high gamma band suggest an interaction between these two factors. Previous evidence suggests that looming stimuli activate sensorimotor areas, even in the absence of an intended action. The current results show that threat disrupts the synchronization over the sensorimotor areas that are likely activated by the presentation of a looming stimulus.

Effect of mechanical tactile noise on amplitude of visual evoked potentials: multisensory stochastic resonance.

The present investigation documents the electrophysiological occurrence of multisensory stochastic resonance in the human visual pathway elicited by tactile noise. We define multisensory stochastic resonance of brain evoked potentials as the phenomenon in which an intermediate level of input noise of one sensory modality enhances the brain evoked response of another sensory modality. Here we examined this phenomenon in visual evoked potentials (VEPs) modulated by the addition of tactile noise. Specifically, we examined whether a particular level of mechanical Gaussian noise applied to the index finger can improve the amplitude of the VEP. We compared the amplitude of the positive P100 VEP component between zero noise (ZN), optimal noise (ON), and high mechanical noise (HN). The data disclosed an inverted U-like graph for all the subjects, thus demonstrating the occurrence of a multisensory stochastic resonance in the P100 VEP.

A VEP study in sleeping and awake one-month-old infants and its relation with social behavior

With the present study we aimed to analyze the relationship between infants’ behavior and their visual evoked-potential (VEPs) response. Specifically, we want to verify differences regarding the VEP response in sleeping and awake infants and if an association between VEP components, in both groups, with neurobehavioral outcome could be identified. To do so, thirty-two full-term and healthy infants, approximately 1-month of age, were assessed through a VEP unpatterned flashlight stimuli paradigm, offered in two different intensities, and were assessed using a neurobehavioral scale. However, only 18 infants have both assessments, and therefore, these is the total included in both analysis. Infants displayed a mature neurobehavioral outcome, expected for their age. We observed that P2 and N3 components were present in both sleeping and awake infants. Differences between intensities were found regarding the P2 amplitude, but only in awake infants. Regression analysis showed that N3 amplitude predicted an adequate social interactive and internal regulatory behavior in infants who were awake during the stimuli presentation. Taking into account that social orientation and regulatory behaviors are fundamental keys for social-like behavior in 1-month-old infants, this study provides an important approach for assessing physiological biomarkers (VEPs) and its relation with social behavior, very early in postnatal development. Moreover, we evidence the importance of the infant’s state when studying differences regarding visual threshold processing and its association with behavioral outcome.

The developmental effects of extremely low frequency electric fields on visual and somatosensory evoked potentials in adult rats

The purpose of our study was to investigate the developmental effects of extremely low frequency electric fields (ELF-EFs) on visual evoked potentials (VEPs) and somatosensory-evoked potentials (SEPs) and to examine the relationship between lipid peroxidation and changes of these potentials. In this context, thiobarbituric acid reactive substances (TBARS) levels were determined as an indicator of lipid peroxidation. Wistar albino female rats were divided into four groups; Control (C), gestational (prenatal) exposure (Pr), gestational+ postnatal exposure (PP) and postnatal exposure (Po) groups. Pregnant rats of Pr and PP groups were exposed to 50 Hz electric field (EF) (12 kV/m; 1 h/day), while those of C and Po groups were placed in an inactive system during pregnancy. Following parturition, rats of PP and Po groups were exposed to ELF-EFs whereas rats of C and Pr groups were kept under the same experimental conditions without being exposed to any EF during 68 days. On postnatal day 90, rats were prepared for VEP and SEP recordings. The latencies of VEP components in all experimental groups were significantly prolonged versus C group. For SEPs, all components of PP group, P2, N2 components of Pr group and P1, P2, N2 components of Po group were delayed versus C group. As brain TBARS levels were significantly increased in Pr and Po groups, retina TBARS levels were significantly elevated in all experimental groups versus C group. In conclusion, alterations seen in evoked potentials, at least partly, could be explained by lipid peroxidation in the retina and brain.

The effect of ingested sulfite on visual evoked potentials, lipid peroxidation, and antioxidant status of brain in normal and sulfite oxidase-deficient aged rats.

Sulfite, commonly used as a preservative in foods, beverages, and pharmaceuticals, is a very reactive and potentially toxic molecule which is detoxified by sulfite oxidase (SOX). Changes induced by aging may be exacerbated by exogenous chemicals like sulfite. The aim of this study was to investigate the effects of ingested sulfite on visual evoked potentials (VEPs) and brain antioxidant statuses by measuring superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities. Brain lipid oxidation status was also determined via thiobarbituric acid reactive substances (TBARS) in normal- and SOX-deficient aged rats. Rats do not mimic the sulfite responses seen in humans because of their relatively high SOX activity level. Therefore this study used SOX-deficient rats since they are more appropriate models for studying sulfite toxicity. Forty male Wistar rats aged 24 months were randomly assigned to four groups: control (C), sulfite (S), SOX-deficient (D) and SOX-deficient + sulfite (DS). SOX deficiency was established by feeding rats with low molybdenum (Mo) diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite in the form of sodium metabisulfite (25 mg kg(-1) day(-1)) was given by gavage. Treatment continued for 6 weeks. At the end of the experimental period, flash VEPs were recorded. Hepatic SOX activity was measured to confirm SOX deficiency. SOX-deficient rats had an approximately 10-fold decrease in hepatic SOX activity compared with the normal rats. The activity of SOX in deficient rats was thus in the range of humans. There was no significant difference between control and treated groups in either latence or amplitude of VEP components. Brain SOD, CAT, and GPx activities and brain TBARS levels were similar in all experimental groups compared with the control group. Our results indicate that exogenous administration of sulfite does not affect VEP components and the antioxidant/oxidant status of aged rat brains.

Inhibition of neutral sphingomyelinase decreases elevated levels of inducible nitric oxide synthase and apoptotic cell death in ocular hypertensive rats

Endoplasmic reticulum (ER) stress and excessive nitric oxide production via induction of inducible nitric oxide synthase (NOS2) have been implicated in the pathogenesis of neuronal retinal cell death in ocular hypertension. Neutral sphingomyelinase (N-SMase)/ceramide pathway can regulate NOS2 expression, hence this study determined the role of selective neutral sphingomyelinase (N-SMase) inhibition on retinal NOS2 levels, ER stress, apoptosis and visual evoked potentials (VEPs) in a rat model of elevated intraocular pressure (EIOP). NOS2 expression and retinal protein nitration were significantly greater in EIOP and significantly decreased with N-SMase inhibition. A significant increase was observed in retinal ER stress markers pPERK, CHOP and GRP78 in EIOP, which were not significantly altered by N-SMase inhibition. Retinal TUNEL staining showed increased apoptosis in all EIOP groups; however N-SMase inhibition significantly decreased the percent of apoptotic cells in EIOP. Caspase-3, -8 and -9 activities were significantly increased in EIOP and returned to baseline levels following N-SMase inhibition. Latencies of all VEP components were significantly prolonged in EIOP and shortened following N-SMase inhibition. Data confirm the role of nitrative injury in EIOP and highlight the protective effect of N-SMase inhibition in EIOP via down-regulation of NOS2 levels and nitrative stress.

Basic visual dysfunction allows classification of patients with schizophrenia with exceptional accuracy

Basic visual dysfunctions are commonly reported in schizophrenia; however their value as diagnostic tools remains uncertain. This study reports a novel electrophysiological approach using checkerboard visual evoked potentials (VEP). Sources of spectral resolution VEP-components C1, P1 and N1 were estimated by LORETA, and the band-effects (BSE) on these estimated sources were explored in each subject. BSEs were Z-transformed for each component and relationships with clinical variables were assessed. Clinical effects were evaluated by ROC-curves and predictive values. Forty-eight patients with schizophrenia (SZ) and 55 healthy controls participated in the study. For each of the 48 patients, the three VEP components were localized to both dorsal and ventral brain areas and also deviated from a normal distribution. P1 and N1 deviations were independent of treatment, illness chronicity or gender. Results from LORETA also suggest that deficits in thalamus, posterior cingulum, precuneus, superior parietal and medial occipitotemporal areas were associated with symptom severity. While positive symptoms were more strongly related to sensory processing deficits (P1), negative symptoms were more strongly related to perceptual processing dysfunction (N1). Clinical validation revealed positive and negative predictive values for correctly classifying SZ of 100% and 77%, respectively. Classification in an additional independent sample of 30 SZ corroborated these results. In summary, this novel approach revealed basic visual dysfunctions in all patients with schizophrenia, suggesting these visual dysfunctions represent a promising candidate as a biomarker for schizophrenia.

The cruciform model of striate generation of the early VEP, re-illustrated, not revoked: A reply to Ales et al. (2013)

Here we summarize the points raised in our dialog with Ales and colleagues on the cortical generators of the early visual evoked potential (VEP), and offer observations on the results of additional simulations that were run in response to our original comment. For small stimuli placed at locations in the upper and lower visual field for which the human VEP has been well characterized, simulated scalp projections of each of the visual areas V1, V2 and V3 invert in polarity. However, the empirically measured, earliest VEP component, “C1,” matches the simulated V1 generators in terms of polarity and topography, but not the simulated V2 and V3 generators. We thus conclude that, 1) consistent with the title of Ales et al. (2010a), polarity inversion on its own is not a sufficient criterion for inferring neuroelectric sources in primary visual cortex; but 2) inconsistent with additional claims made in Ales et al. (2010a), the simulated topographies provide additional evidence for – not against – the tenet that the C1 component is generated in V1.

Contrast sensitivity of pattern transient VEP components: Contribution from M and P pathways.

The purpose of this study was to compare contrast sensitivity estimated from transient visual evoked potentials (VEPs) elicited by achromatic pattern-reversal and pattern-onset/offset modes. The stimuli were 2-cpd, achromatic horizontal gratings presented either as a 1 Hz pattern reversal or a 300 ms onset/700 ms offset stimulus. Contrast thresholds were estimated by linear regression to amplitudes of VEP components vs. the logarithm of the stimulus contrasts, and these regressions were extrapolated to the zero amplitude level. Contrast sensitivity was defined as the inverse of contrast threshold. For pattern reversal, the relation between the P100 amplitude and log of the stimulus contrast was best described by two separate linear regressions. For the N135 component, a single straight line was sufficient. In the case of pattern onset/offset for both the C1 and C2 components, single straight lines described their amplitude vs. log contrast relations in the medium-to-low contrast range. Some saturation was observed for C2 components. The contrast sensitivity estimated from the low-contrast limb of the P100, from the N135, and from the C2 were all similar but higher than those obtained from the high-contrast limb of the P100 and C1 data, which were also similar to each other. With 2 cpd stimuli, a mechanism possibly driven by the M pathway appeared to contribute to the P100 component at medium-to-low contrasts and to the N135 and C2 components at all contrast levels, whereas another mechanism, possibly driven by the P and M pathways, appeared to contribute to the P100 component at high contrast and C1 component at all contrast levels.

The effect of different strengths of extremely low-frequency electric fields on antioxidant status, lipid peroxidation, and visual evoked potentials

The aim of the study was to investigate the effects of extremely low-frequency electric field (ELF EF) on visual evoked potential (VEP), thiobarbituric acid reactive substances (TBARS), total antioxidant status (TAS), total oxidant status (TOS), and oxidant stress index (OSI). Thirty female Wistar rats, aged 3 months, were divided into three equal groups: Control (C), the group exposed to EF at 12 kV/m strength (E12), and the group exposed to EF at 18 kV/m strength (E18). Electric field was applied to the E12 and E18 groups for 14 days (1 h/day). Brain and retina TBARS, TOS, and OSI were significantly increased in the E12 and E18 groups with respect to the control group. Also, TBARS levels were significantly increased in the E18 group compared with the E12 group. Electric fields significantly decreased TAS levels in both brain and retina in E12 and E18 groups with respect to the control group. All VEP components were significantly prolonged in rats exposed to electric fields compared to control group. In addition, all latencies of VEP components were increased in the E18 group with respect to the E12 group. It is conceivable to suggest that EF-induced lipid peroxidation may play an important role in changes of VEP parameters.

Hemispheric differences in VEPs to lateralised stimuli are a marker of recovery from neglect

Visual-evoked potentials (VEPs) were recorded in seventeen patients with unilateral lesions of the right hemisphere (RH) and visuospatial neglect. Hemispheric differences were detected for VEP components in the time window from 130 to 280 msec; this result replicates data from a previous study using a larger group of patients (Di Russo et al., 2008). Three patients were tested twice; their hemispheric differences, i.e., the differences in latency and amplitude of VEPs to ipsilesional and contralesional stimuli, were evaluated at the beginning and end of visuospatial rehabilitation training for neglect. The hemispheric differences were limited to components anterior N1 (N1a), posterior N1 (N1p) and P2 (not C1 and P1) and showed a significant decrease after training; amelioration at the behavioural level was also observed. Fourteen patients were tested only once, at different steps of their training. For the overall group, we determined the correlation between VEP hemispheric differences and the number of sessions attended by the patients at the time of VEP recording. The correlation was negative, the higher the number of sessions, the lower the hemispheric asymmetry, and high, ranging from .45 to .64, for both the latency and amplitude of the N1p and P2 components, and for the amplitude of the N1a component. The correlation between VEP hemispheric differences and time from onset (TFO) of the pathological event was not significant. Overall, the hemispheric differences between specific components of the VEP responses to lateralised stimuli appear to be a good marker of recovery from neglect.

Impaired early visual response modulations to spatial information in chronic schizophrenia

Early visual processing stages have been demonstrated to be impaired in schizophrenia patients and their first-degree relatives. The amplitude and topography of the P1 component of the visual evoked potential (VEP) are both affected; the latter of which indicates alterations in active brain networks between populations. At least two issues remain unresolved. First, the specificity of this deficit (and suitability as an endophenotype) has yet to be established, with evidence for impaired P1 responses in other clinical populations. Second, it remains unknown whether schizophrenia patients exhibit intact functional modulation of the P1 VEP component; an aspect that may assist in distinguishing effects specific to schizophrenia. We applied electrical neuroimaging analyses to VEPs from chronic schizophrenia patients and healthy controls in response to variation in the parafoveal spatial extent of stimuli. Healthy controls demonstrated robust modulation of the VEP strength and topography as a function of the spatial extent of stimuli during the P1 component. By contrast, no such modulations were evident at early latencies in the responses from patients with schizophrenia. Source estimations localized these deficits to the left precuneus and medial inferior parietal cortex. These findings provide insights on potential underlying low-level impairments in schizophrenia.

Manganese porphyrin reduces retinal injury induced by ocular hypertension in rats

This study aimed to clarify the possible therapeutic benefit of preferential nitric oxide synthase (NOS) inhibition and catalytic antioxidant Mn (III) meso-tetrakis ( N-n-hexylpyridinium-2-yl) porphyrin (MnTnHex-2-PyP 5+) treatment in a rat model of elevated intraocular pressure (EIOP). Rats were randomly divided into different experimental groups which received either intraperitoneal MnTnHex-2-PyP 5+ (0.1 mg/kg/day), intragastric NOS inhibitor (S-methylthiourea: SMT; 5 mg/kg/day) or both agents for a period of 6 weeks. Ocular hypertension was induced by unilaterally cauterizing three episcleral vessels and the unoperated eye served as control. Neuroprotective effects of given treatments were determined via electrophysiological measurements of visual evoked potentials (VEP) while retina and vitreous levels of MnTnHex-2-PyP 5+ were measured via LC-MS/MS. Latencies of all VEP components (P 1, N 1, P 2, N 2, P 3) were significantly prolonged ( p < 0.05) in EIOP and returned to control levels following all three treatment protocols. Ocular hypertension significantly increased retinal protein nitration ( p < 0.001) which returned to baseline levels in all treated groups. NOS-2 expression and nitrate/nitrite levels were significantly greater in non-treated rats with EIOP. Retinal TUNEL staining showed apoptosis in all ocular hypertensive rats. The presented data confirm the role of oxidative injury in EIOP and highlight the protective effect of MnTnHex-2-PyP 5+ treatment and NOS inhibition in ocular hypertension.