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We report an observational case study which showed that the rod pathway may have a significant effect on the multifocal electroretinogram (mfERG). A 68-year-old lady diagnosed with Vitamin A deficiency underwent standard ERG and mfERG. ERG rod and cone function were analysed and the first order mfERG responses were determined. At presentation, there was no demonstrable rod function on ERG testing and normal cone function. mfERG P1 amplitude responses were normal but mfERG P1 latency responses were significantly delayed. Four weeks after initiating treatment with intramuscular Vitamin A, ERG rod function significantly improved. However, cone amplitude was reduced and the 30 Hz flicker latencies decreased. Furthermore, mfERG P1 latency returned to normal and interestingly mfERG P1 amplitude responses showed a significant reduction. These results alter our understanding of the mfERG response by indicating that there is a possible inhibitory influence on mfERG responses from rod pathway systems.

The purpose of this study was to document the standard full field electroretinographic (ERG) and wide field multifocal electroretinographic (WF-mfERG) findings in eyes with recent onset hemi-retinal vein occlusion (HRVO) and to compare the electro-diagnostic findings in the affected and fellow eyes with reference to normative data. Eight patients with HRVO were assessed using ERG and WF-mfERG. WF-mfERG first order responses from the affected hemi-retinae and the unaffected hemi-retinae in each affected eye were compared. WF-mfERG responses from each affected hemi-retina and from the symmetrical hemi-retina of each fellow eye were compared. ERG responses between affected and unaffected eyes were also compared. All electrodiagnostic tests were compared to normative data (5-95% confidence limits derived from age-related controls). WF-mfERG P1 and N1 implicit times were greater for the affected hemi-retinae than for the unaffected hemi-retinae (p <0.05). WF-mfERG N1 and P1 implicit times were prolonged (p < 0.05) and WF-mfERG P1/N1 amplitude ratios were significantly reduced (p < 0.05) for the affected eyes when compared with the fellow eyes. Maximal b-wave, cone b-wave and flicker implicit times were prolonged (p < 0.05) when comparing affected and fellow eyes. These results indicate that retinal injury due to HRVO culminates in significant delay of both ERG and WF-mfERG implicit times. These results suggest that WF-mfERG in combination with ERG may have a role in the management of HRVO.

Purpose: To determine the features of wide-field multifocal electroretinography (WF-mfERG) recorded in patients with central retinal vein occlusion (CRVO) and to compare WF-mfERG responses of the affected and fellow eyes. In addition, WF-mfERG responses were also compared by using standard electroretinography (ERG)., Methods: WF-mfERG and ERG responses were recorded from both eyes of 56 patients with CRVO. The WF-mfERG responses, obtained using a custom-built system were grouped into central and peripheral rings. The P1 amplitudes, and P1 and N1 implicit times were grouped and averaged within both rings. Nonparametric statistical analysis was used to compare the ERG results from the affected and fellow eyes. The results were also compared with normative data (5% to 95% confidence limits)., Results: CRVO markedly affected all the parameters of the WF-mfERG. In the affected eyes, 98% of the central and 91% of the peripheral P1 implicit times fell outside the normal range, as opposed to 35% of the 30-Hz flicker implicit times. The WF-mfERG responses obtained from eyes with CRVO were significantly different (P<0.01) from those derived from the fellow eye. The central and peripheral P1 implicit times were also abnormal in 59.2% and 46.9% of the fellow eyes, respectively., Conclusions: WF-mfERG is more susceptible than the standard ERG to changes in the nonlinear dynamics of the eye due to the multiple frequencies of stimulation used to record WF-mfERG responses. WF-mfERG could be a sensitive indicator of the underlying disease affecting the retina in eyes with CRVO and may have a role in the clinical setting.

The aim of this study was to confirm the existence of and identify the receptor subtypes for neuropeptide Y that are present post-junctionally in myocardium. The effects of the selective agonists, [Leu31, Pro34] neuropeptide Y (neuropeptide Y Y1 receptors), neuropeptide Y-(13-36) and peptide YY-(3-36) (neuropeptide Y Y2 receptors), and neuropeptide Y and the related peptide YY, which have differential action at neuropeptide Y Y3 receptors, on amplitudes of contraction of adult rat ventricular cardiomyocytes were studied. Also, the effect of the neuropeptide Y Y1-selective antagonist, bis(31/31')[[Cys31, Trp32, Nva34] neuropeptide Y-(31-36)] on neuropeptide Y-mediated changes in myocyte contraction was investigated. Neuropeptide Y, peptide YY, neuropeptide Y-(13-36) and peptide YY-(3-36) attenuated the isoprenaline (10(-7) M)-stimulated contractile response, and the EC50 values were 9.0 x 10(-9), 4.3 x 10(-10), 3.1 x 10(-11) and 8.5 x 10(-11) M, respectively. [Leu31, Pro34] neuropeptide Y increased the contractile response of cardiomyocytes, and the EC50 values were 8.1 x 10(-9) and 1.5 x 10(-9) M, in the absence and presence of isoprenaline, respectively. Since [Leu31, Pro34] neuropeptide Y caused a positive effect on ventricular myocyte contraction and neuropeptide Y-(13-36) and peptide YY (3-36) produced the most potent negative effects, it is proposed that both neuropeptide Y Y1 and neuropeptide Y Y2 receptors, linked respectively to the positive and negative responses, are expressed in cardiomyocytes. The finding of receptors with neuropeptide Y Y2 characteristics on cardiomyocytes represents a further example of a postjunctional location for this subtype. As there was no significant discrepancy between the potencies of peptide YY and neuropeptide Y to attenuate the contractile response, it appears that neuropeptide Y Y3-like receptors are not linked principally to contractile function in rat cardiomyocytes. Bis(31/31')[[Cys31, Trp32, Nva34] neuropeptide Y-(31-36)] antagonised the neuropeptide Y-mediated stimulation of contractile activity through neuropeptide Y Y1 receptors, but the compound also inhibited the attenuation of isoprenaline-stimulated contraction, apparently by acting as a partial agonist at the neuropeptide Y Y2 receptors.