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Joelle Lavoie, Martin Beaulieu, Marc Hebert; Possible Implication of Dopamine in ERG Anomalies Reported in Psyciatric Disorders. Invest. Ophthalmol. Vis. Sci. 2011;52(14):3522.
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Electroretinogram (ERG) anomalies have been reported in patients with seasonal affective disorder (SAD) and in young offspring at high risk (HR) to develop schizophrenia or bipolar disorder. Whereas a decrease in rod sensitivity was reported in SAD patients and a reduction in rod b-wave amplitude was observed in HR offspring. Since dopamine dysfunction is hypothesized to be at the origin of many psychiatric disorders, it is believed that these ERG anomalies could be associated with a dopaminergic disruption. The purpose of this study was to investigate if a dopaminergic dysfunction at the levels of D1 or D2 receptors or in the expression of central dopamine could impact the ERG in a similar manner to that observed in SAD patients and HR offspring.
ERGs (DTL fiber, ground in the tail, reference in the mouth) were performed on anesthetized (ketamine-xylazine) dopamine transporter knockout mice (DAT-KO) in which a five-fold increase in extracellular dopamine is observed and in D1 or D2 receptor knockout mice (D1R-KO and D2R-KO). Photopic and scotopic luminance response function protocols were used from which two parameters were derived, namely Vmax, that is the maximal b-wave amplitude observed on the luminance response function and logK interpreted as retinal sensitivity and representing the intensity necessary to reach half of Vmax. Homozygote (HO) knockout mice were paired with wildtype (WT) mice.
A decrease in rod sensitivity was observed in DAT-KO mice (WT = -1.91 log units, HO = -1.78 log units; P = 0.0213) with no change for the cones. D1R-KO mice showed a significant decrease of Vmax in both the photopic (WT = 340.54 µV, HO = 267.05 µV; P = 0.0023) and scotopic ERGs (WT = 491.42 µV, HO = 393.43 µV; P < 0.0001). No change was found in the D2R-KO mice.
Dopamine level and dopaminergic D1 receptor appear to impact the ERG. The decrease in the rod Vmax in D1R-KO mice is similar to the one observed in HR offspring and the decrease in scotopic retinal sensitivity in DAT-KO mice is similar in magnitude to that observed in SAD. These data support the hypothesis that dopamine disruption could be at the origin of the ERG anomalies observed in some psychiatric disorders.
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