The Electroretinogram as a Biomarker of Central Dopamine and Serotonin: Potential Relevance to Psychiatric Disorders

Lavoie, Jessie R.; Illiano, Placido; Sotnikova, Tatyana D.; Gainetdinov, Raul R.; Beaulieu, Jean‐Martin; Hébert, Marc

doi:10.1016/j.biopsych.2012.11.024

Cited by 84 publications

(69 citation statements)

References 52 publications

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“…and cats 42 and by genetic KO in mice, 43,44 but is opposite that which is seen in rabbits. 45 We also found that suppression of the b-wave and summed OP amplitudes by the D1R antagonist SCH39166 resembled the ERG phenotype of the D1R-KO mice.…”

Section: D1r-dependent Mechanism Of Apomorphine In Myopiamentioning

confidence: 86%

Dopamine D1 Receptors Contribute Critically to the Apomorphine-Induced Inhibition of Form-Deprivation Myopia in Mice

Huang

Zhang

Wang

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To determine the roles of dopamine D2 receptors (D2Rs) and dopamine D1 receptors (D1Rs) in the inhibition of form-deprivation myopia (FDM) by the nonselective dopamine agonist apomorphine (APO) in D2R-knockout (D2R-KO) and D1R-KO mice. METHODS.Retinal layer thicknesses and electroretinograms (ERGs) were analyzed in KO mice and in D2R and D1R antagonist-treated mice. D2R-KO or D1R-KO mice and wild-type (WT) littermates were subjected to form deprivation during postnatal weeks 5 to 8. Both groups were intraperitoneally injected daily with either APO (5 lg/g body weight) dissolved in 1 lg/ lL ascorbic acid or vehicle alone. Refraction, vitreous chamber depth (VCD), and axial length (AL), among other parameters, were measured prior to and at the end of the treatment period.RESULTS. The retinal layer thicknesses and ERGs in KO mice were similar to those treated with D2R and D1R antagonists. APO administration in WT mice inhibited the development of FDM by approximately 80%. FDM in D2R-KO mice was inhibited approximately 50% compared with WT mice and was further inhibited by APO to a level similar to that in APO-treated WT mice. FDM development in D1R-KO mice was similar to that in WT mice and was not affected by APO administration. The changes in VCD and AL were consistent with refraction data.CONCLUSIONS. In mice, APO-mediated FDM inhibition was abolished by D1R KO but not D2R KO. This indicates the specificity of D1Rs for the pharmacologic inhibitory effect of APO on FDM and a nonessential role of D2Rs in this process in mice.

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Section: D1r-dependent Mechanism Of Apomorphine In Myopiamentioning

confidence: 86%

Dopamine D1 Receptors Contribute Critically to the Apomorphine-Induced Inhibition of Form-Deprivation Myopia in Mice

Huang

Zhang

Wang

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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“…This mutation results in a reduction of brain 5-HT synthesis by B40% in R/H heterozygous (HET) and B80% in H/H homozygous (HO) animals (Beaulieu et al, 2008). Tph2-KI mice replicate alterations in mood disorder and serotonin-related biomarkers observed in human pathologies (Jacobsen et al, 2012b;Lavoie et al, 2013), which provide the opportunity to use R439H Tph2-KI mice as a model with construct, face, and predictive validity to investigate consequences of 5-HT depletions (Dzirasa et al, 2013;Jacobsen et al, 2012a).…”

Section: Introductionmentioning

confidence: 99%

Stimulation of 5-HT2C Receptors Improves Cognitive Deficits Induced by Human Tryptophan Hydroxylase 2 Loss of Function Mutation

Del’Guidice

Lemay

Lemasson

et al. 2013

Neuropsychopharmacol

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Polymorphisms in the gene encoding the serotonin synthesis enzyme Tph2 have been identified in mental illnesses, including bipolar disorder, major depression, autism, schizophrenia, and ADHD. Deficits in cognitive flexibility and perseverative behaviors are shared common symptoms in these disorders. However, little is known about the impact of Tph2 gene variants on cognition. Mice expressing a human TPH2 variant (Tph2-KI) were used to investigate cognitive consequences of TPH2 loss of function and pharmacological treatments. We applied a recently developed behavioral assay, the automated H-maze, to study cognitive functions in Tph2-KI mice. This assay involves the consecutive discovery of three different rules: a delayed alternation task, a non-alternation task, and a delayed reversal task. Possible contribution of locomotion, reward, and sensory perception were also investigated. The expression of loss-of-function mutant Tph2 in mice was associated with impairments in reversal learning and cognitive flexibility, accompanied by perseverative behaviors similar to those observed in human clinical studies. Pharmacological restoration of 5-HT synthesis with 5-hydroxytryptophan or treatment with the 5-HT 2C receptor agonist CP809.101 reduced cognitive deficits in Tph2-KI mice and abolished perseveration. In contrast, treatment with the psychostimulant methylphenidate exacerbated cognitive deficits in mutant mice. Results from this study suggest a contribution of TPH2 in the regulation of cognition. Furthermore, identification of a role for a 5-HT 2 receptor agonist as a cognition-enhancing agent in mutant mice suggests a potential avenue to explore for the personalized treatment of cognitive symptoms in humans with reduced 5-HT synthesis and TPH2 polymorphisms.

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“…, n=3) in photopic and scotopic conditions to assess the cone and rod systems activity, respectively, according to a previously described procedure (Lavoie et al, 2014). Detailed information is available in supplementary Materials and Methods.…”

Section: Erg Recording and Analysismentioning

confidence: 99%

Retinal development anomalies and cone photoreceptors degeneration upon Bmi1 deficiency

et al. 2016

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Retinal development occurs through the sequential but overlapping generation of six types of neuronal cells and one glial cell type. Of these, rod and cone photoreceptors represent the functional unit of light detection and phototransduction and are frequently affected in retinal degenerative diseases. During mouse development, the Polycomb group protein Bmi1 is expressed in immature retinal progenitors and differentiated retinal neurons, including cones. We show here that Bmi1 is required to prevent post natal degeneration of cone photoreceptors and bipolar neurons and that inactivation of Chk2 or p53 could improve but not overcome cone degeneration in Bmi1 −/− mice. The retinal phenotype of Bmi1 −/− mice was also characterized by loss of heterochromatin, activation of tandem repeats, oxidative stress and Rip3-associated necroptosis. In the human retina, BMI1 was preferentially expressed in cones at heterochromatic foci. BMI1 inactivation in human embryonic stem cells was compatible with retinal induction but impaired cone terminal differentiation. Despite this developmental arrest, BMI1-deficient cones recapitulated several anomalies observed in Bmi1 −/− photoreceptors, such as loss of heterochromatin, activation of tandem repeats and induction of p53, revealing partly conserved biological functions between mouse and man.

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The Electroretinogram as a Biomarker of Central Dopamine and Serotonin: Potential Relevance to Psychiatric Disorders

Cited by 84 publications

References 52 publications

Dopamine D1 Receptors Contribute Critically to the Apomorphine-Induced Inhibition of Form-Deprivation Myopia in Mice

Dopamine D1 Receptors Contribute Critically to the Apomorphine-Induced Inhibition of Form-Deprivation Myopia in Mice

Stimulation of 5-HT2C Receptors Improves Cognitive Deficits Induced by Human Tryptophan Hydroxylase 2 Loss of Function Mutation

Retinal development anomalies and cone photoreceptors degeneration upon Bmi1 deficiency

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