Expression of circadian clock genes in retinal dopaminergic cells

Dorenbos, Ronald; Contini, Massimo; Hirasawa, Hajime; Gustincich, Stefano; Raviola, Elio

doi:10.1017/s0952523807070538

Cited by 51 publications

(38 citation statements)

References 25 publications

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“…Thus, the presence of GABA in the intercellular spaces of the IPL may be essential in counteracting the spillover of signals from the OFF and ON sublaminae, and thus contribute to Roska and Werblin's 'vertical inhibition' between strata. (v) DA cells contain a circadian clock that anticipates predictable variations in retinal illumination [64]. (vi) In addition to dopamine and GABA, DA cells synthesize a large repertory of additional molecules: these include ferritin, the neuropeptide CART, the cytokine IFN-a, the chemokine MCP-1 and the hormone insulin [12], suggesting that a large portion of the DA cell proteome is still uncharacterized.…”

Section: Dopaminergic Amacrine Cells: Retina's Jack Of All Tradesmentioning

confidence: 99%

Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons

Hirasawa

Contini

Raviola

2015

Phil. Trans. R. Soc. B

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One contribution of 16 to a discussion meeting issue 'Release of chemical transmitters from cell bodies and dendrites of nerve cells'. In the mouse retina, dopaminergic amacrine (DA) cells synthesize both dopamine and GABA. Both transmitters are released extrasynaptically and act on neighbouring and distant retinal neurons by volume transmission. In simultaneous recordings of dopamine and GABA release from isolated perikarya of DA cells, a proportion of the events of dopamine and GABA exocytosis were simultaneous, suggesting co-release. In addition, DA cells establish GABAergic synapses onto AII amacrine cells, the neurons that transfer rod bipolar signals to cone bipolars. GABA A but not dopamine receptors are clustered in the postsynaptic membrane. Therefore, dopamine, irrespective of its site of release-synaptic or extrasynaptic-exclusively acts by volume transmission. Dopamine is released upon illumination and sets the gain of retinal neurons for vision in bright light. The GABA released at DA cells' synapses probably prevents signals from the saturated rods from entering the cone pathway when the dark-adapted retina is exposed to bright illumination. The GABA released extrasynaptically by DA and other amacrine cells may set a 'GABAergic tone' in the inner plexiform layer and thus counteract the effects of a spillover of glutamate released at the bipolar cell synapses of adjacent OFF and ON strata, thus preserving segregation of signals between ON and OFF pathways.

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Section: Dopaminergic Amacrine Cells: Retina's Jack Of All Tradesmentioning

confidence: 99%

Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons

Hirasawa

Contini

Raviola

2015

Phil. Trans. R. Soc. B

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“…First, dopamine is implicated in circadian mechanisms including the light input and adaptation in the retina [102,103] and the regulation of specific hormones, such as cortisol, prolactin, and melatonin [104]. The interaction between dopamine and melatonin [105], a major regulator of the circadian rhythm, seems to be closely linked to Parkinson's disease progression [106,107].…”

Section: Sleep-wake Neurobiology In Prodromal Parkinson's Diseasementioning

confidence: 99%

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

Bargiotas

Schuepbach

Bassetti

2016

Current Opinion in Neurology

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Purpose of reviewReview of recent literature pertaining to frequency, associations, mechanisms, and overall significance of sleep-wake disturbances (SWD) in the premotor and early phase of Parkinson's disease.Recent findings SWD are frequent in Parkinson's disease and their prevalence increases with disease progression. Recent studies confirm previous findings that SWD can appear as initial manifestation of Parkinson's disease even decades before motor signs appear and highlight their clinical associations in these early stages. More intriguingly, new evidence underpins their role as risk factors, predictors, or even as driving force for the neurodegenerative process. As our understanding of sleep-wake neurobiology increases, new hypotheses emerge concerning the pathophysiology of SWD in early Parkinson's disease stages involving dopaminergic and nondopaminergic mechanisms. INTRODUCTIONSleep-wake disturbances (SWD) are frequent in Parkinson's disease and are typically attributed to Parkinson's disease medications, poor sleep hygiene, and other nonmotor symptoms (NMS) such as nocturnal akinesia, pain, cramping, and nycturia. Over the past decade, notable advances have been made in the understanding of the role of the dopaminergic system in circadian mechanisms and sleep-wake physiology [1]. In addition, nondopaminergic systems are involved early in the pathogenesis of SWD in Parkinson's disease [2,3]. These findings suggest that SWD are no longer solely a complication of advanced PD but can emerge, among other NMS, in the premotor stages as a primary manifestation of neurodegeneration [4] and increase in frequency with Parkinson's disease progression (Fig. 1). Considering the importance of early diagnosis and intervention, the possibility that SWD may have prognostic value for the development of Parkinson's disease is intriguing.This review will discuss first the most recent literature on SWD in the context of premotor and early stage of Parkinson's disease and then important recent evidence on the pathophysiology of SWD in early Parkinson's disease. SUBJECTIVE SLEEP DISTURBANCES/ INSOMNIATwo thirds of patients with Parkinson's disease report poor sleep quality [5], many of them very early in the course of the disease [6,7]. Recent studies confirm the high prevalence of subjective sleep disturbances in the early stages of Parkinson's disease and highlight their association with low quality of life [8,9&& ,10 && ] and other NMS such as global cognitive impairment, anxiety, depression and nocturia [8]. Individuals later diagnosed with

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“…Among other molecules involved in sleep regulation and dysregulation, dopamine (DA) is a key neurotransmitter involved in up-regulating arousal [9–13], and thus conceptualized as contributing to insomnia and shorter sleep duration [14]. DA also plays a role in the circadian regulation of sleep, which if dysregulated, can also contribute to insomnia complaints [15–17]. …”

Section: Introductionmentioning

confidence: 99%

Sleep onset insomnia, daytime sleepiness and sleep duration in relationship toToxoplasma gondiiIgG seropositivity and serointensity

et al. 2017

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AbstractToxoplasma gondii (T. gondii) infects central nervous tissue and is kept in relative dormancy by a healthy immune system. Sleep disturbances have been found to precipitate mental illness, suicidal behavior and car accidents, which have been previously linked to T. gondii as well. We speculated that if sleep disruption, particularly insomnia, would mediate, at least partly, the link between T. gondii infection and related behavioral dysregulation, then we would be able to identify significant associations between sleep disruption and T. gondii. The mechanisms for such an association may involve dopamine (DA) production by T. gondii, or collateral effects of immune activation necessary to keep T. gondii in check. Sleep questionnaires from 2031 Old Order Amish were analyzed in relationship to T. gondii-IgG antibodies measured by enzyme-linked immunosorbent assay (ELISA). Toxoplasma gondii seropositivity and serointensity were not associated with any of the sleep latency variables or Epworth Sleepiness Scale (ESS). A secondary analysis identified, after adjustment for age group, a statistical trend toward shorter sleep duration in seropositive men (p=0.07). In conclusion, it is unlikely that sleep disruption mediates links between T. gondii and mental illness or behavioral dysregulation. Trending gender differences in associations between T. gondii and shorter sleep need further investigation.

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Expression of circadian clock genes in retinal dopaminergic cells

Cited by 51 publications

References 25 publications

Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons

Extrasynaptic release of GABA and dopamine by retinal dopaminergic neurons

Sleep-wake disturbances in the premotor and early stage of Parkinson's disease

Sleep onset insomnia, daytime sleepiness and sleep duration in relationship toToxoplasma gondiiIgG seropositivity and serointensity

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