Dopamine differentially affects retinal circuits to shape the retinal code.

Dopamine has long been reported to enhance antagonistic surrounds of retinal ganglion cells (RGCs). Yet, the retina contains many different RGC subtypes and the effects of dopamine can be subtype-specific. Using multielectrode array (MEA) recordings we investigated how dopamine shapes the receptive fields of RGCs in the mouse retina.

Topographic Variations in Retinal Encoding of Visual Space.

A retina completely devoid of topographic variations would be homogenous, encoding any given feature uniformly across the visual field. In a naive view, such homogeneity would appear advantageous. However, it is now clear that retinal topographic variations exist across mammalian species in a variety of forms and patterns.

Inhomogeneous Encoding of the Visual Field in the Mouse Retina.

Stimulus characteristics of the mouse's visual field differ above and below the skyline. Here, we show for the first time that retinal ganglion cells (RGCs), the output neurons of the retina, gradually change their functional properties along the ventral-dorsal axis to allow better representation of the different stimulus characteristics. We conducted two-photon targeted recordings of transient-Offα-RGCs and found that they gradually became more sustained along the ventral-dorsal axis, revealing >5-fold-longer duration responses in the dorsal retina.

Involvement of aberrant calcium signalling in herpetic neuralgia.

Alpha-herpesviruses, herpes simplex viruses (HSV) and varicella zoster virus (VZV), are pathogens of the peripheral nervous system. After primary infection, these viruses establish latency within sensory ganglia, while retaining the ability to reactivate. Reactivation of VZV results in herpes zoster, a condition characterized by skin lesions that leads to post-herpetic neuralgia.

Glutamate release from satellite glial cells of the murine trigeminal ganglion.

It has been proposed that glutamate serves as a mediator between neurons and satellite glial cells (SGCs) in sensory ganglia and that SGCs release glutamate. Using a novel method, we studied glutamate release from SGCs from murine trigeminal ganglia. Sensory neurons with adhering SGCs were enzymatically isolated from wild type and transgenic mice in which vesicular exocytosis was suppressed in glial cells.

Satellite glial cells in dorsal root ganglia are activated in experimental autoimmune encephalomyelitis.

Pain is a serious and common problem with patients suffering from multiple sclerosis (MS). Very little has been done to investigate the peripheral mechanisms of pain in MS. Here we used a mouse model of experimental autoimmune encephalomyelitis (EAE) to investigate the possible contribution of satellite glial cells (SGCs) to pain in MS.