Dynamic encoding of saccade sequences in primate frontal eye field.

The frontal eye field (FEF) is a key part of the oculomotor system, with dominant responses to the direction of single saccades. However, whether and how FEF contributes to sequential saccades remain largely unknown. By training rhesus monkeys to perform saccade sequences, we found sequence-related activities in FEF neurons, whose selectivity to saccade direction undergoes dynamic changes during sequential vs.

Different functional susceptibilities of mouse retinal ganglion cell subtypes to optic nerve crush injury.

In optic neuropathies, the progressive deterioration of retinal ganglion cell (RGC) function leads to irreversible vision loss. Increasing experimental evidence suggests differing susceptibility for RGC functional subtypes. Here with multi-electrode array recordings, RGC functional loss was characterized at multiple time points in a mouse model of optic nerve crush.

Overexpression of Brain-Derived Neurotrophic Factor Protects Large Retinal Ganglion Cells After Optic Nerve Crush in Mice.

Brain-derived neurotrophic factor (BDNF), a neurotrophin essential for neuron survival and function, plays an important role in neuroprotection during neurodegenerative diseases. In this study, we examined whether a modest increase of retinal BDNF promotes retinal ganglion cell (RGC) survival after acute injury of the optic nerve in mice. We adopted an inducible Cre-recombinase transgenic system to up-regulate BDNF in the mouse retina and then examined RGC survival after optic nerve crush by imaging.

Optical Detection of Early Damage in Retinal Ganglion Cells in a Mouse Model of Partial Optic Nerve Crush Injury.

Purpose: Elastic light backscattering spectroscopy (ELBS) has exquisite sensitivity to the ultrastructural properties of tissue and thus has been applied to detect various diseases associated with ultrastructural alterations in their early stages. This study aims to test whether ELBS can detect early damage in retinal ganglion cells (RGCs).

Methods: We used a mouse model of partial optic nerve crush (pONC) to induce rapid RGC death.

Retinal Ganglion Cell Loss is Delayed Following Optic Nerve Crush in NLRP3 Knockout Mice.

The NLRP3 inflammasome, a sensor for a variety of pathogen- and host-derived threats, consists of the adaptor ASC (Apoptosis-associated Speck-like protein containing a Caspase Activation and Recruitment Domain (CARD)), pro-caspase-1, and NLRP3 (NOD-Like Receptor family Pyrin domain containing 3). NLRP3-induced neuroinflammation is implicated in the pathogenesis and progression of eye diseases, but it remains unclear whether activation of NLRP3 inflammasome contributes to retinal ganglion cell (RGC) death. Here we examined NLRP3-induced neuroinflammation and RGC survival following partial optic nerve crush (pONC) injury.

Subtype-dependent Morphological and Functional Degeneration of Retinal Ganglion Cells in Mouse Models of Experimental Glaucoma.

In this short review, Puyang and her colleagues compared the results from three laboratories on the dendritic and functional degeneration of retinal ganglion cells (RGCs) in mouse models of experimental glaucoma [1-4]. Acute or chronic ocular hypertension was induced in mice, and different techniques were applied to identify RGC types. The dendritic alternations of RGCs were examined following the induction of ocular hypertension, and their light response properties were characterized by the multi-electrode array (MEA) recording.

Progressive degeneration of retinal and superior collicular functions in mice with sustained ocular hypertension.

Purpose: We investigated the progressive degeneration of retinal and superior collicular functions in a mouse model of sustained ocular hypertension.

Methods: Focal laser illumination and injection of polystyrene microbeads were used to induce chronic ocular hypertension. Retinal ganglion cell (RGC) loss was characterized by in vivo optical coherence tomography (OCT) and immunohistochemistry.