In this study, we report that partial unilateral optic nerve crush in the rat affects the number of retinal ganglion cells of the contralateral eye still in continuity with the ipsilateral superior colliculus. The reduction in cell number of the uncrossed retinal projection was accompanied by a microglia response and could be prevented by the local intravitreal application of the anti-inflammatory agent dexamethasone. Interestingly, the level of neuronal activity after optic nerve crush as evidenced by thallium autometallography was enhanced in the termination area of the uncrossed projection, the rostro-medial superior colliculus, suggesting that a dying-back mechanism is not involved. We propose that injury signals from the damaged optic nerve and retina are transduced to the unaffected eye.

SummaryCalneuron-1 and -2 are members of the neuronal calcium-binding protein family (nCaBP). They are transmembrane Calmodulin-like EF-hand Ca 2+ -sensors, and a function in the control of Golgi-to-plasma membrane vesicle trafficking has been assigned to both proteins. In this paper, we describe the distribution of Calneuron-1 in rat and human brains. We show that Calneuron-1 is ubiquitously expressed in all brain regions examined. The protein is most abundant in Purkinje cells of the cerebellum and principal neurons of the cortex and limbic brain whereas no expression in glial cells is apparent. In addition, we identify two novel splice isoforms of Calneuron-1 with extended N-termini. These isoforms are particular abundant in the cerebellum. Taken together, these data set grounds for a better understanding of the cellular function of Calneurons. (J Histochem Cytochem 63:793-804, 2015)