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In a screen to identify genes that are expressed differentially in the retina after partial optic nerve crush, we identified MAP1B as an up-regulated transcript. Western blot analysis of inner retina protein preparations confirmed changes in the protein composition of the microtubule-associated cytoskeleton of crushed vs. uncrushed nerve. MAP1B immunoreactivity and transcript levels were elevated for two weeks after crush. Immunostaining and Western blots with monoclonal antibodies directed against developmentally regulated phosphorylation sites on MAP1B revealed a gradient of MAP1B phosphorylation from the proximal optic nerve stump to the soma of retinal ganglion cells. Most interestingly, using antibodies directed against developmentally regulated phosphorylation sites on MAP1B, we observed that a significant number of crushed optic nerve axons develop MAP1B-immunopositive growth cones, which cross the crush site and migrate along the distal nerve fragment. In parallel, an abnormal distribution of highly phosphorylated neurofilament protein (pNF-H) in the cell soma and dendrites of presumably axotomized retinal ganglion cells was observed following partial nerve crush. This redistribution is present for the period between day 7 and 28 postcrush and is not seen in cells that stay connected to the superior colliculus. Axotomized ganglion cells, which contain pNF-H in soma and dendrites appear to have been disconnected from the colliculus at an early stage but survive axonal trauma for long periods.

Neurons in primary visual cortex (V1) respond preferentially to stimuli of a particular orientation falling within a circumscribed region of visual space known as their receptive field (RF). However, the response to an optimally oriented stimulus presented within the RF can be enhanced by the simultaneous presentation of co-oriented, co-linearly aligned flank stimuli falling outside the RF which, when presented alone, fail to activate the cell. This type of contextual effect, termed colinear facilitation, presumably forms the physiological substrate for the integration of the line elements of a contour and the perceptual saliency of a contour in a complex environment. Here we show that colinear facilitation in single cells of cat area V1 can be substantially reduced or abolished by focal inactivation of laterally remote cells in the same area which respond strongly to the co-oriented, colinear flank stimulus inducing the facilitatory effect. The results provide evidence that horizontal intrinsic connections between cells with co-oriented and co-linearly aligned RFs make a major contribution to colinear facilitation in V1. They imply that the neuronal circuitry underlying contour integration and saliency is already present at the earliest stage of visual cortical information processing.

Individuals suffering from classical migraine report an astonishing diversity of migraine auras. A frequently reported symptom is a visual hallucination known as fortification illusion (FI). Here we demonstrate that the typical zig-zag pattern of the FI can be reproduced using experimental data of orientation maps of the primary visual cortex (V1) assuming that a continuous excitation front propagates across V1. We put forward a model in which the cortical neurons within this excitation wave are activated sufficiently to contribute to conscious perception. It is shown that the discontinuous repetitive nature of the zig-zag pattern of the FI can reflect the specific layout of visual cortical orientation maps. Additionally, dynamic features of the FI are predicted based on our model.